TY  - JOUR
AU  - Lazarević, Milica
AU  - Battaglia, Giuseppe
AU  - Jevtić, Bojan
AU  - Nikolovski, Neda
AU  - Bruno, Valeria
AU  - Cavalli, Eugenio
AU  - Miljković, Đorđe
AU  - Nicoletti, Ferdinando
AU  - Momčilović, Miljana
AU  - Fagone, Paolo
PY  - 2020
UR  - https://www.mdpi.com/2076-3921/9/7/608
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32664399
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3819
AB  - The aim of this study was to examine the in vitro effects of the slow-releasing H2S donor GYY4137 on the immune cells involved in the pathogenesis of the central nervous system (CNS) autoimmune disease, multiple sclerosis (MS). GYY4137 specifically potentiated TGF-β expression and production in dendritic cells and significantly reduced IFN-γ and IL-17 production in the lymph node and spinal cord T cells obtained from mice immunized with CNS antigens. Both the proportion of FoxP3+ regulatory CD4+ T cells in the lymph node cells, and the percentage of IL-17+ CD4+ T cells in the spinal cord cells were reduced upon culturing with GYY4137. Interestingly, the peripheral blood mononuclear cells obtained from the MS patients had a lower expression of the H2S-producing enzyme, 3-mercaptopyruvate-sulfurtransferase (MPST), in comparison to those obtained from healthy donors. A significant inverse correlation between the expression of MPST and several pro-inflammatory factors was also observed. Further studies on the relevance of the observed results for the pathogenesis and therapy of MS are warranted.
PB  - MDPI AG
T2  - Antioxidants (Basel, Switzerland)
T2  - Antioxidants (Basel, Switzerland)
T1  - Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis.
IS  - 7
VL  - 9
DO  - 10.3390/antiox9070608
SP  - 608
ER  - 

@article{
author = "Lazarević, Milica and Battaglia, Giuseppe and Jevtić, Bojan and Nikolovski, Neda and Bruno, Valeria and Cavalli, Eugenio and Miljković, Đorđe and Nicoletti, Ferdinando and Momčilović, Miljana and Fagone, Paolo",
year = "2020",
abstract = "The aim of this study was to examine the in vitro effects of the slow-releasing H2S donor GYY4137 on the immune cells involved in the pathogenesis of the central nervous system (CNS) autoimmune disease, multiple sclerosis (MS). GYY4137 specifically potentiated TGF-β expression and production in dendritic cells and significantly reduced IFN-γ and IL-17 production in the lymph node and spinal cord T cells obtained from mice immunized with CNS antigens. Both the proportion of FoxP3+ regulatory CD4+ T cells in the lymph node cells, and the percentage of IL-17+ CD4+ T cells in the spinal cord cells were reduced upon culturing with GYY4137. Interestingly, the peripheral blood mononuclear cells obtained from the MS patients had a lower expression of the H2S-producing enzyme, 3-mercaptopyruvate-sulfurtransferase (MPST), in comparison to those obtained from healthy donors. A significant inverse correlation between the expression of MPST and several pro-inflammatory factors was also observed. Further studies on the relevance of the observed results for the pathogenesis and therapy of MS are warranted.",
publisher = "MDPI AG",
journal = "Antioxidants (Basel, Switzerland), Antioxidants (Basel, Switzerland)",
title = "Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis.",
number = "7",
volume = "9",
doi = "10.3390/antiox9070608",
pages = "608"
}

Lazarević, M., Battaglia, G., Jevtić, B., Nikolovski, N., Bruno, V., Cavalli, E., Miljković, Đ., Nicoletti, F., Momčilović, M.,& Fagone, P.. (2020). Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis.. in Antioxidants (Basel, Switzerland)
MDPI AG., 9(7), 608.
https://doi.org/10.3390/antiox9070608

Lazarević M, Battaglia G, Jevtić B, Nikolovski N, Bruno V, Cavalli E, Miljković Đ, Nicoletti F, Momčilović M, Fagone P. Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis.. in Antioxidants (Basel, Switzerland). 2020;9(7):608.
doi:10.3390/antiox9070608 .

Lazarević, Milica, Battaglia, Giuseppe, Jevtić, Bojan, Nikolovski, Neda, Bruno, Valeria, Cavalli, Eugenio, Miljković, Đorđe, Nicoletti, Ferdinando, Momčilović, Miljana, Fagone, Paolo, "Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis." in Antioxidants (Basel, Switzerland), 9, no. 7 (2020):608,
https://doi.org/10.3390/antiox9070608 . .

TY  - JOUR
AU  - Mijatović, Sanja
AU  - Bramanti, Alessia
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Kaluđerović, Goran N.
AU  - Maksimović-Ivanić, Danijela
PY  - 2018
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0734975018300739
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29656090
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3045
AB  - Differentiation of cancer cells entails the reversion of phenotype from malignant to the original. The conversion to cell type characteristic for another tissue is named transdifferentiation. Differentiation/transdifferentiation of malignant cells in high grade tumor mass could serve as a nonaggressive approach that potentially limits tumor progression and augments chemosensitivity. While this therapeutic strategy is already being used for treatment of hematological cancers, its feasibility for solid malignancies is still debated. We will presently discuss the natural compounds that show these properties, with focus on anthraquinones from Aloe vera, Senna, Rheum sp. and hop derived prenylflavonoids.
T2  - Biotechnology Advances
T1  - Naturally occurring compounds in differentiation based therapy of cancer.
DO  - 10.1016/j.biotechadv.2018.04.001
ER  - 

@article{
author = "Mijatović, Sanja and Bramanti, Alessia and Nicoletti, Ferdinando and Fagone, Paolo and Kaluđerović, Goran N. and Maksimović-Ivanić, Danijela",
year = "2018",
abstract = "Differentiation of cancer cells entails the reversion of phenotype from malignant to the original. The conversion to cell type characteristic for another tissue is named transdifferentiation. Differentiation/transdifferentiation of malignant cells in high grade tumor mass could serve as a nonaggressive approach that potentially limits tumor progression and augments chemosensitivity. While this therapeutic strategy is already being used for treatment of hematological cancers, its feasibility for solid malignancies is still debated. We will presently discuss the natural compounds that show these properties, with focus on anthraquinones from Aloe vera, Senna, Rheum sp. and hop derived prenylflavonoids.",
journal = "Biotechnology Advances",
title = "Naturally occurring compounds in differentiation based therapy of cancer.",
doi = "10.1016/j.biotechadv.2018.04.001"
}

Mijatović, S., Bramanti, A., Nicoletti, F., Fagone, P., Kaluđerović, G. N.,& Maksimović-Ivanić, D.. (2018). Naturally occurring compounds in differentiation based therapy of cancer.. in Biotechnology Advances.
https://doi.org/10.1016/j.biotechadv.2018.04.001

Mijatović S, Bramanti A, Nicoletti F, Fagone P, Kaluđerović GN, Maksimović-Ivanić D. Naturally occurring compounds in differentiation based therapy of cancer.. in Biotechnology Advances. 2018;.
doi:10.1016/j.biotechadv.2018.04.001 .

Mijatović, Sanja, Bramanti, Alessia, Nicoletti, Ferdinando, Fagone, Paolo, Kaluđerović, Goran N., Maksimović-Ivanić, Danijela, "Naturally occurring compounds in differentiation based therapy of cancer." in Biotechnology Advances (2018),
https://doi.org/10.1016/j.biotechadv.2018.04.001 . .

TY  - JOUR
AU  - Nikolić, Ivana
AU  - Stojanović, Ivana D.
AU  - Vujičić, Milica
AU  - Fagone, Paolo
AU  - Mangano, Katia
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
AU  - Saksida, Tamara
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0171298516303746
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2484
AB  - Bovine colostrum is a rich source of nutrients and immunologically active components that play a role in conveying passive immunity to the offspring, protection and maturation of new-born's gastrointestinal tract. Colostrum has exerted positive effects in diseases affecting gastrointestinal tract, as well as type 2 diabetes (T2D). However, health-promoting effects in type 1 diabetes have not been reported. The aim of this study was to investigate therapeutic value of oral administration of standardized bovine colostrum derivative (SBCD) in three models of type 1 diabetes (T1D): spontaneously developed T1D in NOD mice and BB-DP rats, and in chemically induced T1D in C57BL/6 mice with multiple low doses of streptozotocin (MLDS). SBCD was administered per os and the disease development was evaluated by weekly measurement of blood glucose and by histological analyses of the pancreas. SBCD administration prevented diabetes development in all three models, as indicated by euglicaemia. Ex vivo analysis of cytokine expression and production in the spleen and mesenteric lymph nodes (MLN) in MLDS challenged mice revealed a strong modulation of the immune response. In the MLN cells SBCD disrupted harmful Th17 response induced by MLDS. Expression of Th1 signature cytokine IFN-γ was down-regulated in MLN cells of SBCD-treated mice, while IL-4 secretion (Th2 cytokine) was up-regulated in comparison to diabetic group. Modulation of the immune response seen in the MLN protruded to the spleen, giving overall less infiltration of immune cells to the pancreas. SBCD acted on immune cells and halted (auto) aggression towards pancreatic beta cells. Moreover, SBCD induced beta cell proliferation. Hence, this derivative could be tested in diabetes and other similar diseases with aberrant immune response.
T2  - Immunobiology
T1  - Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents
IS  - 2
VL  - 222
DO  - 10.1016/j.imbio.2016.09.013
SP  - 272
EP  - 279
ER  - 

@article{
author = "Nikolić, Ivana and Stojanović, Ivana D. and Vujičić, Milica and Fagone, Paolo and Mangano, Katia and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando and Saksida, Tamara",
year = "2017",
abstract = "Bovine colostrum is a rich source of nutrients and immunologically active components that play a role in conveying passive immunity to the offspring, protection and maturation of new-born's gastrointestinal tract. Colostrum has exerted positive effects in diseases affecting gastrointestinal tract, as well as type 2 diabetes (T2D). However, health-promoting effects in type 1 diabetes have not been reported. The aim of this study was to investigate therapeutic value of oral administration of standardized bovine colostrum derivative (SBCD) in three models of type 1 diabetes (T1D): spontaneously developed T1D in NOD mice and BB-DP rats, and in chemically induced T1D in C57BL/6 mice with multiple low doses of streptozotocin (MLDS). SBCD was administered per os and the disease development was evaluated by weekly measurement of blood glucose and by histological analyses of the pancreas. SBCD administration prevented diabetes development in all three models, as indicated by euglicaemia. Ex vivo analysis of cytokine expression and production in the spleen and mesenteric lymph nodes (MLN) in MLDS challenged mice revealed a strong modulation of the immune response. In the MLN cells SBCD disrupted harmful Th17 response induced by MLDS. Expression of Th1 signature cytokine IFN-γ was down-regulated in MLN cells of SBCD-treated mice, while IL-4 secretion (Th2 cytokine) was up-regulated in comparison to diabetic group. Modulation of the immune response seen in the MLN protruded to the spleen, giving overall less infiltration of immune cells to the pancreas. SBCD acted on immune cells and halted (auto) aggression towards pancreatic beta cells. Moreover, SBCD induced beta cell proliferation. Hence, this derivative could be tested in diabetes and other similar diseases with aberrant immune response.",
journal = "Immunobiology",
title = "Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents",
number = "2",
volume = "222",
doi = "10.1016/j.imbio.2016.09.013",
pages = "272-279"
}

Nikolić, I., Stojanović, I. D., Vujičić, M., Fagone, P., Mangano, K., Stošić-Grujičić, S., Nicoletti, F.,& Saksida, T.. (2017). Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents. in Immunobiology, 222(2), 272-279.
https://doi.org/10.1016/j.imbio.2016.09.013

Nikolić I, Stojanović ID, Vujičić M, Fagone P, Mangano K, Stošić-Grujičić S, Nicoletti F, Saksida T. Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents. in Immunobiology. 2017;222(2):272-279.
doi:10.1016/j.imbio.2016.09.013 .

Nikolić, Ivana, Stojanović, Ivana D., Vujičić, Milica, Fagone, Paolo, Mangano, Katia, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, Saksida, Tamara, "Standardized bovine colostrum derivative impedes development of type 1 diabetes in rodents" in Immunobiology, 222, no. 2 (2017):272-279,
https://doi.org/10.1016/j.imbio.2016.09.013 . .

