TY  - CHAP
AU  - Kapor, Sunčica
AU  - Momčilović, Sanja
AU  - Kapor, Slobodan
AU  - Mojsilović, Slavko
AU  - Radojković, Milica
AU  - Apostolović, Milica
AU  - Filipović, Branka
AU  - Gotić, Mirjana
AU  - Čokić, Vladan
AU  - Santibanez, Juan F.
AU  - Simon, Felipe
PY  - 2023
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1391
AB  - The Philadelphia-negative myeloproliferative neoplasms (MPNs), defined as clonal disorders of the hematopoietic stem cells, are characterized by the proliferation of mature myeloid cells in the bone marrow and a chronic inflammatory status impacting the initiation, progression, and symptomatology of the malignancies. There are three main entities defined as essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF), and genetically classified by JAK2V617F, CALR, or MPL mutations. In MPNs, due to the overproduction of inflammatory cytokines by the neoplastic cells and non-transformed immune cells, chronic inflammation may provoke the generation and expansion of myeloid-derived suppressors cells (MDSCs) that highly influence the adaptive immune response. Although peripheral blood MDSC levels are elevated, their frequency in the bone marrow of MPNs patients is not well elucidated yet. Our results indicated increased levels of total (T)-MDSCs (CD33+HLA-DR−/low) and polymorphonuclear (PMN)-MDSCs (CD33+/HLA-DRlow/CD15+/CD14−) in the bone marrow and peripheral blood of all three types of MPNs malignancies. However, these bone marrow MDSCs-increased frequencies did not correlate with the clinical parameters, such as hepatomegaly, leukocytes, hemoglobin, or platelet levels, or with JAK2 and CALR mutations. Besides, bone marrow MDSCs, from ET, PV, and PMF patients, exhibited immunosuppressive function, determined as T-cell proliferation inhibition. Notably, the highest T-MDSCs and PMN-MDSC levels were found in PMF samples, and the increased MDSCs frequency strongly correlated with the degree of myelofibrosis. Thus, these data together indicate that the immunosuppressive MDSCs population is increased in the bone marrow of MPNs patients and may be implicated in generating a fibrotic microenvironment.
PB  - Springer Nature
T2  - Advances in Molecular Pathology
T1  - Increase in Frequency of Myeloid-Derived Suppressor Cells in the Bone Marrow of Myeloproliferative Neoplasm: Potential Implications in Myelofibrosis
EP  - 290
SP  - 273
VL  - 1408
DO  - 10.1007/978-3-031-26163-3_15
ER  - 

@inbook{
author = "Kapor, Sunčica and Momčilović, Sanja and Kapor, Slobodan and Mojsilović, Slavko and Radojković, Milica and Apostolović, Milica and Filipović, Branka and Gotić, Mirjana and Čokić, Vladan and Santibanez, Juan F. and Simon, Felipe",
year = "2023",
abstract = "The Philadelphia-negative myeloproliferative neoplasms (MPNs), defined as clonal disorders of the hematopoietic stem cells, are characterized by the proliferation of mature myeloid cells in the bone marrow and a chronic inflammatory status impacting the initiation, progression, and symptomatology of the malignancies. There are three main entities defined as essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF), and genetically classified by JAK2V617F, CALR, or MPL mutations. In MPNs, due to the overproduction of inflammatory cytokines by the neoplastic cells and non-transformed immune cells, chronic inflammation may provoke the generation and expansion of myeloid-derived suppressors cells (MDSCs) that highly influence the adaptive immune response. Although peripheral blood MDSC levels are elevated, their frequency in the bone marrow of MPNs patients is not well elucidated yet. Our results indicated increased levels of total (T)-MDSCs (CD33+HLA-DR−/low) and polymorphonuclear (PMN)-MDSCs (CD33+/HLA-DRlow/CD15+/CD14−) in the bone marrow and peripheral blood of all three types of MPNs malignancies. However, these bone marrow MDSCs-increased frequencies did not correlate with the clinical parameters, such as hepatomegaly, leukocytes, hemoglobin, or platelet levels, or with JAK2 and CALR mutations. Besides, bone marrow MDSCs, from ET, PV, and PMF patients, exhibited immunosuppressive function, determined as T-cell proliferation inhibition. Notably, the highest T-MDSCs and PMN-MDSC levels were found in PMF samples, and the increased MDSCs frequency strongly correlated with the degree of myelofibrosis. Thus, these data together indicate that the immunosuppressive MDSCs population is increased in the bone marrow of MPNs patients and may be implicated in generating a fibrotic microenvironment.",
publisher = "Springer Nature",
journal = "Advances in Molecular Pathology",
booktitle = "Increase in Frequency of Myeloid-Derived Suppressor Cells in the Bone Marrow of Myeloproliferative Neoplasm: Potential Implications in Myelofibrosis",
pages = "290-273",
volume = "1408",
doi = "10.1007/978-3-031-26163-3_15"
}

Kapor, S., Momčilović, S., Kapor, S., Mojsilović, S., Radojković, M., Apostolović, M., Filipović, B., Gotić, M., Čokić, V., Santibanez, J. F.,& Simon, F.. (2023). Increase in Frequency of Myeloid-Derived Suppressor Cells in the Bone Marrow of Myeloproliferative Neoplasm: Potential Implications in Myelofibrosis. in Advances in Molecular Pathology
Springer Nature., 1408, 273-290.
https://doi.org/10.1007/978-3-031-26163-3_15

Kapor S, Momčilović S, Kapor S, Mojsilović S, Radojković M, Apostolović M, Filipović B, Gotić M, Čokić V, Santibanez JF, Simon F. Increase in Frequency of Myeloid-Derived Suppressor Cells in the Bone Marrow of Myeloproliferative Neoplasm: Potential Implications in Myelofibrosis. in Advances in Molecular Pathology. 2023;1408:273-290.
doi:10.1007/978-3-031-26163-3_15 .

Kapor, Sunčica, Momčilović, Sanja, Kapor, Slobodan, Mojsilović, Slavko, Radojković, Milica, Apostolović, Milica, Filipović, Branka, Gotić, Mirjana, Čokić, Vladan, Santibanez, Juan F., Simon, Felipe, "Increase in Frequency of Myeloid-Derived Suppressor Cells in the Bone Marrow of Myeloproliferative Neoplasm: Potential Implications in Myelofibrosis" in Advances in Molecular Pathology, 1408 (2023):273-290,
https://doi.org/10.1007/978-3-031-26163-3_15 . .

TY  - JOUR
AU  - Vukotić, Milica
AU  - Kapor, Sunčica
AU  - Dragojević, Teodora
AU  - Đikić, Dragoslava
AU  - Mitrović-Ajtić, Olivera
AU  - Diklić, Miloš
AU  - Subotički, Tijana
AU  - Živković, Emilija
AU  - Beleslin-Čokić, Bojana
AU  - Vojvodić, Aleksandar
AU  - Santibanez, Juan F.
AU  - Gotić, Mirjana
AU  - Čokić, Vladan
PY  - 2022
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1226
AB  - Although bone marrow-derived mesenchymal stromal cells (BM-MSCs) have been identified as a major cellular source of fibrosis, the exact molecular mechanism and signaling pathways involved have not been identified thus far. Here, we show that BM-MSCs contribute to fibrosis in myeloproliferative neoplasms (MPNs) by differentiating into αSMA-positive myofibroblasts. These cells display a dysregulated extracellular matrix with increased FN1 production and secretion of profibrotic MMP9 compared to healthy donor cells. Fibrogenic TGFβ and inflammatory JAK2/STAT3 and NFκB signaling pathway activity is increased in BM-MSCs of MPN patients. Moreover, coculture with mononuclear cells from MPN patients was sufficient to induce fibrosis in healthy BM-MSCs. Inhibition of JAK1/2, SMAD3 or NFκB significantly reduced the fibrotic phenotype of MPN BM-MSCs and was able to prevent the development of fibrosis induced by coculture of healthy BM-MSCs and MPN mononuclear cells with overly active JAK/STAT signaling, underlining their involvement in fibrosis. Combined treatment with JAK1/2 and SMAD3 inhibitors showed synergistic and the most favorable effects on αSMA and FN1 expression in BM-MSCs. These results support the combined inhibition of TGFβ and inflammatory signaling to extenuate fibrosis in MPN.
PB  - Korean Society of Medical Biochemistry and Molecular Biology [Associate Organisation]
PB  - Springer Nature [Commercial Publisher]
T2  - Experimental & Molecular Medicine
T1  - Inhibition of proinflammatory signaling impairs fibrosis of bone marrow mesenchymal stromal cells in myeloproliferative neoplasms
EP  - 284
IS  - 3
SP  - 273
VL  - 54
DO  - 10.1038/s12276-022-00742-y
ER  - 