TY  - JOUR
AU  - Maksimović-Ivanić, Danijela
AU  - Fagone, Paolo
AU  - McCubrey, James
AU  - Bendtzen, Klaus
AU  - Mijatović, Sanja
AU  - Nicoletti, Ferdinando
PY  - 2017
UR  - http://doi.wiley.com/10.1002/ijc.30529
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2553
AB  - The possible use of HIV protease inhibitors (HIV-PI) as new therapeutic option for the treatment of cancer primarily originated from their success in treating HIV-related Kaposi's sarcoma (KS). While these findings were initially attributed to immune reconstitution and better control of oncogenic viral infections, the number of reports on solid tumors, KS, lymphoma, fibrosarcoma, multiple myeloma and prostate cancer suggest other mechanisms for the anti-neoplastic activity of PIs. However, a major drawback for the possible adoption of HIV-PIs in the therapy of cancer relies on their relatively weak anticancer potency and important side effects. This has propelled several groups to generate derivatives of HIV-PIs for anticancer use, through modifications such as attachment of different moieties, ligands and transporters, including saquinavir-loaded folic acid conjugated nanoparticles and nitric oxide (NO) derivatives of HIV-PIs. In this article, we discuss the current preclinical and clinical evidences for the potential use of HIV-PIs, and of novel derivatives, such as saquinavir-NO in the treatment of cancer.
T2  - International Journal of Cancer
T1  - HIV-protease inhibitors for the treatment of cancer: Repositioning HIV protease inhibitors while developing more potent NO-hybridized derivatives?
DO  - 10.1002/ijc.30529
ER  - 

@article{
author = "Maksimović-Ivanić, Danijela and Fagone, Paolo and McCubrey, James and Bendtzen, Klaus and Mijatović, Sanja and Nicoletti, Ferdinando",
year = "2017",
abstract = "The possible use of HIV protease inhibitors (HIV-PI) as new therapeutic option for the treatment of cancer primarily originated from their success in treating HIV-related Kaposi's sarcoma (KS). While these findings were initially attributed to immune reconstitution and better control of oncogenic viral infections, the number of reports on solid tumors, KS, lymphoma, fibrosarcoma, multiple myeloma and prostate cancer suggest other mechanisms for the anti-neoplastic activity of PIs. However, a major drawback for the possible adoption of HIV-PIs in the therapy of cancer relies on their relatively weak anticancer potency and important side effects. This has propelled several groups to generate derivatives of HIV-PIs for anticancer use, through modifications such as attachment of different moieties, ligands and transporters, including saquinavir-loaded folic acid conjugated nanoparticles and nitric oxide (NO) derivatives of HIV-PIs. In this article, we discuss the current preclinical and clinical evidences for the potential use of HIV-PIs, and of novel derivatives, such as saquinavir-NO in the treatment of cancer.",
journal = "International Journal of Cancer",
title = "HIV-protease inhibitors for the treatment of cancer: Repositioning HIV protease inhibitors while developing more potent NO-hybridized derivatives?",
doi = "10.1002/ijc.30529"
}

Maksimović-Ivanić, D., Fagone, P., McCubrey, J., Bendtzen, K., Mijatović, S.,& Nicoletti, F.. (2017). HIV-protease inhibitors for the treatment of cancer: Repositioning HIV protease inhibitors while developing more potent NO-hybridized derivatives?. in International Journal of Cancer.
https://doi.org/10.1002/ijc.30529

Maksimović-Ivanić D, Fagone P, McCubrey J, Bendtzen K, Mijatović S, Nicoletti F. HIV-protease inhibitors for the treatment of cancer: Repositioning HIV protease inhibitors while developing more potent NO-hybridized derivatives?. in International Journal of Cancer. 2017;.
doi:10.1002/ijc.30529 .

Maksimović-Ivanić, Danijela, Fagone, Paolo, McCubrey, James, Bendtzen, Klaus, Mijatović, Sanja, Nicoletti, Ferdinando, "HIV-protease inhibitors for the treatment of cancer: Repositioning HIV protease inhibitors while developing more potent NO-hybridized derivatives?" in International Journal of Cancer (2017),
https://doi.org/10.1002/ijc.30529 . .

TY  - JOUR
AU  - Maksimović-Ivanić, Danijela
AU  - Mojić, Marija
AU  - Bulatović, Mirna Z.
AU  - Radojkovic, Milica
AU  - Kuzmanovic, Milos
AU  - Ristic, Slobodan
AU  - Stošić-Grujičić, Stanislava
AU  - Miljković, Đorđe
AU  - Cavalli, Eugenio
AU  - Libra, Massimo
AU  - Fagone, Paolo
AU  - McCubrey, James
AU  - Nicoletti, Ferdinando
AU  - Mijatović, Sanja
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2353
AB  - Covalent attachment of NO to the first approved HIV protease inhibitor
   Saquinavir (Saq-NO) expands the therapeutic potential of the original
   drug. Apart from retained antiviral activity, the modified drug exerts
   strong antitumor effects and lower toxicity. In the present study, we
   have evaluated the sensitivity of different hematological malignancies
   to Saq-NO. Saq-NO efficiently diminished the viability of Jurkat, Raji,
   HL-60 and K562 cells. While Jurkat and Raji cells (established from
   pediatric patients) displayed abrogated proliferative potential, HL-60
   and K652 cells (originated from adults) exposed to Saq-NO treatment
   underwent caspase dependent apoptosis. In addition, similar sensitivity
   to Saq-NO was observed in mononuclear blood cells obtained from
   pediatric patients with acute lymphoblastic leukemia (ALL) and adult
   patients with acute myeloid leukemia (AML). Western blot analysis
   indicated p70S6 kinase as a possible intracellular target of Saq-NO
   action. Moreover, the addition of a NO moiety to Lopinavir resulted in
   improved antitumor potential as compared to the parental compound,
   suggesting that NO-derived HIV protease inhibitors are a potential new
   source of anticancer drugs with unique mode of action. (C) 2015 Elsevier
   Ltd. All rights reserved.
T2  - Leukemia Research
T1  - The NO-modified HIV protease inhibitor as a valuable drug for
 hematological malignancies: Role of p70S6K
IS  - 10
VL  - 39
DO  - 10.1016/j.leukres.2015.06.013
SP  - 1088
EP  - 1095
ER  - 

@article{
author = "Maksimović-Ivanić, Danijela and Mojić, Marija and Bulatović, Mirna Z. and Radojkovic, Milica and Kuzmanovic, Milos and Ristic, Slobodan and Stošić-Grujičić, Stanislava and Miljković, Đorđe and Cavalli, Eugenio and Libra, Massimo and Fagone, Paolo and McCubrey, James and Nicoletti, Ferdinando and Mijatović, Sanja",
year = "2015",
abstract = "Covalent attachment of NO to the first approved HIV protease inhibitor
   Saquinavir (Saq-NO) expands the therapeutic potential of the original
   drug. Apart from retained antiviral activity, the modified drug exerts
   strong antitumor effects and lower toxicity. In the present study, we
   have evaluated the sensitivity of different hematological malignancies
   to Saq-NO. Saq-NO efficiently diminished the viability of Jurkat, Raji,
   HL-60 and K562 cells. While Jurkat and Raji cells (established from
   pediatric patients) displayed abrogated proliferative potential, HL-60
   and K652 cells (originated from adults) exposed to Saq-NO treatment
   underwent caspase dependent apoptosis. In addition, similar sensitivity
   to Saq-NO was observed in mononuclear blood cells obtained from
   pediatric patients with acute lymphoblastic leukemia (ALL) and adult
   patients with acute myeloid leukemia (AML). Western blot analysis
   indicated p70S6 kinase as a possible intracellular target of Saq-NO
   action. Moreover, the addition of a NO moiety to Lopinavir resulted in
   improved antitumor potential as compared to the parental compound,
   suggesting that NO-derived HIV protease inhibitors are a potential new
   source of anticancer drugs with unique mode of action. (C) 2015 Elsevier
   Ltd. All rights reserved.",
journal = "Leukemia Research",
title = "The NO-modified HIV protease inhibitor as a valuable drug for
 hematological malignancies: Role of p70S6K",
number = "10",
volume = "39",
doi = "10.1016/j.leukres.2015.06.013",
pages = "1088-1095"
}

Maksimović-Ivanić, D., Mojić, M., Bulatović, M. Z., Radojkovic, M., Kuzmanovic, M., Ristic, S., Stošić-Grujičić, S., Miljković, Đ., Cavalli, E., Libra, M., Fagone, P., McCubrey, J., Nicoletti, F.,& Mijatović, S.. (2015). The NO-modified HIV protease inhibitor as a valuable drug for
 hematological malignancies: Role of p70S6K. in Leukemia Research, 39(10), 1088-1095.
https://doi.org/10.1016/j.leukres.2015.06.013

Maksimović-Ivanić D, Mojić M, Bulatović MZ, Radojkovic M, Kuzmanovic M, Ristic S, Stošić-Grujičić S, Miljković Đ, Cavalli E, Libra M, Fagone P, McCubrey J, Nicoletti F, Mijatović S. The NO-modified HIV protease inhibitor as a valuable drug for
 hematological malignancies: Role of p70S6K. in Leukemia Research. 2015;39(10):1088-1095.
doi:10.1016/j.leukres.2015.06.013 .

Maksimović-Ivanić, Danijela, Mojić, Marija, Bulatović, Mirna Z., Radojkovic, Milica, Kuzmanovic, Milos, Ristic, Slobodan, Stošić-Grujičić, Stanislava, Miljković, Đorđe, Cavalli, Eugenio, Libra, Massimo, Fagone, Paolo, McCubrey, James, Nicoletti, Ferdinando, Mijatović, Sanja, "The NO-modified HIV protease inhibitor as a valuable drug for
 hematological malignancies: Role of p70S6K" in Leukemia Research, 39, no. 10 (2015):1088-1095,
https://doi.org/10.1016/j.leukres.2015.06.013 . .

TY  - CONF
AU  - Steelman, Linda S.
AU  - Davis, Nicole M.
AU  - Sokolosky, Melissa
AU  - Abrams, Stephen L.
AU  - Martelli, Alberto M.
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Mazzarino, Clorinda
AU  - Malponte, Graziella
AU  - Libra, Massimo
AU  - Cervello, Melchiorre
AU  - Montalto, Giuseppe
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Umezawa, Kazuo
AU  - McCubrey, James A.
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2278
C3  - International Journal of Molecular Medicine
T1  - Inhibition of GSK-3 beta activity can result in drug and hormonal
 resistance and alter sensitivity to targeted therapy in breast cancer
IS  - 1
VL  - 34
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_2278
ER  - 

@conference{
author = "Steelman, Linda S. and Davis, Nicole M. and Sokolosky, Melissa and Abrams, Stephen L. and Martelli, Alberto M. and Nicoletti, Ferdinando and Fagone, Paolo and Mazzarino, Clorinda and Malponte, Graziella and Libra, Massimo and Cervello, Melchiorre and Montalto, Giuseppe and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Umezawa, Kazuo and McCubrey, James A.",
year = "2014",
journal = "International Journal of Molecular Medicine",
title = "Inhibition of GSK-3 beta activity can result in drug and hormonal
 resistance and alter sensitivity to targeted therapy in breast cancer",
number = "1",
volume = "34",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_2278"
}

Steelman, L. S., Davis, N. M., Sokolosky, M., Abrams, S. L., Martelli, A. M., Nicoletti, F., Fagone, P., Mazzarino, C., Malponte, G., Libra, M., Cervello, M., Montalto, G., Maksimović-Ivanić, D., Mijatović, S., Umezawa, K.,& McCubrey, J. A.. (2014). Inhibition of GSK-3 beta activity can result in drug and hormonal
 resistance and alter sensitivity to targeted therapy in breast cancer. in International Journal of Molecular Medicine, 34(1).
https://hdl.handle.net/21.15107/rcub_ibiss_2278

Steelman LS, Davis NM, Sokolosky M, Abrams SL, Martelli AM, Nicoletti F, Fagone P, Mazzarino C, Malponte G, Libra M, Cervello M, Montalto G, Maksimović-Ivanić D, Mijatović S, Umezawa K, McCubrey JA. Inhibition of GSK-3 beta activity can result in drug and hormonal
 resistance and alter sensitivity to targeted therapy in breast cancer. in International Journal of Molecular Medicine. 2014;34(1).
https://hdl.handle.net/21.15107/rcub_ibiss_2278 .

Steelman, Linda S., Davis, Nicole M., Sokolosky, Melissa, Abrams, Stephen L., Martelli, Alberto M., Nicoletti, Ferdinando, Fagone, Paolo, Mazzarino, Clorinda, Malponte, Graziella, Libra, Massimo, Cervello, Melchiorre, Montalto, Giuseppe, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Umezawa, Kazuo, McCubrey, James A., "Inhibition of GSK-3 beta activity can result in drug and hormonal
 resistance and alter sensitivity to targeted therapy in breast cancer" in International Journal of Molecular Medicine, 34, no. 1 (2014),
https://hdl.handle.net/21.15107/rcub_ibiss_2278 .