@article{
author = "Vukotić, Milica and Kapor, Sunčica and Dragojević, Teodora and Đikić, Dragoslava and Mitrović-Ajtić, Olivera and Diklić, Miloš and Subotički, Tijana and Živković, Emilija and Beleslin-Čokić, Bojana and Vojvodić, Aleksandar and Santibanez, Juan F. and Gotić, Mirjana and Čokić, Vladan",
year = "2022",
abstract = "Although bone marrow-derived mesenchymal stromal cells (BM-MSCs) have been identified as a major cellular source of fibrosis, the exact molecular mechanism and signaling pathways involved have not been identified thus far. Here, we show that BM-MSCs contribute to fibrosis in myeloproliferative neoplasms (MPNs) by differentiating into αSMA-positive myofibroblasts. These cells display a dysregulated extracellular matrix with increased FN1 production and secretion of profibrotic MMP9 compared to healthy donor cells. Fibrogenic TGFβ and inflammatory JAK2/STAT3 and NFκB signaling pathway activity is increased in BM-MSCs of MPN patients. Moreover, coculture with mononuclear cells from MPN patients was sufficient to induce fibrosis in healthy BM-MSCs. Inhibition of JAK1/2, SMAD3 or NFκB significantly reduced the fibrotic phenotype of MPN BM-MSCs and was able to prevent the development of fibrosis induced by coculture of healthy BM-MSCs and MPN mononuclear cells with overly active JAK/STAT signaling, underlining their involvement in fibrosis. Combined treatment with JAK1/2 and SMAD3 inhibitors showed synergistic and the most favorable effects on αSMA and FN1 expression in BM-MSCs. These results support the combined inhibition of TGFβ and inflammatory signaling to extenuate fibrosis in MPN.",
publisher = "Korean Society of Medical Biochemistry and Molecular Biology [Associate Organisation], Springer Nature [Commercial Publisher]",
journal = "Experimental & Molecular Medicine",
title = "Inhibition of proinflammatory signaling impairs fibrosis of bone marrow mesenchymal stromal cells in myeloproliferative neoplasms",
pages = "284-273",
number = "3",
volume = "54",
doi = "10.1038/s12276-022-00742-y"
}

Vukotić, M., Kapor, S., Dragojević, T., Đikić, D., Mitrović-Ajtić, O., Diklić, M., Subotički, T., Živković, E., Beleslin-Čokić, B., Vojvodić, A., Santibanez, J. F., Gotić, M.,& Čokić, V.. (2022). Inhibition of proinflammatory signaling impairs fibrosis of bone marrow mesenchymal stromal cells in myeloproliferative neoplasms. in Experimental & Molecular Medicine
Korean Society of Medical Biochemistry and Molecular Biology [Associate Organisation]., 54(3), 273-284.
https://doi.org/10.1038/s12276-022-00742-y

Vukotić M, Kapor S, Dragojević T, Đikić D, Mitrović-Ajtić O, Diklić M, Subotički T, Živković E, Beleslin-Čokić B, Vojvodić A, Santibanez JF, Gotić M, Čokić V. Inhibition of proinflammatory signaling impairs fibrosis of bone marrow mesenchymal stromal cells in myeloproliferative neoplasms. in Experimental & Molecular Medicine. 2022;54(3):273-284.
doi:10.1038/s12276-022-00742-y .

Vukotić, Milica, Kapor, Sunčica, Dragojević, Teodora, Đikić, Dragoslava, Mitrović-Ajtić, Olivera, Diklić, Miloš, Subotički, Tijana, Živković, Emilija, Beleslin-Čokić, Bojana, Vojvodić, Aleksandar, Santibanez, Juan F., Gotić, Mirjana, Čokić, Vladan, "Inhibition of proinflammatory signaling impairs fibrosis of bone marrow mesenchymal stromal cells in myeloproliferative neoplasms" in Experimental & Molecular Medicine, 54, no. 3 (2022):273-284,
https://doi.org/10.1038/s12276-022-00742-y . .

TY  - JOUR
AU  - Kapor, Sunčica
AU  - Vukotić, Milica
AU  - Subotički, Tijana
AU  - Đikić, Dragoslava
AU  - Mitrović-Ajtić, Olivera
AU  - Radojković, Milica
AU  - Čokić, Vladan
AU  - Santibanez, Juan F.
PY  - 2021
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1172
AB  - Hydroxyurea (HU) is an antineoplastic agent that functions as an antimetabolite compound by inhibiting the ribonucleotide reductase. HU acts mainly as a cytostatic drug that through DNA replication stress may trigger a premature senescence-like cell phenotype, though its influence on bone marrow-derived mesenchymal stem/stromal cell (BMMSC) functions has not elucidated yet. Our results indicate that HU inhibits the growth of human BMMSC alongside senescence-like changes in both morphology and replicative potential, provokes cell cycle arrest at the S phase without affecting cellular viability and induces the expression of senescence-associated β-galactosidase and p16INK4. Moreover, HU-induced senescent BMMSC, although they did not change MSC markers expression, exhibited reduced capacity osteogenic and adipogenic differentiation. Conversely, HU treatment increased immunoregulatory functions of BMMSC compared with untreated cells and determined by T-cell proliferation. Interestingly, HU did not influence the capacity of BMMSC to induce monocytic myeloid-derived suppressor cells. Thus, these results suggest that HU improves the BMMSC functions on the T-cell inhibition and preserves their interaction with myeloid cell compartment. Mechanistically, BMMSC under HU treatment displayed a downregulation of mTOR and p38 MAPK signaling that may explain the reduced cell differentiation and increased immunomodulation activities. Together, the results obtained in this investigation suggest that HU by inducing senescence-like phenotype of BMMSC influences their cellular differentiation and immunoregulatory functions.
PB  - MDPI
T2  - Journal of Personalized Medicine
T1  - Hydroxyurea Induces Bone Marrow Mesenchymal Stromal Cells Senescence and Modifies Cell Functionality In Vitro
IS  - 11
SP  - 1048
VL  - 11
DO  - 10.3390/jpm11111048
ER  - 

@article{
author = "Kapor, Sunčica and Vukotić, Milica and Subotički, Tijana and Đikić, Dragoslava and Mitrović-Ajtić, Olivera and Radojković, Milica and Čokić, Vladan and Santibanez, Juan F.",
year = "2021",
abstract = "Hydroxyurea (HU) is an antineoplastic agent that functions as an antimetabolite compound by inhibiting the ribonucleotide reductase. HU acts mainly as a cytostatic drug that through DNA replication stress may trigger a premature senescence-like cell phenotype, though its influence on bone marrow-derived mesenchymal stem/stromal cell (BMMSC) functions has not elucidated yet. Our results indicate that HU inhibits the growth of human BMMSC alongside senescence-like changes in both morphology and replicative potential, provokes cell cycle arrest at the S phase without affecting cellular viability and induces the expression of senescence-associated β-galactosidase and p16INK4. Moreover, HU-induced senescent BMMSC, although they did not change MSC markers expression, exhibited reduced capacity osteogenic and adipogenic differentiation. Conversely, HU treatment increased immunoregulatory functions of BMMSC compared with untreated cells and determined by T-cell proliferation. Interestingly, HU did not influence the capacity of BMMSC to induce monocytic myeloid-derived suppressor cells. Thus, these results suggest that HU improves the BMMSC functions on the T-cell inhibition and preserves their interaction with myeloid cell compartment. Mechanistically, BMMSC under HU treatment displayed a downregulation of mTOR and p38 MAPK signaling that may explain the reduced cell differentiation and increased immunomodulation activities. Together, the results obtained in this investigation suggest that HU by inducing senescence-like phenotype of BMMSC influences their cellular differentiation and immunoregulatory functions.",
publisher = "MDPI",
journal = "Journal of Personalized Medicine",
title = "Hydroxyurea Induces Bone Marrow Mesenchymal Stromal Cells Senescence and Modifies Cell Functionality In Vitro",
number = "11",
pages = "1048",
volume = "11",
doi = "10.3390/jpm11111048"
}