TY  - JOUR
AU  - Mijatović, Sanja
AU  - Pešić, Milica
AU  - Mojić, Marija
AU  - Banković, Jasna
AU  - Miljković, Đorđe
AU  - Fagone, Paolo
AU  - Mangano, Katia
AU  - Nicoletti, Ferdinando
AU  - Mccubrey, James
AU  - Tanić, Nikola
AU  - Maksimović-Ivanić, Danijela
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/508
AB  - Background: The NO-modified form of the HIV inhibitor saquinavir (Saq-NO) inhibited the growth of a variety of cancer cell lines in vitro and in vivo more potently than the original compound in a nontoxic fashion. In addition, chemo- and immunosensitizing properties were observed. The aim of the present study was to evaluate its anticancer action against non-small cell lung carcinoma cells in their doxorubicin (DOXO) sensitive and resistant phenotype (NCI-H460 and NCI-H460/R). Methods: The viability of cells was analyzed by MTT and crystal violet assays. DR5 expression was estimated by real time RT-PCR and flow cytometry. Activity of P-glycoprotein (P-gp) pumps was evaluated by the Rho123 accumulation assay. Results: Saq-NO diminished the viability of lung cancer cells through induction of cell cycle arrest in the G0/G1 phase independently of the overexpression of the P-gp pumps. In addition, Saq-NO elevated or completely reconstituted the doxorubicin efficacy in NCI-H460 and NCI-H460/R, respectively. The chemosensitizing effect in DOXO resistant cells was a consequence of P-gp inhibition which was found to be more potent than that observed with dex-verapamil, a conventional inhibitor of P-gp. Sensitization to DOXO upon Saq-NO was accompanied by elevated DR5 expression, but the resistance to TRAIL was not abrogated. Conclusions: The NO-modified HIV inhibitor saquinavir displayed equal antiproliferative and chemosensitizing properties in DOXO sensitive and resistant non-small cell lung carcinoma cells, suggesting the importance of the evaluation of this drug as an antineoplastic agent.
AB  - Uvod: Inhibitor HIV proteaze - sakvinavir nakon modifikacije kovalentnim vezivanjem NO (Saq-NO) gubi toksična svojstva dok potentnije od originalnog jedinjenja inhibira in vitro i in vivo rast brojnih ćelijskih linija kancera. Pored direktnog antitumorskog delovanja, Saq-NO povećava osetljivost ćelija kancera na antitumorski imunski odgovor i konvencionalnu hemioterapiju. Ova studija je imala za cilj ispitivanje antitumorskog potencijala Saq-NO na ćelijskim linijama nesitnoćelijskog karcinoma pluća, senzitivnim (NCI-H460), odnosno rezistentnim (NCI-H460/R) na doksorubicin. Metode: Vijabilitet ćelija je evaluiran testovima MTT i 'kristal violet'. Ekspresija receptora DR5 je procenjivana me-odom RT-PCR u realnom vremenu i protočnom citofluorimetrijom. Aktivnost P-gp pumpi određivana je akumulacionim testom Rho123. Rezultati: Saq-NO inhibira rast ćelija kancera pluća zaustavljanjem ćelija u fazi G0/G1 ćelijskog ciklusa a zapaženi efekat nije oslabljen povećanjem ekspresije P-gp pumpi. Pored toga, Saq-NO povećava osetljivost NCI-H460 ćelija, dok u slučaju rezistentne forme, NCI-H460/R, potpuno rekonstituiše njihovu osetljivost na doksorubicin. Efekat hemosenzitizacije je posledica inhibicije P-gp pumpi, što Saq-NO čini potentnijim od deksverapamila, uobičajenog inhibitora P-gp. Opisani fenomen je praćen povećanjem ekspresije receptora DR5 na genskom i membranskom nivou, ali time rezistencija na molekul TRAIL nije ukinuta. Zaključak: Saq-NO pokazuje značajan antiproliferativan i hemosenzitizujući potencijal na ćelijama nesitnoćelijskog kancera pluća nezavisno od njihove osetljivosti odnosno rezistencije na doksorubicin, ukazujući na potrebu daljeg ispitivanja ovog jedinjenja u svojstvu potencijalnog antineoplastičnog agensa.
T2  - Journal of Medical Biochemistry
T1  - Modifikovana forma sakvinavira efikasno suprimira rast ćelija nesitnoćelijskog karcinoma pluća različite osetljivosti na doksorubicin
T1  - No-modified saquinavir is equally efficient against doxorubicin sensitive and resistant non-small cell lung carcinoma cells
IS  - 4
VL  - 32
DO  - 10.2478/jomb-2013-0050
SP  - 406
EP  - 416
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_508
ER  - 

@article{
author = "Mijatović, Sanja and Pešić, Milica and Mojić, Marija and Banković, Jasna and Miljković, Đorđe and Fagone, Paolo and Mangano, Katia and Nicoletti, Ferdinando and Mccubrey, James and Tanić, Nikola and Maksimović-Ivanić, Danijela",
year = "2013, 2013",
abstract = "Background: The NO-modified form of the HIV inhibitor saquinavir (Saq-NO) inhibited the growth of a variety of cancer cell lines in vitro and in vivo more potently than the original compound in a nontoxic fashion. In addition, chemo- and immunosensitizing properties were observed. The aim of the present study was to evaluate its anticancer action against non-small cell lung carcinoma cells in their doxorubicin (DOXO) sensitive and resistant phenotype (NCI-H460 and NCI-H460/R). Methods: The viability of cells was analyzed by MTT and crystal violet assays. DR5 expression was estimated by real time RT-PCR and flow cytometry. Activity of P-glycoprotein (P-gp) pumps was evaluated by the Rho123 accumulation assay. Results: Saq-NO diminished the viability of lung cancer cells through induction of cell cycle arrest in the G0/G1 phase independently of the overexpression of the P-gp pumps. In addition, Saq-NO elevated or completely reconstituted the doxorubicin efficacy in NCI-H460 and NCI-H460/R, respectively. The chemosensitizing effect in DOXO resistant cells was a consequence of P-gp inhibition which was found to be more potent than that observed with dex-verapamil, a conventional inhibitor of P-gp. Sensitization to DOXO upon Saq-NO was accompanied by elevated DR5 expression, but the resistance to TRAIL was not abrogated. Conclusions: The NO-modified HIV inhibitor saquinavir displayed equal antiproliferative and chemosensitizing properties in DOXO sensitive and resistant non-small cell lung carcinoma cells, suggesting the importance of the evaluation of this drug as an antineoplastic agent., Uvod: Inhibitor HIV proteaze - sakvinavir nakon modifikacije kovalentnim vezivanjem NO (Saq-NO) gubi toksična svojstva dok potentnije od originalnog jedinjenja inhibira in vitro i in vivo rast brojnih ćelijskih linija kancera. Pored direktnog antitumorskog delovanja, Saq-NO povećava osetljivost ćelija kancera na antitumorski imunski odgovor i konvencionalnu hemioterapiju. Ova studija je imala za cilj ispitivanje antitumorskog potencijala Saq-NO na ćelijskim linijama nesitnoćelijskog karcinoma pluća, senzitivnim (NCI-H460), odnosno rezistentnim (NCI-H460/R) na doksorubicin. Metode: Vijabilitet ćelija je evaluiran testovima MTT i 'kristal violet'. Ekspresija receptora DR5 je procenjivana me-odom RT-PCR u realnom vremenu i protočnom citofluorimetrijom. Aktivnost P-gp pumpi određivana je akumulacionim testom Rho123. Rezultati: Saq-NO inhibira rast ćelija kancera pluća zaustavljanjem ćelija u fazi G0/G1 ćelijskog ciklusa a zapaženi efekat nije oslabljen povećanjem ekspresije P-gp pumpi. Pored toga, Saq-NO povećava osetljivost NCI-H460 ćelija, dok u slučaju rezistentne forme, NCI-H460/R, potpuno rekonstituiše njihovu osetljivost na doksorubicin. Efekat hemosenzitizacije je posledica inhibicije P-gp pumpi, što Saq-NO čini potentnijim od deksverapamila, uobičajenog inhibitora P-gp. Opisani fenomen je praćen povećanjem ekspresije receptora DR5 na genskom i membranskom nivou, ali time rezistencija na molekul TRAIL nije ukinuta. Zaključak: Saq-NO pokazuje značajan antiproliferativan i hemosenzitizujući potencijal na ćelijama nesitnoćelijskog kancera pluća nezavisno od njihove osetljivosti odnosno rezistencije na doksorubicin, ukazujući na potrebu daljeg ispitivanja ovog jedinjenja u svojstvu potencijalnog antineoplastičnog agensa.",
journal = "Journal of Medical Biochemistry",
title = "Modifikovana forma sakvinavira efikasno suprimira rast ćelija nesitnoćelijskog karcinoma pluća različite osetljivosti na doksorubicin, No-modified saquinavir is equally efficient against doxorubicin sensitive and resistant non-small cell lung carcinoma cells",
number = "4",
volume = "32",
doi = "10.2478/jomb-2013-0050",
pages = "406-416",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_508"
}

Mijatović, S., Pešić, M., Mojić, M., Banković, J., Miljković, Đ., Fagone, P., Mangano, K., Nicoletti, F., Mccubrey, J., Tanić, N.,& Maksimović-Ivanić, D.. (2013). Modifikovana forma sakvinavira efikasno suprimira rast ćelija nesitnoćelijskog karcinoma pluća različite osetljivosti na doksorubicin. in Journal of Medical Biochemistry, 32(4), 406-416.
https://doi.org/10.2478/jomb-2013-0050
https://hdl.handle.net/21.15107/rcub_ibiss_508

Mijatović S, Pešić M, Mojić M, Banković J, Miljković Đ, Fagone P, Mangano K, Nicoletti F, Mccubrey J, Tanić N, Maksimović-Ivanić D. Modifikovana forma sakvinavira efikasno suprimira rast ćelija nesitnoćelijskog karcinoma pluća različite osetljivosti na doksorubicin. in Journal of Medical Biochemistry. 2013;32(4):406-416.
doi:10.2478/jomb-2013-0050
https://hdl.handle.net/21.15107/rcub_ibiss_508 .

Mijatović, Sanja, Pešić, Milica, Mojić, Marija, Banković, Jasna, Miljković, Đorđe, Fagone, Paolo, Mangano, Katia, Nicoletti, Ferdinando, Mccubrey, James, Tanić, Nikola, Maksimović-Ivanić, Danijela, "Modifikovana forma sakvinavira efikasno suprimira rast ćelija nesitnoćelijskog karcinoma pluća različite osetljivosti na doksorubicin" in Journal of Medical Biochemistry, 32, no. 4 (2013):406-416,
https://doi.org/10.2478/jomb-2013-0050 .,
https://hdl.handle.net/21.15107/rcub_ibiss_508 .

TY  - JOUR
AU  - Petković, Filip
AU  - Blaževski, Jana
AU  - Momčilović, Miljana
AU  - Timotijević, Gordana
AU  - Zocca, Mai-Britt
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Mangano, Katia
AU  - Fagone, Paolo
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
AU  - Miljković, Đorđe
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/998
AB  - NO-hybridization of the HIV protease inhibitor Saquinavir generates a new chemical entity named Saq-NO, that retains the anti-viral activity and exerts lower toxicity. We show that Saq-NO inhibited the generation of various cytokines in ConA-stimulated unfractionated murine spleen cells and rat lymph nodes stimulated with ConA as well as in purified CD4(+) T cells in vitro and reduced the circulating levels of cytokines in mice challenged with anti-CD3 antibody. Furthermore, Saq-NO reduced IL-17 and IFN-gamma production in myelin basic protein (MBP)-specific cells isolated from rats immunized with MBP. These findings translated well into the in vivo setting as Saq-NO ameliorated the course of the disease in two preclinical models of multiple sclerosis. Our results demonstrate that Saq-NO exerts immunomodulatory effects that warrant studies on its application in autoimmune diseases. (c) 2013 Elsevier B.V. All rights reserved.
PB  - Amsterdam: Elsevier
T2  - Journal of Neuroimmunology
T1  - Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis
IS  - 1-2
VL  - 259
DO  - 10.1016/j.jneuroim.2013.03.010
SP  - 55
EP  - 65
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_998
ER  - 

@article{
author = "Petković, Filip and Blaževski, Jana and Momčilović, Miljana and Timotijević, Gordana and Zocca, Mai-Britt and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Mangano, Katia and Fagone, Paolo and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando and Miljković, Đorđe",
year = "2013",
abstract = "NO-hybridization of the HIV protease inhibitor Saquinavir generates a new chemical entity named Saq-NO, that retains the anti-viral activity and exerts lower toxicity. We show that Saq-NO inhibited the generation of various cytokines in ConA-stimulated unfractionated murine spleen cells and rat lymph nodes stimulated with ConA as well as in purified CD4(+) T cells in vitro and reduced the circulating levels of cytokines in mice challenged with anti-CD3 antibody. Furthermore, Saq-NO reduced IL-17 and IFN-gamma production in myelin basic protein (MBP)-specific cells isolated from rats immunized with MBP. These findings translated well into the in vivo setting as Saq-NO ameliorated the course of the disease in two preclinical models of multiple sclerosis. Our results demonstrate that Saq-NO exerts immunomodulatory effects that warrant studies on its application in autoimmune diseases. (c) 2013 Elsevier B.V. All rights reserved.",
publisher = "Amsterdam: Elsevier",
journal = "Journal of Neuroimmunology",
title = "Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis",
number = "1-2",
volume = "259",
doi = "10.1016/j.jneuroim.2013.03.010",
pages = "55-65",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_998"
}

Petković, F., Blaževski, J., Momčilović, M., Timotijević, G., Zocca, M., Mijatović, S., Maksimović-Ivanić, D., Mangano, K., Fagone, P., Stošić-Grujičić, S., Nicoletti, F.,& Miljković, Đ.. (2013). Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology
Amsterdam: Elsevier., 259(1-2), 55-65.
https://doi.org/10.1016/j.jneuroim.2013.03.010
https://hdl.handle.net/21.15107/rcub_ibiss_998

Petković F, Blaževski J, Momčilović M, Timotijević G, Zocca M, Mijatović S, Maksimović-Ivanić D, Mangano K, Fagone P, Stošić-Grujičić S, Nicoletti F, Miljković Đ. Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology. 2013;259(1-2):55-65.
doi:10.1016/j.jneuroim.2013.03.010
https://hdl.handle.net/21.15107/rcub_ibiss_998 .

Petković, Filip, Blaževski, Jana, Momčilović, Miljana, Timotijević, Gordana, Zocca, Mai-Britt, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Mangano, Katia, Fagone, Paolo, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, Miljković, Đorđe, "Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis" in Journal of Neuroimmunology, 259, no. 1-2 (2013):55-65,
https://doi.org/10.1016/j.jneuroim.2013.03.010 .,
https://hdl.handle.net/21.15107/rcub_ibiss_998 .

TY  - JOUR
AU  - Saksida, Tamara
AU  - Miljković, Đorđe
AU  - Timotijević, Gordana S
AU  - Stojanović, Ivana D.
AU  - Mijatović, Sanja
AU  - Fagone, Paolo
AU  - Mangano, Katia
AU  - Mammana, Santa
AU  - Farina, Claudio
AU  - Ascione, Ester
AU  - Maiello, Valentina
AU  - Nicoletti, Ferdinando
AU  - Stošić-Grujičić, Stanislava
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/965
AB  - Transferrin (Tf) has a major role in T cell activation and proliferation. Here, we investigated whether Tf exerts immunomodulatory effects on T cells and in development of T-cell driven experimental autoimmune encephalomyelitis (EAE). While treatment of concanavalin A-stimulated splenocytes with apotransferrin (ApoTf) did not affect release of IL-1 beta, TNF, INF-gamma, IL-17, IL-4, and IL-10, it markedly and dose-dependently down-regulated synthesis of IL-2 in these cells. ApoTf also inhibited IL-2 generation in purified CD3(+) T cells and the effect was accompanied with down-regulation of MAPK p44/42 and NF kappa B signaling. Despite impeded IL-2 release, proliferation of splenocytes was not inhibited by ApoTf. Importantly, ApoTf ameliorated EAE in mice and significantly reduced ex vivo IL-2 production in proteolipid protein-specific lymphocytes. Thus ApoTf may be a promising beneficial agent for multiple sclerosis. (C) 2013 Elsevier B.V. All rights reserved.
T2  - Journal of Neuroimmunology
T1  - Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis
IS  - 1-2
VL  - 262
SP  - 63
EP  - 78
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_965
ER  - 

@article{
author = "Saksida, Tamara and Miljković, Đorđe and Timotijević, Gordana S and Stojanović, Ivana D. and Mijatović, Sanja and Fagone, Paolo and Mangano, Katia and Mammana, Santa and Farina, Claudio and Ascione, Ester and Maiello, Valentina and Nicoletti, Ferdinando and Stošić-Grujičić, Stanislava",
year = "2013",
abstract = "Transferrin (Tf) has a major role in T cell activation and proliferation. Here, we investigated whether Tf exerts immunomodulatory effects on T cells and in development of T-cell driven experimental autoimmune encephalomyelitis (EAE). While treatment of concanavalin A-stimulated splenocytes with apotransferrin (ApoTf) did not affect release of IL-1 beta, TNF, INF-gamma, IL-17, IL-4, and IL-10, it markedly and dose-dependently down-regulated synthesis of IL-2 in these cells. ApoTf also inhibited IL-2 generation in purified CD3(+) T cells and the effect was accompanied with down-regulation of MAPK p44/42 and NF kappa B signaling. Despite impeded IL-2 release, proliferation of splenocytes was not inhibited by ApoTf. Importantly, ApoTf ameliorated EAE in mice and significantly reduced ex vivo IL-2 production in proteolipid protein-specific lymphocytes. Thus ApoTf may be a promising beneficial agent for multiple sclerosis. (C) 2013 Elsevier B.V. All rights reserved.",
journal = "Journal of Neuroimmunology",
title = "Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis",
number = "1-2",
volume = "262",
pages = "63-78",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_965"
}

Saksida, T., Miljković, Đ., Timotijević, G. S., Stojanović, I. D., Mijatović, S., Fagone, P., Mangano, K., Mammana, S., Farina, C., Ascione, E., Maiello, V., Nicoletti, F.,& Stošić-Grujičić, S.. (2013). Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology, 262(1-2), 63-78.
https://hdl.handle.net/21.15107/rcub_ibiss_965

Saksida T, Miljković Đ, Timotijević GS, Stojanović ID, Mijatović S, Fagone P, Mangano K, Mammana S, Farina C, Ascione E, Maiello V, Nicoletti F, Stošić-Grujičić S. Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology. 2013;262(1-2):63-78.
https://hdl.handle.net/21.15107/rcub_ibiss_965 .

Saksida, Tamara, Miljković, Đorđe, Timotijević, Gordana S, Stojanović, Ivana D., Mijatović, Sanja, Fagone, Paolo, Mangano, Katia, Mammana, Santa, Farina, Claudio, Ascione, Ester, Maiello, Valentina, Nicoletti, Ferdinando, Stošić-Grujičić, Stanislava, "Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis" in Journal of Neuroimmunology, 262, no. 1-2 (2013):63-78,
https://hdl.handle.net/21.15107/rcub_ibiss_965 .

TY  - JOUR
AU  - Mangano, Katia
AU  - Fagone, Paolo
AU  - Di Mauro, M
AU  - Ascione, E
AU  - Maiello, V
AU  - Milicić, Tanja
AU  - Jotić, Aleksandra Z
AU  - Lalić, Nebojsa M
AU  - Saksida, Tamara
AU  - Stojanović, Ivana D.
AU  - Selmi, C
AU  - Farina, C
AU  - Stošić-Grujičić, Stanislava
AU  - Meroni, P
AU  - Nicoletti, Ferdinando
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1119
AB  - The transferrin (Tf) family of iron binding proteins includes important endogenous modulators of the immune function that may modulate autoimmune diseases. To define more clearly the role of apotransferrin (apoTf) in type 1 diabetes we determined the impact of this protein on type 1 diabetes as investigated in islet cells, animal models and patient sera. First, we demonstrated that recombinant apoTf counteracts the cytokine-induced death of murine pancreatic islet cells. Secondly, human apoTf administration favourably influences the course of type 1 diabetes in animal models, resulting in protection against disease development that was associated with reduction of insulitis and reduced levels of proinflammatory cytokines. Finally, we confirmed that patients with newly diagnosed type 1 diabetes manifest significantly lower apoTf serum levels compared to healthy controls and patients with long-lasting disease. In conclusion, our data suggest the apoTf pivotal role in the perpetuation of type 1 diabetes pathology.
T2  - Clinical and Experimental Immunology
T1  - The immunobiology of apotransferrin in type 1 diabetes
IS  - 3
VL  - 169
SP  - 5
EP  - 252
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1119
ER  - 

@article{
author = "Mangano, Katia and Fagone, Paolo and Di Mauro, M and Ascione, E and Maiello, V and Milicić, Tanja and Jotić, Aleksandra Z and Lalić, Nebojsa M and Saksida, Tamara and Stojanović, Ivana D. and Selmi, C and Farina, C and Stošić-Grujičić, Stanislava and Meroni, P and Nicoletti, Ferdinando",
year = "2012",
abstract = "The transferrin (Tf) family of iron binding proteins includes important endogenous modulators of the immune function that may modulate autoimmune diseases. To define more clearly the role of apotransferrin (apoTf) in type 1 diabetes we determined the impact of this protein on type 1 diabetes as investigated in islet cells, animal models and patient sera. First, we demonstrated that recombinant apoTf counteracts the cytokine-induced death of murine pancreatic islet cells. Secondly, human apoTf administration favourably influences the course of type 1 diabetes in animal models, resulting in protection against disease development that was associated with reduction of insulitis and reduced levels of proinflammatory cytokines. Finally, we confirmed that patients with newly diagnosed type 1 diabetes manifest significantly lower apoTf serum levels compared to healthy controls and patients with long-lasting disease. In conclusion, our data suggest the apoTf pivotal role in the perpetuation of type 1 diabetes pathology.",
journal = "Clinical and Experimental Immunology",
title = "The immunobiology of apotransferrin in type 1 diabetes",
number = "3",
volume = "169",
pages = "5-252",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1119"
}

Mangano, K., Fagone, P., Di Mauro, M., Ascione, E., Maiello, V., Milicić, T., Jotić, A. Z., Lalić, N. M., Saksida, T., Stojanović, I. D., Selmi, C., Farina, C., Stošić-Grujičić, S., Meroni, P.,& Nicoletti, F.. (2012). The immunobiology of apotransferrin in type 1 diabetes. in Clinical and Experimental Immunology, 169(3), 5-252.
https://hdl.handle.net/21.15107/rcub_ibiss_1119

Mangano K, Fagone P, Di Mauro M, Ascione E, Maiello V, Milicić T, Jotić AZ, Lalić NM, Saksida T, Stojanović ID, Selmi C, Farina C, Stošić-Grujičić S, Meroni P, Nicoletti F. The immunobiology of apotransferrin in type 1 diabetes. in Clinical and Experimental Immunology. 2012;169(3):5-252.
https://hdl.handle.net/21.15107/rcub_ibiss_1119 .

Mangano, Katia, Fagone, Paolo, Di Mauro, M, Ascione, E, Maiello, V, Milicić, Tanja, Jotić, Aleksandra Z, Lalić, Nebojsa M, Saksida, Tamara, Stojanović, Ivana D., Selmi, C, Farina, C, Stošić-Grujičić, Stanislava, Meroni, P, Nicoletti, Ferdinando, "The immunobiology of apotransferrin in type 1 diabetes" in Clinical and Experimental Immunology, 169, no. 3 (2012):5-252,
https://hdl.handle.net/21.15107/rcub_ibiss_1119 .

TY  - JOUR
AU  - Tumino, Salvatore
AU  - Mojić, Marija
AU  - Dinić, Svetlana
AU  - Fagone, Paolo
AU  - Mangano, Katia
AU  - Maksimović-Ivanić, Danijela
AU  - Grdović, Nevena
AU  - Zocca, Mai-Britt
AU  - Miljković, Đorđe
AU  - Al-Abed, Yousef
AU  - Mijatović, Sanja
AU  - McCubrey, James A
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1199
AB  - We previously reported that the NO-modified form of HIV protease inhibitor Saquinavir ( Saq) is a potent antitumoral agent efficient against numerous tumor cell lines in vitro and in vivo. In acute toxicity studies, doses of Saq-NO equivalent to DL100 of the parental drug were completely nontoxic. Beside direct effect on malignant cell growth, Saq-NO sensitizes certain type of cells to tumor necrosis factor-related apoptosis-inducing ligand ( TRAIL)-mediated cell death. In this study, we evaluated the effects of Saq-NO on androgen-dependent prostate cancer LNCaP. Saq-NO inhibited both the growth of LNCaP cells in vitro and in xenograft models. Suppression of tumor growth was accompanied with cell cycle arrest in G(0)/G(1) phase and established a persistent inhibition of proliferation. Furthermore, Saq-NO reverted sensitivity of LNCaP cells to TRAIL but not to TNF. Treatment of cells with Saq-NO induced transient upregulation of Akt and ERK1/2. This, however, did not represent the primary mode of action of Saq-NO, as elimination with specific inhibitors did not compromise the chemotherapic efficacy of the drug. However, permanent abrogation of phosphorylation of the S6 protein, which is the downstream target of both signaling pathways, was observed. Diminished S6 phosphorylation was associated with re-established sensitivity to TRAIL and reduction of X-linked inhibitor of apoptosis protein (XIAP). In summary, NO modification of Saq led to a new chemical entity with stronger and more pleiotropic antitumor activity than the parental drug.
T2  - Cell Cycle
T1  - Saquinavir-NO-targeted S6 protein mediates sensitivity of androgen-dependent prostate cancer cells to TRAIL
IS  - 6
VL  - 11
EP  - 1182
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1199
ER  - 

@article{
author = "Tumino, Salvatore and Mojić, Marija and Dinić, Svetlana and Fagone, Paolo and Mangano, Katia and Maksimović-Ivanić, Danijela and Grdović, Nevena and Zocca, Mai-Britt and Miljković, Đorđe and Al-Abed, Yousef and Mijatović, Sanja and McCubrey, James A and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando",
year = "2012",
abstract = "We previously reported that the NO-modified form of HIV protease inhibitor Saquinavir ( Saq) is a potent antitumoral agent efficient against numerous tumor cell lines in vitro and in vivo. In acute toxicity studies, doses of Saq-NO equivalent to DL100 of the parental drug were completely nontoxic. Beside direct effect on malignant cell growth, Saq-NO sensitizes certain type of cells to tumor necrosis factor-related apoptosis-inducing ligand ( TRAIL)-mediated cell death. In this study, we evaluated the effects of Saq-NO on androgen-dependent prostate cancer LNCaP. Saq-NO inhibited both the growth of LNCaP cells in vitro and in xenograft models. Suppression of tumor growth was accompanied with cell cycle arrest in G(0)/G(1) phase and established a persistent inhibition of proliferation. Furthermore, Saq-NO reverted sensitivity of LNCaP cells to TRAIL but not to TNF. Treatment of cells with Saq-NO induced transient upregulation of Akt and ERK1/2. This, however, did not represent the primary mode of action of Saq-NO, as elimination with specific inhibitors did not compromise the chemotherapic efficacy of the drug. However, permanent abrogation of phosphorylation of the S6 protein, which is the downstream target of both signaling pathways, was observed. Diminished S6 phosphorylation was associated with re-established sensitivity to TRAIL and reduction of X-linked inhibitor of apoptosis protein (XIAP). In summary, NO modification of Saq led to a new chemical entity with stronger and more pleiotropic antitumor activity than the parental drug.",
journal = "Cell Cycle",
title = "Saquinavir-NO-targeted S6 protein mediates sensitivity of androgen-dependent prostate cancer cells to TRAIL",
number = "6",
volume = "11",
pages = "1182",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1199"
}

Tumino, S., Mojić, M., Dinić, S., Fagone, P., Mangano, K., Maksimović-Ivanić, D., Grdović, N., Zocca, M., Miljković, Đ., Al-Abed, Y., Mijatović, S., McCubrey, J. A., Stošić-Grujičić, S.,& Nicoletti, F.. (2012). Saquinavir-NO-targeted S6 protein mediates sensitivity of androgen-dependent prostate cancer cells to TRAIL. in Cell Cycle, 11(6).
https://hdl.handle.net/21.15107/rcub_ibiss_1199

Tumino S, Mojić M, Dinić S, Fagone P, Mangano K, Maksimović-Ivanić D, Grdović N, Zocca M, Miljković Đ, Al-Abed Y, Mijatović S, McCubrey JA, Stošić-Grujičić S, Nicoletti F. Saquinavir-NO-targeted S6 protein mediates sensitivity of androgen-dependent prostate cancer cells to TRAIL. in Cell Cycle. 2012;11(6):null-1182.
https://hdl.handle.net/21.15107/rcub_ibiss_1199 .