Kapor, S., Vukotić, M., Subotički, T., Đikić, D., Mitrović-Ajtić, O., Radojković, M., Čokić, V.,& Santibanez, J. F.. (2021). Hydroxyurea Induces Bone Marrow Mesenchymal Stromal Cells Senescence and Modifies Cell Functionality In Vitro. in Journal of Personalized Medicine
MDPI., 11(11), 1048.
https://doi.org/10.3390/jpm11111048

Kapor S, Vukotić M, Subotički T, Đikić D, Mitrović-Ajtić O, Radojković M, Čokić V, Santibanez JF. Hydroxyurea Induces Bone Marrow Mesenchymal Stromal Cells Senescence and Modifies Cell Functionality In Vitro. in Journal of Personalized Medicine. 2021;11(11):1048.
doi:10.3390/jpm11111048 .

Kapor, Sunčica, Vukotić, Milica, Subotički, Tijana, Đikić, Dragoslava, Mitrović-Ajtić, Olivera, Radojković, Milica, Čokić, Vladan, Santibanez, Juan F., "Hydroxyurea Induces Bone Marrow Mesenchymal Stromal Cells Senescence and Modifies Cell Functionality In Vitro" in Journal of Personalized Medicine, 11, no. 11 (2021):1048,
https://doi.org/10.3390/jpm11111048 . .

TY  - JOUR
AU  - Kapor, Sunčica
AU  - Santibanez, Juan F.
PY  - 2021
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1163
AB  - Myeloid malignancies arise from an altered hematopoietic stem cell and mainly comprise acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic leukemic cells may influence the growth and differentiation of other hematopoietic cell lineages in peripheral blood and bone marrow. Myeloid-derived suppressor cells (MDSCs) and mesenchymal stromal cells (MSCs) display immunoregulatory properties by controlling the innate and adaptive immune systems that may induce a tolerant and supportive microenvironment for neoplasm development. This review analyzes the main features of MDSCs and MSCs in myeloid malignancies. The number of MDSCs is elevated in myeloid malignancies exhibiting high immunosuppressive capacities, whereas MSCs, in addition to their immunosuppression contribution, regulate myeloid leukemia cell proliferation, apoptosis, and chemotherapy resistance. Moreover, MSCs may promote MDSC expansion, which may mutually contribute to the creation of an immuno-tolerant neoplasm microenvironment. Understanding the implication of MDSCs and MSCs in myeloid malignancies may favor their potential use in immunotherapeutic strategies.
PB  - MDPI
T2  - Journal of Clinical Medicine
T1  - Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies
IS  - 13
SP  - 2788
VL  - 10
DO  - 10.3390/jcm10132788
ER  - 

@article{
author = "Kapor, Sunčica and Santibanez, Juan F.",
year = "2021",
abstract = "Myeloid malignancies arise from an altered hematopoietic stem cell and mainly comprise acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic leukemic cells may influence the growth and differentiation of other hematopoietic cell lineages in peripheral blood and bone marrow. Myeloid-derived suppressor cells (MDSCs) and mesenchymal stromal cells (MSCs) display immunoregulatory properties by controlling the innate and adaptive immune systems that may induce a tolerant and supportive microenvironment for neoplasm development. This review analyzes the main features of MDSCs and MSCs in myeloid malignancies. The number of MDSCs is elevated in myeloid malignancies exhibiting high immunosuppressive capacities, whereas MSCs, in addition to their immunosuppression contribution, regulate myeloid leukemia cell proliferation, apoptosis, and chemotherapy resistance. Moreover, MSCs may promote MDSC expansion, which may mutually contribute to the creation of an immuno-tolerant neoplasm microenvironment. Understanding the implication of MDSCs and MSCs in myeloid malignancies may favor their potential use in immunotherapeutic strategies.",
publisher = "MDPI",
journal = "Journal of Clinical Medicine",
title = "Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies",
number = "13",
pages = "2788",
volume = "10",
doi = "10.3390/jcm10132788"
}

Kapor, S.,& Santibanez, J. F.. (2021). Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies. in Journal of Clinical Medicine
MDPI., 10(13), 2788.
https://doi.org/10.3390/jcm10132788

Kapor S, Santibanez JF. Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies. in Journal of Clinical Medicine. 2021;10(13):2788.
doi:10.3390/jcm10132788 .