Tumino, Salvatore, Mojić, Marija, Dinić, Svetlana, Fagone, Paolo, Mangano, Katia, Maksimović-Ivanić, Danijela, Grdović, Nevena, Zocca, Mai-Britt, Miljković, Đorđe, Al-Abed, Yousef, Mijatović, Sanja, McCubrey, James A, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, "Saquinavir-NO-targeted S6 protein mediates sensitivity of androgen-dependent prostate cancer cells to TRAIL" in Cell Cycle, 11, no. 6 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1199 .

TY  - JOUR
AU  - Mojić, Marija
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Miljković, Đorđe
AU  - Stošić-Grujičić, Stanislava
AU  - Stanković, Marija M
AU  - Mangano, Katia
AU  - Travali, Salvatore
AU  - Donia, Marco
AU  - Fagone, Paolo
AU  - Zocca, Mai-Britt
AU  - Al-Abed, Yousef
AU  - McCubrey, James A
AU  - Nicoletti, Ferdinando
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1099
AB  - We have examined the influence of the nitric oxide (NO)modified anti-inflammatory drug (S, R)-3-phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) named GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116. The effects of the drugs on cell viability, apoptosis, proliferation, and metastatic potential were analyzed. The release of NO and oxygen and nitrogen species was also determined. The efficacy of the drugs was evaluated in vivo in BALB/c mice injected with CT26CL25 cells. Both agents suppressed the growth of colon cancer cells in vitro and reduced tumor volume in syngeneic BALB/c mice. However, their mechanisms of action were different because GIT-27NO released larger amounts of nitrite than Saq-NO in cell cultures and its antitumor action depended on the intracellular NO release inside the cells. On the contrary, Saq-NO released barely detectable amounts of NO and its antitumor action was NO-independent. In fact, cotreatment with an NO-peroxynitrite scavenger revealed that GIT-27NO but not Saq-NO acts through peroxynitrite-mediated cell destruction. At the cellular level, GIT-27NO prevalently induced proapoptotic signals followed by caspase-dependent apoptosis. In contrast, Saq-NO blocked cell proliferation, changed the adhesive, migratory, and invasive properties of the cells, and decreased metastatic potential in vivo. In conclusion, differences in NO release and oxidative stress generation between GIT-27NO and Saq-NO resulted in different mechanisms that caused cell death.
T2  - Molecular Pharmacology
T1  - Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells
IS  - 4
VL  - 82
SP  - 203
EP  - 710
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1099
ER  - 

@article{
author = "Mojić, Marija and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Miljković, Đorđe and Stošić-Grujičić, Stanislava and Stanković, Marija M and Mangano, Katia and Travali, Salvatore and Donia, Marco and Fagone, Paolo and Zocca, Mai-Britt and Al-Abed, Yousef and McCubrey, James A and Nicoletti, Ferdinando",
year = "2012",
abstract = "We have examined the influence of the nitric oxide (NO)modified anti-inflammatory drug (S, R)-3-phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) named GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116. The effects of the drugs on cell viability, apoptosis, proliferation, and metastatic potential were analyzed. The release of NO and oxygen and nitrogen species was also determined. The efficacy of the drugs was evaluated in vivo in BALB/c mice injected with CT26CL25 cells. Both agents suppressed the growth of colon cancer cells in vitro and reduced tumor volume in syngeneic BALB/c mice. However, their mechanisms of action were different because GIT-27NO released larger amounts of nitrite than Saq-NO in cell cultures and its antitumor action depended on the intracellular NO release inside the cells. On the contrary, Saq-NO released barely detectable amounts of NO and its antitumor action was NO-independent. In fact, cotreatment with an NO-peroxynitrite scavenger revealed that GIT-27NO but not Saq-NO acts through peroxynitrite-mediated cell destruction. At the cellular level, GIT-27NO prevalently induced proapoptotic signals followed by caspase-dependent apoptosis. In contrast, Saq-NO blocked cell proliferation, changed the adhesive, migratory, and invasive properties of the cells, and decreased metastatic potential in vivo. In conclusion, differences in NO release and oxidative stress generation between GIT-27NO and Saq-NO resulted in different mechanisms that caused cell death.",
journal = "Molecular Pharmacology",
title = "Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells",
number = "4",
volume = "82",
pages = "203-710",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1099"
}

Mojić, M., Mijatović, S., Maksimović-Ivanić, D., Miljković, Đ., Stošić-Grujičić, S., Stanković, M. M., Mangano, K., Travali, S., Donia, M., Fagone, P., Zocca, M., Al-Abed, Y., McCubrey, J. A.,& Nicoletti, F.. (2012). Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells. in Molecular Pharmacology, 82(4), 203-710.
https://hdl.handle.net/21.15107/rcub_ibiss_1099

Mojić M, Mijatović S, Maksimović-Ivanić D, Miljković Đ, Stošić-Grujičić S, Stanković MM, Mangano K, Travali S, Donia M, Fagone P, Zocca M, Al-Abed Y, McCubrey JA, Nicoletti F. Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells. in Molecular Pharmacology. 2012;82(4):203-710.
https://hdl.handle.net/21.15107/rcub_ibiss_1099 .

Mojić, Marija, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Miljković, Đorđe, Stošić-Grujičić, Stanislava, Stanković, Marija M, Mangano, Katia, Travali, Salvatore, Donia, Marco, Fagone, Paolo, Zocca, Mai-Britt, Al-Abed, Yousef, McCubrey, James A, Nicoletti, Ferdinando, "Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells" in Molecular Pharmacology, 82, no. 4 (2012):203-710,
https://hdl.handle.net/21.15107/rcub_ibiss_1099 .

TY  - JOUR
AU  - McCubrey, James A
AU  - Steelman, Linda S
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Franklin, Richard A
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Libra, Massimo
AU  - Candido, Saverio
AU  - Malaponte, Graziella
AU  - Mazzarino, Maria C
AU  - Fagone, Paolo
AU  - Nicoletti, Ferdinando
AU  - Baesecke, Joerg
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Chiarini, Francesca
AU  - Evangelisti, Camilla
AU  - Cocco, Lucio
AU  - Martelli, Alberto M
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1096
AB  - The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have been investigated in pre-clinical and clinical investigations and then discuss how cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance.
T2  - Oncotarget
T1  - Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascade Inhibitors: How Mutations Can Result in Therapy Resistance and How to Overcome Resistance
IS  - 10
VL  - 3
DO  - 10.18632/oncotarget.659
SP  - 389
EP  - 1111
ER  - 

@article{
author = "McCubrey, James A and Steelman, Linda S and Chappell, William H and Abrams, Stephen L and Franklin, Richard A and Montalto, Giuseppe and Cervello, Melchiorre and Libra, Massimo and Candido, Saverio and Malaponte, Graziella and Mazzarino, Maria C and Fagone, Paolo and Nicoletti, Ferdinando and Baesecke, Joerg and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Milella, Michele and Tafuri, Agostino and Chiarini, Francesca and Evangelisti, Camilla and Cocco, Lucio and Martelli, Alberto M",
year = "2012",
abstract = "The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have been investigated in pre-clinical and clinical investigations and then discuss how cancers can become insensitive to various inhibitors and potential strategies to overcome this resistance.",
journal = "Oncotarget",
title = "Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascade Inhibitors: How Mutations Can Result in Therapy Resistance and How to Overcome Resistance",
number = "10",
volume = "3",
doi = "10.18632/oncotarget.659",
pages = "389-1111"
}

McCubrey, J. A., Steelman, L. S., Chappell, W. H., Abrams, S. L., Franklin, R. A., Montalto, G., Cervello, M., Libra, M., Candido, S., Malaponte, G., Mazzarino, M. C., Fagone, P., Nicoletti, F., Baesecke, J., Mijatović, S., Maksimović-Ivanić, D., Milella, M., Tafuri, A., Chiarini, F., Evangelisti, C., Cocco, L.,& Martelli, A. M.. (2012). Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascade Inhibitors: How Mutations Can Result in Therapy Resistance and How to Overcome Resistance. in Oncotarget, 3(10), 389-1111.
https://doi.org/10.18632/oncotarget.659

McCubrey JA, Steelman LS, Chappell WH, Abrams SL, Franklin RA, Montalto G, Cervello M, Libra M, Candido S, Malaponte G, Mazzarino MC, Fagone P, Nicoletti F, Baesecke J, Mijatović S, Maksimović-Ivanić D, Milella M, Tafuri A, Chiarini F, Evangelisti C, Cocco L, Martelli AM. Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascade Inhibitors: How Mutations Can Result in Therapy Resistance and How to Overcome Resistance. in Oncotarget. 2012;3(10):389-1111.
doi:10.18632/oncotarget.659 .

McCubrey, James A, Steelman, Linda S, Chappell, William H, Abrams, Stephen L, Franklin, Richard A, Montalto, Giuseppe, Cervello, Melchiorre, Libra, Massimo, Candido, Saverio, Malaponte, Graziella, Mazzarino, Maria C, Fagone, Paolo, Nicoletti, Ferdinando, Baesecke, Joerg, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Milella, Michele, Tafuri, Agostino, Chiarini, Francesca, Evangelisti, Camilla, Cocco, Lucio, Martelli, Alberto M, "Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascade Inhibitors: How Mutations Can Result in Therapy Resistance and How to Overcome Resistance" in Oncotarget, 3, no. 10 (2012):389-1111,
https://doi.org/10.18632/oncotarget.659 . .

TY  - JOUR
AU  - McCubrey, James A
AU  - Steelman, Linda S
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Malaponte, Graziella
AU  - Mazzarino, Maria C
AU  - Candido, Saverio
AU  - Libra, Massimo
AU  - Baesecke, Joerg
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Cocco, Lucio
AU  - Evangelisti, Camilla
AU  - Chiarini, Francesca
AU  - Martelli, Alberto M
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1109
AB  - The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cascades can contribute to: resistance to other pathway inhibitors, chemotherapeutic drug resistance, premature aging as well as other diseases. This review will first describe these pathways and discuss how genetic mutations and epigenetic alterations can result in resistance to various inhibitors.
T2  - Oncotarget
T1  - Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.
IS  - 9
VL  - 3
DO  - 10.18632/oncotarget.652
SP  - 153
EP  - 987
ER  - 

@article{
author = "McCubrey, James A and Steelman, Linda S and Chappell, William H and Abrams, Stephen L and Montalto, Giuseppe and Cervello, Melchiorre and Nicoletti, Ferdinando and Fagone, Paolo and Malaponte, Graziella and Mazzarino, Maria C and Candido, Saverio and Libra, Massimo and Baesecke, Joerg and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Milella, Michele and Tafuri, Agostino and Cocco, Lucio and Evangelisti, Camilla and Chiarini, Francesca and Martelli, Alberto M",
year = "2012",
abstract = "The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cascades can contribute to: resistance to other pathway inhibitors, chemotherapeutic drug resistance, premature aging as well as other diseases. This review will first describe these pathways and discuss how genetic mutations and epigenetic alterations can result in resistance to various inhibitors.",
journal = "Oncotarget",
title = "Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.",
number = "9",
volume = "3",
doi = "10.18632/oncotarget.652",
pages = "153-987"
}

McCubrey, J. A., Steelman, L. S., Chappell, W. H., Abrams, S. L., Montalto, G., Cervello, M., Nicoletti, F., Fagone, P., Malaponte, G., Mazzarino, M. C., Candido, S., Libra, M., Baesecke, J., Mijatović, S., Maksimović-Ivanić, D., Milella, M., Tafuri, A., Cocco, L., Evangelisti, C., Chiarini, F.,& Martelli, A. M.. (2012). Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.. in Oncotarget, 3(9), 153-987.
https://doi.org/10.18632/oncotarget.652

McCubrey JA, Steelman LS, Chappell WH, Abrams SL, Montalto G, Cervello M, Nicoletti F, Fagone P, Malaponte G, Mazzarino MC, Candido S, Libra M, Baesecke J, Mijatović S, Maksimović-Ivanić D, Milella M, Tafuri A, Cocco L, Evangelisti C, Chiarini F, Martelli AM. Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.. in Oncotarget. 2012;3(9):153-987.
doi:10.18632/oncotarget.652 .