Kapor, Sunčica, Santibanez, Juan F., "Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies" in Journal of Clinical Medicine, 10, no. 13 (2021):2788,
https://doi.org/10.3390/jcm10132788 . .

TY  - JOUR
AU  - Kapor, Sunčica
AU  - Čokić, Vladan
AU  - Santibanez, Juan F.
PY  - 2021
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1174
AB  - Hydroxyurea (HU) is a water-soluble antiproliferative agent used for decades in neoplastic and nonneoplastic conditions. HU is considered an essential medicine because of its cytoreduction functions. HU is an antimetabolite that inhibits ribonucleotide reductase, which causes a depletion of the deoxyribonucleotide pool and dramatically reduces cell proliferation. The proliferation arrest, depending on drug concentration and exposure, may promote a cellular senescence phenotype associated with cancer cell therapy resistance and inflammation, influencing neighboring cell functions, immunosuppression, and potential cancer relapse. HU can induce cellular senescence in both healthy and transformed cells in vitro, in part, because of increased reactive oxygen species (ROS). Here, we analyze the main molecular mechanisms involved in cytotoxic/genotoxic HU function, the potential to increase intracellular ROS levels, and the principal features of cellular senescence induction. Understanding the mechanisms involved in HU's ability to induce cellular senescence may help to improve current chemotherapy strategies and control undesirable treatment effects in cancer patients and other diseases.
PB  - Hindawi
T2  - Oxidative Medicine and Cellular Longevity
T1  - Mechanisms of Hydroxyurea-Induced Cellular Senescence: An Oxidative Stress Connection?
SP  - e7753857
VL  - 2021
DO  - 10.1155/2021/7753857
ER  - 

@article{
author = "Kapor, Sunčica and Čokić, Vladan and Santibanez, Juan F.",
year = "2021",
abstract = "Hydroxyurea (HU) is a water-soluble antiproliferative agent used for decades in neoplastic and nonneoplastic conditions. HU is considered an essential medicine because of its cytoreduction functions. HU is an antimetabolite that inhibits ribonucleotide reductase, which causes a depletion of the deoxyribonucleotide pool and dramatically reduces cell proliferation. The proliferation arrest, depending on drug concentration and exposure, may promote a cellular senescence phenotype associated with cancer cell therapy resistance and inflammation, influencing neighboring cell functions, immunosuppression, and potential cancer relapse. HU can induce cellular senescence in both healthy and transformed cells in vitro, in part, because of increased reactive oxygen species (ROS). Here, we analyze the main molecular mechanisms involved in cytotoxic/genotoxic HU function, the potential to increase intracellular ROS levels, and the principal features of cellular senescence induction. Understanding the mechanisms involved in HU's ability to induce cellular senescence may help to improve current chemotherapy strategies and control undesirable treatment effects in cancer patients and other diseases.",
publisher = "Hindawi",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Mechanisms of Hydroxyurea-Induced Cellular Senescence: An Oxidative Stress Connection?",
pages = "e7753857",
volume = "2021",
doi = "10.1155/2021/7753857"
}

Kapor, S., Čokić, V.,& Santibanez, J. F.. (2021). Mechanisms of Hydroxyurea-Induced Cellular Senescence: An Oxidative Stress Connection?. in Oxidative Medicine and Cellular Longevity
Hindawi., 2021, e7753857.
https://doi.org/10.1155/2021/7753857

Kapor S, Čokić V, Santibanez JF. Mechanisms of Hydroxyurea-Induced Cellular Senescence: An Oxidative Stress Connection?. in Oxidative Medicine and Cellular Longevity. 2021;2021:e7753857.
doi:10.1155/2021/7753857 .

Kapor, Sunčica, Čokić, Vladan, Santibanez, Juan F., "Mechanisms of Hydroxyurea-Induced Cellular Senescence: An Oxidative Stress Connection?" in Oxidative Medicine and Cellular Longevity, 2021 (2021):e7753857,
https://doi.org/10.1155/2021/7753857 . .