McCubrey, James A, Steelman, Linda S, Chappell, William H, Abrams, Stephen L, Montalto, Giuseppe, Cervello, Melchiorre, Nicoletti, Ferdinando, Fagone, Paolo, Malaponte, Graziella, Mazzarino, Maria C, Candido, Saverio, Libra, Massimo, Baesecke, Joerg, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Milella, Michele, Tafuri, Agostino, Cocco, Lucio, Evangelisti, Camilla, Chiarini, Francesca, Martelli, Alberto M, "Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response." in Oncotarget, 3, no. 9 (2012):153-987,
https://doi.org/10.18632/oncotarget.652 . .

TY  - JOUR
AU  - McCubrey, James A
AU  - Steelman, Linda S
AU  - Chappell, William H
AU  - Sun, Lin
AU  - Davis, Nicole M
AU  - Abrams, Stephen L
AU  - Franklin, Richard A
AU  - Cocco, Lucio
AU  - Evangelisti, Camilla
AU  - Chiarini, Francesca
AU  - Martelli, Alberto M
AU  - Libra, Massimo
AU  - Candido, Saverio
AU  - Ligresti, Giovanni
AU  - Malaponte, Graziella
AU  - Mazzarino, Maria C
AU  - Fagone, Paolo
AU  - Donia, Marco
AU  - Nicoletti, Ferdinando
AU  - Polesel, Jerry
AU  - Talamini, Renato
AU  - Baesecke, Joerg
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Dulinska-Litewka, Joanna
AU  - Laidler, Piotr
AU  - D'Assoro, Antonio B
AU  - Drobot, Lyudmyla
AU  - Umezawa, Kazuo
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Demidenko, Zoya N
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1071
AB  - Over the past few years, significant advances have occurred in both our understanding of the complexity of signal transduction pathways as well as the isolation of specific inhibitors which target key components in those pathways. Furthermore critical information is being accrued regarding how genetic mutations can affect the sensitivity of various types of patients to targeted therapy. Finally, genetic mechanisms responsible for the development of resistance after targeted therapy are being discovered which may allow the creation of alternative therapies to overcome resistance. This review will discuss some of the highlights over the past few years on the roles of key signaling pathways in various diseases, the targeting of signal transduction pathways and the genetic mechanisms governing sensitivity and resistance to targeted therapies.
T2  - Oncotarget
T1  - Advances in Targeting Signal Transduction Pathways
IS  - 12
VL  - 3
SP  - 69
EP  - 1521
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1071
ER  - 

@article{
author = "McCubrey, James A and Steelman, Linda S and Chappell, William H and Sun, Lin and Davis, Nicole M and Abrams, Stephen L and Franklin, Richard A and Cocco, Lucio and Evangelisti, Camilla and Chiarini, Francesca and Martelli, Alberto M and Libra, Massimo and Candido, Saverio and Ligresti, Giovanni and Malaponte, Graziella and Mazzarino, Maria C and Fagone, Paolo and Donia, Marco and Nicoletti, Ferdinando and Polesel, Jerry and Talamini, Renato and Baesecke, Joerg and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Milella, Michele and Tafuri, Agostino and Dulinska-Litewka, Joanna and Laidler, Piotr and D'Assoro, Antonio B and Drobot, Lyudmyla and Umezawa, Kazuo and Montalto, Giuseppe and Cervello, Melchiorre and Demidenko, Zoya N",
year = "2012",
abstract = "Over the past few years, significant advances have occurred in both our understanding of the complexity of signal transduction pathways as well as the isolation of specific inhibitors which target key components in those pathways. Furthermore critical information is being accrued regarding how genetic mutations can affect the sensitivity of various types of patients to targeted therapy. Finally, genetic mechanisms responsible for the development of resistance after targeted therapy are being discovered which may allow the creation of alternative therapies to overcome resistance. This review will discuss some of the highlights over the past few years on the roles of key signaling pathways in various diseases, the targeting of signal transduction pathways and the genetic mechanisms governing sensitivity and resistance to targeted therapies.",
journal = "Oncotarget",
title = "Advances in Targeting Signal Transduction Pathways",
number = "12",
volume = "3",
pages = "69-1521",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1071"
}

McCubrey, J. A., Steelman, L. S., Chappell, W. H., Sun, L., Davis, N. M., Abrams, S. L., Franklin, R. A., Cocco, L., Evangelisti, C., Chiarini, F., Martelli, A. M., Libra, M., Candido, S., Ligresti, G., Malaponte, G., Mazzarino, M. C., Fagone, P., Donia, M., Nicoletti, F., Polesel, J., Talamini, R., Baesecke, J., Mijatović, S., Maksimović-Ivanić, D., Milella, M., Tafuri, A., Dulinska-Litewka, J., Laidler, P., D'Assoro, A. B., Drobot, L., Umezawa, K., Montalto, G., Cervello, M.,& Demidenko, Z. N.. (2012). Advances in Targeting Signal Transduction Pathways. in Oncotarget, 3(12), 69-1521.
https://hdl.handle.net/21.15107/rcub_ibiss_1071

McCubrey JA, Steelman LS, Chappell WH, Sun L, Davis NM, Abrams SL, Franklin RA, Cocco L, Evangelisti C, Chiarini F, Martelli AM, Libra M, Candido S, Ligresti G, Malaponte G, Mazzarino MC, Fagone P, Donia M, Nicoletti F, Polesel J, Talamini R, Baesecke J, Mijatović S, Maksimović-Ivanić D, Milella M, Tafuri A, Dulinska-Litewka J, Laidler P, D'Assoro AB, Drobot L, Umezawa K, Montalto G, Cervello M, Demidenko ZN. Advances in Targeting Signal Transduction Pathways. in Oncotarget. 2012;3(12):69-1521.
https://hdl.handle.net/21.15107/rcub_ibiss_1071 .

McCubrey, James A, Steelman, Linda S, Chappell, William H, Sun, Lin, Davis, Nicole M, Abrams, Stephen L, Franklin, Richard A, Cocco, Lucio, Evangelisti, Camilla, Chiarini, Francesca, Martelli, Alberto M, Libra, Massimo, Candido, Saverio, Ligresti, Giovanni, Malaponte, Graziella, Mazzarino, Maria C, Fagone, Paolo, Donia, Marco, Nicoletti, Ferdinando, Polesel, Jerry, Talamini, Renato, Baesecke, Joerg, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Milella, Michele, Tafuri, Agostino, Dulinska-Litewka, Joanna, Laidler, Piotr, D'Assoro, Antonio B, Drobot, Lyudmyla, Umezawa, Kazuo, Montalto, Giuseppe, Cervello, Melchiorre, Demidenko, Zoya N, "Advances in Targeting Signal Transduction Pathways" in Oncotarget, 3, no. 12 (2012):69-1521,
https://hdl.handle.net/21.15107/rcub_ibiss_1071 .

TY  - JOUR
AU  - Donia, Marco
AU  - Mangano, Katia
AU  - Fagone, Paolo
AU  - De Pasquale, R
AU  - Dinotta, F
AU  - Coco, Marinella
AU  - Padron, J
AU  - Al-Abed, Yousef
AU  - Lombardo, GAG
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Zocca, Mai-Britt
AU  - Perciavalle, V
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1157
AB  - We have recently shown that covalent attachment of the nitric oxide (NO) moiety to the HIV protease inhibitor Saquinavir (Saq) produced a qualitatively new chemical entity, named Saquinavir-NO (Saq-NO), with enhanced anticancer properties and reduced toxicity both in vitro and in vivo. The aim of this study was to address several unanswered questions both on the pharmacological profile of Saq-NO as well as on the in vivo role of NO in the oncogenesis of A375 human melanoma cells. To this end, we have evaluated here the impact of single and combined effects of Saq-NO, Saq, the NO-donor DETA NONOate and the iNOS inhibitor L-NAME on the in vitro as well as in vivo growth of the iNOS positive A375 cells. Our data confirm clear-cut evidence for a strong and powerful anti-melanoma action of Saq-NO that is not duplicable by the combined use of Saq and DETA NONOate. Surprisingly, but also in agreement with the complex and multifaceted role of endogenous NO in A375 cells, both DETA NONOate and L-NAME significantly suppressed the in vivo growth of xenotransplants.
T2  - Oncology Reports
T1  - Unique antineoplastic profile of Saquinavir-NO, a novel NO-derivative of the protease inhibitor Saquinavir, on the in vitro and in vivo tumor formation of A375 human melanoma cells
IS  - 2
VL  - 28
SP  - 323
EP  - 688
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1157
ER  - 

@article{
author = "Donia, Marco and Mangano, Katia and Fagone, Paolo and De Pasquale, R and Dinotta, F and Coco, Marinella and Padron, J and Al-Abed, Yousef and Lombardo, GAG and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Zocca, Mai-Britt and Perciavalle, V and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando",
year = "2012",
abstract = "We have recently shown that covalent attachment of the nitric oxide (NO) moiety to the HIV protease inhibitor Saquinavir (Saq) produced a qualitatively new chemical entity, named Saquinavir-NO (Saq-NO), with enhanced anticancer properties and reduced toxicity both in vitro and in vivo. The aim of this study was to address several unanswered questions both on the pharmacological profile of Saq-NO as well as on the in vivo role of NO in the oncogenesis of A375 human melanoma cells. To this end, we have evaluated here the impact of single and combined effects of Saq-NO, Saq, the NO-donor DETA NONOate and the iNOS inhibitor L-NAME on the in vitro as well as in vivo growth of the iNOS positive A375 cells. Our data confirm clear-cut evidence for a strong and powerful anti-melanoma action of Saq-NO that is not duplicable by the combined use of Saq and DETA NONOate. Surprisingly, but also in agreement with the complex and multifaceted role of endogenous NO in A375 cells, both DETA NONOate and L-NAME significantly suppressed the in vivo growth of xenotransplants.",
journal = "Oncology Reports",
title = "Unique antineoplastic profile of Saquinavir-NO, a novel NO-derivative of the protease inhibitor Saquinavir, on the in vitro and in vivo tumor formation of A375 human melanoma cells",
number = "2",
volume = "28",
pages = "323-688",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1157"
}

Donia, M., Mangano, K., Fagone, P., De Pasquale, R., Dinotta, F., Coco, M., Padron, J., Al-Abed, Y., Lombardo, G., Maksimović-Ivanić, D., Mijatović, S., Zocca, M., Perciavalle, V., Stošić-Grujičić, S.,& Nicoletti, F.. (2012). Unique antineoplastic profile of Saquinavir-NO, a novel NO-derivative of the protease inhibitor Saquinavir, on the in vitro and in vivo tumor formation of A375 human melanoma cells. in Oncology Reports, 28(2), 323-688.
https://hdl.handle.net/21.15107/rcub_ibiss_1157

Donia M, Mangano K, Fagone P, De Pasquale R, Dinotta F, Coco M, Padron J, Al-Abed Y, Lombardo G, Maksimović-Ivanić D, Mijatović S, Zocca M, Perciavalle V, Stošić-Grujičić S, Nicoletti F. Unique antineoplastic profile of Saquinavir-NO, a novel NO-derivative of the protease inhibitor Saquinavir, on the in vitro and in vivo tumor formation of A375 human melanoma cells. in Oncology Reports. 2012;28(2):323-688.
https://hdl.handle.net/21.15107/rcub_ibiss_1157 .

Donia, Marco, Mangano, Katia, Fagone, Paolo, De Pasquale, R, Dinotta, F, Coco, Marinella, Padron, J, Al-Abed, Yousef, Lombardo, GAG, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Zocca, Mai-Britt, Perciavalle, V, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, "Unique antineoplastic profile of Saquinavir-NO, a novel NO-derivative of the protease inhibitor Saquinavir, on the in vitro and in vivo tumor formation of A375 human melanoma cells" in Oncology Reports, 28, no. 2 (2012):323-688,
https://hdl.handle.net/21.15107/rcub_ibiss_1157 .

TY  - CONF
AU  - McCubrey, James A
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Martelli, Alberto M
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Libra, Massimo
AU  - Cervello, Melchiorre
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Polesel, Jerry
AU  - Talamini, Renato
AU  - Maestro, Roberta
AU  - Steelman, Linda S
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1219
C3  - International Journal of Molecular Medicine
T1  - Role of NGAL (Lcn2) in prostate cancer invasion
IS  - null
VL  - 30
EP  - S25
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1219
ER  - 

@conference{
author = "McCubrey, James A and Chappell, William H and Abrams, Stephen L and Martelli, Alberto M and Nicoletti, Ferdinando and Fagone, Paolo and Libra, Massimo and Cervello, Melchiorre and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Polesel, Jerry and Talamini, Renato and Maestro, Roberta and Steelman, Linda S",
year = "2012",
journal = "International Journal of Molecular Medicine",
title = "Role of NGAL (Lcn2) in prostate cancer invasion",
number = "null",
volume = "30",
pages = "S25",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1219"
}

McCubrey, J. A., Chappell, W. H., Abrams, S. L., Martelli, A. M., Nicoletti, F., Fagone, P., Libra, M., Cervello, M., Maksimović-Ivanić, D., Mijatović, S., Polesel, J., Talamini, R., Maestro, R.,& Steelman, L. S.. (2012). Role of NGAL (Lcn2) in prostate cancer invasion. in International Journal of Molecular Medicine, 30(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1219

McCubrey JA, Chappell WH, Abrams SL, Martelli AM, Nicoletti F, Fagone P, Libra M, Cervello M, Maksimović-Ivanić D, Mijatović S, Polesel J, Talamini R, Maestro R, Steelman LS. Role of NGAL (Lcn2) in prostate cancer invasion. in International Journal of Molecular Medicine. 2012;30(null):null-S25.
https://hdl.handle.net/21.15107/rcub_ibiss_1219 .

McCubrey, James A, Chappell, William H, Abrams, Stephen L, Martelli, Alberto M, Nicoletti, Ferdinando, Fagone, Paolo, Libra, Massimo, Cervello, Melchiorre, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Polesel, Jerry, Talamini, Renato, Maestro, Roberta, Steelman, Linda S, "Role of NGAL (Lcn2) in prostate cancer invasion" in International Journal of Molecular Medicine, 30, no. null (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1219 .

TY  - CONF
AU  - Steelman, Linda S
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Martelli, Alberto M
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Mazzarino, Clorinda
AU  - Malaponte, Graziella
AU  - Libra, Massimo
AU  - Cervello, Melchiorre
AU  - Montalto, Giuseppe
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Umezawa, Kazuo
AU  - McCubrey, James A
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1221
C3  - International Journal of Molecular Medicine
T1  - Targeting signaling pathways in prostate cancer
IS  - null
VL  - 30
EP  - S50
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1221
ER  - 

@conference{
author = "Steelman, Linda S and Chappell, William H and Abrams, Stephen L and Martelli, Alberto M and Nicoletti, Ferdinando and Fagone, Paolo and Mazzarino, Clorinda and Malaponte, Graziella and Libra, Massimo and Cervello, Melchiorre and Montalto, Giuseppe and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Umezawa, Kazuo and McCubrey, James A",
year = "2012",
journal = "International Journal of Molecular Medicine",
title = "Targeting signaling pathways in prostate cancer",
number = "null",
volume = "30",
pages = "S50",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1221"
}

Steelman, L. S., Chappell, W. H., Abrams, S. L., Martelli, A. M., Nicoletti, F., Fagone, P., Mazzarino, C., Malaponte, G., Libra, M., Cervello, M., Montalto, G., Maksimović-Ivanić, D., Mijatović, S., Umezawa, K.,& McCubrey, J. A.. (2012). Targeting signaling pathways in prostate cancer. in International Journal of Molecular Medicine, 30(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1221

Steelman LS, Chappell WH, Abrams SL, Martelli AM, Nicoletti F, Fagone P, Mazzarino C, Malaponte G, Libra M, Cervello M, Montalto G, Maksimović-Ivanić D, Mijatović S, Umezawa K, McCubrey JA. Targeting signaling pathways in prostate cancer. in International Journal of Molecular Medicine. 2012;30(null):null-S50.
https://hdl.handle.net/21.15107/rcub_ibiss_1221 .

Steelman, Linda S, Chappell, William H, Abrams, Stephen L, Martelli, Alberto M, Nicoletti, Ferdinando, Fagone, Paolo, Mazzarino, Clorinda, Malaponte, Graziella, Libra, Massimo, Cervello, Melchiorre, Montalto, Giuseppe, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Umezawa, Kazuo, McCubrey, James A, "Targeting signaling pathways in prostate cancer" in International Journal of Molecular Medicine, 30, no. null (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1221 .

TY  - CONF
AU  - Nicoletti, Ferdinando
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Fagone, Paolo
AU  - Zocca, Mai-Britt
AU  - Stošić-Grujičić, Stanislava
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1220
C3  - International Journal of Molecular Medicine
T1  - NO-hybridized protease inhibitors as a new class of anticancer compounds. Saquinavir-NO as prototypical example?
IS  - null
VL  - 30
EP  - S37
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1220
ER  - 

@conference{
author = "Nicoletti, Ferdinando and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Fagone, Paolo and Zocca, Mai-Britt and Stošić-Grujičić, Stanislava",
year = "2012",
journal = "International Journal of Molecular Medicine",
title = "NO-hybridized protease inhibitors as a new class of anticancer compounds. Saquinavir-NO as prototypical example?",
number = "null",
volume = "30",
pages = "S37",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1220"
}

Nicoletti, F., Maksimović-Ivanić, D., Mijatović, S., Fagone, P., Zocca, M.,& Stošić-Grujičić, S.. (2012). NO-hybridized protease inhibitors as a new class of anticancer compounds. Saquinavir-NO as prototypical example?. in International Journal of Molecular Medicine, 30(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1220

Nicoletti F, Maksimović-Ivanić D, Mijatović S, Fagone P, Zocca M, Stošić-Grujičić S. NO-hybridized protease inhibitors as a new class of anticancer compounds. Saquinavir-NO as prototypical example?. in International Journal of Molecular Medicine. 2012;30(null):null-S37.
https://hdl.handle.net/21.15107/rcub_ibiss_1220 .

Nicoletti, Ferdinando, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Fagone, Paolo, Zocca, Mai-Britt, Stošić-Grujičić, Stanislava, "NO-hybridized protease inhibitors as a new class of anticancer compounds. Saquinavir-NO as prototypical example?" in International Journal of Molecular Medicine, 30, no. null (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1220 .

TY  - JOUR
AU  - Steelman, Linda S
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Kempf, C Ruth
AU  - Long, Jacquelyn M
AU  - Laidler, Piotr
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Stivala, Franca
AU  - Mazzarino, Maria C
AU  - Donia, Marco
AU  - Fagone, Paolo
AU  - Malaponte, Graziella
AU  - Nicoletti, Ferdinando
AU  - Libra, Massimo
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Bonati, Antonio
AU  - Baesecke, Joerg
AU  - Cocco, Lucio
AU  - Evangelisti, Camilla
AU  - Martelli, Alberto M
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - McCubrey, James A
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1302
UR  - https://www.aging-us.com/article/100296
AB  - Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described roles of these pathways in cancer stem cells, cellular senescence and aging will be evaluated. Controlling the expression of these pathways could ameliorate human health.
T2  - Aging-US
T1  - Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging
IS  - 3
VL  - 3
DO  - 10.18632/aging.100296
EP  - 222
ER  - 

@article{
author = "Steelman, Linda S and Chappell, William H and Abrams, Stephen L and Kempf, C Ruth and Long, Jacquelyn M and Laidler, Piotr and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Stivala, Franca and Mazzarino, Maria C and Donia, Marco and Fagone, Paolo and Malaponte, Graziella and Nicoletti, Ferdinando and Libra, Massimo and Milella, Michele and Tafuri, Agostino and Bonati, Antonio and Baesecke, Joerg and Cocco, Lucio and Evangelisti, Camilla and Martelli, Alberto M and Montalto, Giuseppe and Cervello, Melchiorre and McCubrey, James A",
year = "2011",
abstract = "Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described roles of these pathways in cancer stem cells, cellular senescence and aging will be evaluated. Controlling the expression of these pathways could ameliorate human health.",
journal = "Aging-US",
title = "Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging",
number = "3",
volume = "3",
doi = "10.18632/aging.100296",
pages = "222"
}

Steelman, L. S., Chappell, W. H., Abrams, S. L., Kempf, C. R., Long, J. M., Laidler, P., Mijatović, S., Maksimović-Ivanić, D., Stivala, F., Mazzarino, M. C., Donia, M., Fagone, P., Malaponte, G., Nicoletti, F., Libra, M., Milella, M., Tafuri, A., Bonati, A., Baesecke, J., Cocco, L., Evangelisti, C., Martelli, A. M., Montalto, G., Cervello, M.,& McCubrey, J. A.. (2011). Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging. in Aging-US, 3(3).
https://doi.org/10.18632/aging.100296

Steelman LS, Chappell WH, Abrams SL, Kempf CR, Long JM, Laidler P, Mijatović S, Maksimović-Ivanić D, Stivala F, Mazzarino MC, Donia M, Fagone P, Malaponte G, Nicoletti F, Libra M, Milella M, Tafuri A, Bonati A, Baesecke J, Cocco L, Evangelisti C, Martelli AM, Montalto G, Cervello M, McCubrey JA. Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging. in Aging-US. 2011;3(3):null-222.
doi:10.18632/aging.100296 .

Steelman, Linda S, Chappell, William H, Abrams, Stephen L, Kempf, C Ruth, Long, Jacquelyn M, Laidler, Piotr, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Stivala, Franca, Mazzarino, Maria C, Donia, Marco, Fagone, Paolo, Malaponte, Graziella, Nicoletti, Ferdinando, Libra, Massimo, Milella, Michele, Tafuri, Agostino, Bonati, Antonio, Baesecke, Joerg, Cocco, Lucio, Evangelisti, Camilla, Martelli, Alberto M, Montalto, Giuseppe, Cervello, Melchiorre, McCubrey, James A, "Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging" in Aging-US, 3, no. 3 (2011),
https://doi.org/10.18632/aging.100296 . .

TY  - JOUR
AU  - Donia, Marco
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Mojić, Marija
AU  - Miljković, Đorđe
AU  - Timotijević, Gordana S
AU  - Fagone, Paolo
AU  - Caponnetto, Salvatore
AU  - Al-Abed, Yousef
AU  - McCubrey, James A
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1309
AB  - The NO-derivative of the HIV protease inhibitor saquinavir (Saq-NO) is a nontoxic variant of the parental drug with enhanced anticancer activity on several cell lines. However, it is still unclear whether the p53 status of the target cell might influence the sensitivity to Saq-NO. In this study we evaluated the in vitro and in vivo activity of Saq-NO on the p53-deficient hormone resistant prostate cancer PC-3 cells. We demonstrate that the absence of functional p53 is not essential for the capacity of Saq-NO to reduce prostate cancer cell growth. In contrast to its previously described cytostatic action in B16 and C6 cell lines, Saq-NO exerted cytotoxic effects in PC-3 cells leading to dominant induction of apoptosis and enhanced production of proapoptotic Bim. In addition, differently from saquinavir, Saq-NO restored TRAIL sensitivity that was correlated with increased expression of DR5 independent from ROS/RNS production and YY1 repression. NF kappa B activation may be responsible of the Saq-NO induced DR5 expression. Moreover, Saq-NO but not saquinavir, exerted synergistic activity with conventional cytostatic therapy. In agreement with these in vitro studies, Saq-NO inhibited the in vivo growth of PC-3 cells xenotransplants to a greater extent than the parental compound. Taken together, these data indicate that Saq-NO possesses powerful and suitable in vitro and in vivo chemotherapeutic potential to be further studied as a novel drug for the treatment of prostate cancer in the clinical setting.
T2  - Cell Cycle
T1  - In vitro and in vivo anticancer action of Saquinavir-NO, a novel nitric oxide-derivative of the protease inhibitor saquinavir, on hormone resistant prostate cancer cells
IS  - 3
VL  - 10
EP  - 499
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1309
ER  - 

@article{
author = "Donia, Marco and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Mojić, Marija and Miljković, Đorđe and Timotijević, Gordana S and Fagone, Paolo and Caponnetto, Salvatore and Al-Abed, Yousef and McCubrey, James A and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando",
year = "2011",
abstract = "The NO-derivative of the HIV protease inhibitor saquinavir (Saq-NO) is a nontoxic variant of the parental drug with enhanced anticancer activity on several cell lines. However, it is still unclear whether the p53 status of the target cell might influence the sensitivity to Saq-NO. In this study we evaluated the in vitro and in vivo activity of Saq-NO on the p53-deficient hormone resistant prostate cancer PC-3 cells. We demonstrate that the absence of functional p53 is not essential for the capacity of Saq-NO to reduce prostate cancer cell growth. In contrast to its previously described cytostatic action in B16 and C6 cell lines, Saq-NO exerted cytotoxic effects in PC-3 cells leading to dominant induction of apoptosis and enhanced production of proapoptotic Bim. In addition, differently from saquinavir, Saq-NO restored TRAIL sensitivity that was correlated with increased expression of DR5 independent from ROS/RNS production and YY1 repression. NF kappa B activation may be responsible of the Saq-NO induced DR5 expression. Moreover, Saq-NO but not saquinavir, exerted synergistic activity with conventional cytostatic therapy. In agreement with these in vitro studies, Saq-NO inhibited the in vivo growth of PC-3 cells xenotransplants to a greater extent than the parental compound. Taken together, these data indicate that Saq-NO possesses powerful and suitable in vitro and in vivo chemotherapeutic potential to be further studied as a novel drug for the treatment of prostate cancer in the clinical setting.",
journal = "Cell Cycle",
title = "In vitro and in vivo anticancer action of Saquinavir-NO, a novel nitric oxide-derivative of the protease inhibitor saquinavir, on hormone resistant prostate cancer cells",
number = "3",
volume = "10",
pages = "499",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1309"
}

Donia, M., Maksimović-Ivanić, D., Mijatović, S., Mojić, M., Miljković, Đ., Timotijević, G. S., Fagone, P., Caponnetto, S., Al-Abed, Y., McCubrey, J. A., Stošić-Grujičić, S.,& Nicoletti, F.. (2011). In vitro and in vivo anticancer action of Saquinavir-NO, a novel nitric oxide-derivative of the protease inhibitor saquinavir, on hormone resistant prostate cancer cells. in Cell Cycle, 10(3).
https://hdl.handle.net/21.15107/rcub_ibiss_1309

Donia M, Maksimović-Ivanić D, Mijatović S, Mojić M, Miljković Đ, Timotijević GS, Fagone P, Caponnetto S, Al-Abed Y, McCubrey JA, Stošić-Grujičić S, Nicoletti F. In vitro and in vivo anticancer action of Saquinavir-NO, a novel nitric oxide-derivative of the protease inhibitor saquinavir, on hormone resistant prostate cancer cells. in Cell Cycle. 2011;10(3):null-499.
https://hdl.handle.net/21.15107/rcub_ibiss_1309 .

Donia, Marco, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Mojić, Marija, Miljković, Đorđe, Timotijević, Gordana S, Fagone, Paolo, Caponnetto, Salvatore, Al-Abed, Yousef, McCubrey, James A, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, "In vitro and in vivo anticancer action of Saquinavir-NO, a novel nitric oxide-derivative of the protease inhibitor saquinavir, on hormone resistant prostate cancer cells" in Cell Cycle, 10, no. 3 (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1309 .

TY  - JOUR
AU  - Chappell, William H
AU  - Steelman, Linda S
AU  - Long, Jacquelyn M
AU  - Kempf, Ruth C
AU  - Abrams, Stephen L
AU  - Franklin, Richard A
AU  - Baesecke, Joerg
AU  - Stivala, Franca
AU  - Donia, Marco
AU  - Fagone, Paolo
AU  - Malaponte, Graziella
AU  - Mazzarino, Maria C
AU  - Nicoletti, Ferdinando
AU  - Libra, Massimo
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Laidler, Piotr
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Bonati, Antonio
AU  - Evangelisti, Camilla
AU  - Cocco, Lucio
AU  - Martelli, Alberto M
AU  - McCubrey, James A
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1300
AB  - The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Integral components of these pathways, Ras, B-Raf, PI3K, and PTEN are also activated/inactivated by mutations. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of these pathways can contribute to chemotherapeutic drug resistance, proliferation of cancer initiating cells (CICs) and premature aging. This review will evaluate more recently described potential uses of MEK, PI3K, Akt and mTOR inhibitors in the proliferation of malignant cells, suppression of CICs, cellular senescence and prevention of aging. Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways play key roles in the regulation of normal and malignant cell growth. Inhibitors targeting these pathways have many potential uses from suppression of cancer, proliferative diseases as well as aging.
T2  - Oncotarget
T1  - Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health
IS  - 3
VL  - 2
DO  - 10.18632/oncotarget.240
EP  - 164
ER  - 

@article{
author = "Chappell, William H and Steelman, Linda S and Long, Jacquelyn M and Kempf, Ruth C and Abrams, Stephen L and Franklin, Richard A and Baesecke, Joerg and Stivala, Franca and Donia, Marco and Fagone, Paolo and Malaponte, Graziella and Mazzarino, Maria C and Nicoletti, Ferdinando and Libra, Massimo and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Montalto, Giuseppe and Cervello, Melchiorre and Laidler, Piotr and Milella, Michele and Tafuri, Agostino and Bonati, Antonio and Evangelisti, Camilla and Cocco, Lucio and Martelli, Alberto M and McCubrey, James A",
year = "2011",
abstract = "The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Integral components of these pathways, Ras, B-Raf, PI3K, and PTEN are also activated/inactivated by mutations. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of these pathways can contribute to chemotherapeutic drug resistance, proliferation of cancer initiating cells (CICs) and premature aging. This review will evaluate more recently described potential uses of MEK, PI3K, Akt and mTOR inhibitors in the proliferation of malignant cells, suppression of CICs, cellular senescence and prevention of aging. Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways play key roles in the regulation of normal and malignant cell growth. Inhibitors targeting these pathways have many potential uses from suppression of cancer, proliferative diseases as well as aging.",
journal = "Oncotarget",
title = "Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health",
number = "3",
volume = "2",
doi = "10.18632/oncotarget.240",
pages = "164"
}

Chappell, W. H., Steelman, L. S., Long, J. M., Kempf, R. C., Abrams, S. L., Franklin, R. A., Baesecke, J., Stivala, F., Donia, M., Fagone, P., Malaponte, G., Mazzarino, M. C., Nicoletti, F., Libra, M., Maksimović-Ivanić, D., Mijatović, S., Montalto, G., Cervello, M., Laidler, P., Milella, M., Tafuri, A., Bonati, A., Evangelisti, C., Cocco, L., Martelli, A. M.,& McCubrey, J. A.. (2011). Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health. in Oncotarget, 2(3).
https://doi.org/10.18632/oncotarget.240

Chappell WH, Steelman LS, Long JM, Kempf RC, Abrams SL, Franklin RA, Baesecke J, Stivala F, Donia M, Fagone P, Malaponte G, Mazzarino MC, Nicoletti F, Libra M, Maksimović-Ivanić D, Mijatović S, Montalto G, Cervello M, Laidler P, Milella M, Tafuri A, Bonati A, Evangelisti C, Cocco L, Martelli AM, McCubrey JA. Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health. in Oncotarget. 2011;2(3):null-164.
doi:10.18632/oncotarget.240 .

Chappell, William H, Steelman, Linda S, Long, Jacquelyn M, Kempf, Ruth C, Abrams, Stephen L, Franklin, Richard A, Baesecke, Joerg, Stivala, Franca, Donia, Marco, Fagone, Paolo, Malaponte, Graziella, Mazzarino, Maria C, Nicoletti, Ferdinando, Libra, Massimo, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Montalto, Giuseppe, Cervello, Melchiorre, Laidler, Piotr, Milella, Michele, Tafuri, Agostino, Bonati, Antonio, Evangelisti, Camilla, Cocco, Lucio, Martelli, Alberto M, McCubrey, James A, "Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health" in Oncotarget, 2, no. 3 (2011),
https://doi.org/10.18632/oncotarget.240 . .

TY  - CONF
AU  - Steelman, Linda S
AU  - Abrams, Stephen L
AU  - Chappell, William H
AU  - Martelli, Alberto M
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Mazzarino, Clorinda
AU  - Malaponte, Graziella
AU  - Libra, Massimo
AU  - Stivala, Franca
AU  - Cervello, Melchiorre
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - McCubrey, James A
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1313
C3  - International Journal of Molecular Medicine
T1  - Sensitization of cancer stem cells based on inhibiting key signal transduction pathways
IS  - null
VL  - 28
EP  - S18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1313
ER  - 

@conference{
author = "Steelman, Linda S and Abrams, Stephen L and Chappell, William H and Martelli, Alberto M and Nicoletti, Ferdinando and Fagone, Paolo and Mazzarino, Clorinda and Malaponte, Graziella and Libra, Massimo and Stivala, Franca and Cervello, Melchiorre and Mijatović, Sanja and Maksimović-Ivanić, Danijela and McCubrey, James A",
year = "2011",
journal = "International Journal of Molecular Medicine",
title = "Sensitization of cancer stem cells based on inhibiting key signal transduction pathways",
number = "null",
volume = "28",
pages = "S18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1313"
}

Steelman, L. S., Abrams, S. L., Chappell, W. H., Martelli, A. M., Nicoletti, F., Fagone, P., Mazzarino, C., Malaponte, G., Libra, M., Stivala, F., Cervello, M., Mijatović, S., Maksimović-Ivanić, D.,& McCubrey, J. A.. (2011). Sensitization of cancer stem cells based on inhibiting key signal transduction pathways. in International Journal of Molecular Medicine, 28(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1313

Steelman LS, Abrams SL, Chappell WH, Martelli AM, Nicoletti F, Fagone P, Mazzarino C, Malaponte G, Libra M, Stivala F, Cervello M, Mijatović S, Maksimović-Ivanić D, McCubrey JA. Sensitization of cancer stem cells based on inhibiting key signal transduction pathways. in International Journal of Molecular Medicine. 2011;28(null):null-S18.
https://hdl.handle.net/21.15107/rcub_ibiss_1313 .

Steelman, Linda S, Abrams, Stephen L, Chappell, William H, Martelli, Alberto M, Nicoletti, Ferdinando, Fagone, Paolo, Mazzarino, Clorinda, Malaponte, Graziella, Libra, Massimo, Stivala, Franca, Cervello, Melchiorre, Mijatović, Sanja, Maksimović-Ivanić, Danijela, McCubrey, James A, "Sensitization of cancer stem cells based on inhibiting key signal transduction pathways" in International Journal of Molecular Medicine, 28, no. null (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1313 .

TY  - CONF
AU  - McCubrey, James A
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Martelli, Alberto M
AU  - Stivala, Franca
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Mazzarino, Clorinda
AU  - Mulaponte, Graziella
AU  - Libra, Mussimo
AU  - Cervello, Melchiorre
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Steelman, Linda S
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1312
C3  - International Journal of Molecular Medicine
T1  - Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer
IS  - null
VL  - 28
EP  - S18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1312
ER  - 

@conference{
author = "McCubrey, James A and Chappell, William H and Abrams, Stephen L and Martelli, Alberto M and Stivala, Franca and Nicoletti, Ferdinando and Fagone, Paolo and Mazzarino, Clorinda and Mulaponte, Graziella and Libra, Mussimo and Cervello, Melchiorre and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Steelman, Linda S",
year = "2011",
journal = "International Journal of Molecular Medicine",
title = "Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer",
number = "null",
volume = "28",
pages = "S18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1312"
}

McCubrey, J. A., Chappell, W. H., Abrams, S. L., Martelli, A. M., Stivala, F., Nicoletti, F., Fagone, P., Mazzarino, C., Mulaponte, G., Libra, M., Cervello, M., Maksimović-Ivanić, D., Mijatović, S.,& Steelman, L. S.. (2011). Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer. in International Journal of Molecular Medicine, 28(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1312

McCubrey JA, Chappell WH, Abrams SL, Martelli AM, Stivala F, Nicoletti F, Fagone P, Mazzarino C, Mulaponte G, Libra M, Cervello M, Maksimović-Ivanić D, Mijatović S, Steelman LS. Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer. in International Journal of Molecular Medicine. 2011;28(null):null-S18.
https://hdl.handle.net/21.15107/rcub_ibiss_1312 .

McCubrey, James A, Chappell, William H, Abrams, Stephen L, Martelli, Alberto M, Stivala, Franca, Nicoletti, Ferdinando, Fagone, Paolo, Mazzarino, Clorinda, Mulaponte, Graziella, Libra, Mussimo, Cervello, Melchiorre, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Steelman, Linda S, "Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer" in International Journal of Molecular Medicine, 28, no. null (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1312 .

TY  - CONF
AU  - Donia, Marco
AU  - Mijatović, Sanja
AU  - Timotijević, Gordana S
AU  - Miljković, Đorđe
AU  - Stošić-Grujičić, Stanislava
AU  - Caponnetto, Salvatore
AU  - Fagone, Paolo
AU  - Mojić, Marija
AU  - Libra, Massimo
AU  - Maksimović-Ivanić, Danijela
AU  - Mangano, Katia
AU  - Nicoletti, Ferdinando
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1410
C3  - International Journal of Molecular Medicine
T1  - The effects of the nitric oxide-modified HIV protease inhibitor Saquinavir-NO (Saq-NO) on p53-deficient androgen independent prostate cancer cell lines
IS  - null
VL  - 26
EP  - S69
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1410
ER  - 

@conference{
author = "Donia, Marco and Mijatović, Sanja and Timotijević, Gordana S and Miljković, Đorđe and Stošić-Grujičić, Stanislava and Caponnetto, Salvatore and Fagone, Paolo and Mojić, Marija and Libra, Massimo and Maksimović-Ivanić, Danijela and Mangano, Katia and Nicoletti, Ferdinando",
year = "2010",
journal = "International Journal of Molecular Medicine",
title = "The effects of the nitric oxide-modified HIV protease inhibitor Saquinavir-NO (Saq-NO) on p53-deficient androgen independent prostate cancer cell lines",
number = "null",
volume = "26",
pages = "S69",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1410"
}

Donia, M., Mijatović, S., Timotijević, G. S., Miljković, Đ., Stošić-Grujičić, S., Caponnetto, S., Fagone, P., Mojić, M., Libra, M., Maksimović-Ivanić, D., Mangano, K.,& Nicoletti, F.. (2010). The effects of the nitric oxide-modified HIV protease inhibitor Saquinavir-NO (Saq-NO) on p53-deficient androgen independent prostate cancer cell lines. in International Journal of Molecular Medicine, 26(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1410

Donia M, Mijatović S, Timotijević GS, Miljković Đ, Stošić-Grujičić S, Caponnetto S, Fagone P, Mojić M, Libra M, Maksimović-Ivanić D, Mangano K, Nicoletti F. The effects of the nitric oxide-modified HIV protease inhibitor Saquinavir-NO (Saq-NO) on p53-deficient androgen independent prostate cancer cell lines. in International Journal of Molecular Medicine. 2010;26(null):null-S69.
https://hdl.handle.net/21.15107/rcub_ibiss_1410 .

Donia, Marco, Mijatović, Sanja, Timotijević, Gordana S, Miljković, Đorđe, Stošić-Grujičić, Stanislava, Caponnetto, Salvatore, Fagone, Paolo, Mojić, Marija, Libra, Massimo, Maksimović-Ivanić, Danijela, Mangano, Katia, Nicoletti, Ferdinando, "The effects of the nitric oxide-modified HIV protease inhibitor Saquinavir-NO (Saq-NO) on p53-deficient androgen independent prostate cancer cell lines" in International Journal of Molecular Medicine, 26, no. null (2010),
https://hdl.handle.net/21.15107/rcub_ibiss_1410 .