TY  - JOUR
AU  - Kovačić, Marijana
AU  - Mitrović-Ajtić, Olivera
AU  - Beleslin-Čokić, Bojana
AU  - Đikić, Dragoslava
AU  - Subotički, Tijana
AU  - Diklić, Miloš
AU  - Leković, Danijela
AU  - Gotić, Mirjana
AU  - Mossuz, Pascal
AU  - Čokić, Vladan
PY  - 2018
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/834
AB  - Purpose Previously, the family of S 100A proteins has been found to be associated with inflammation and myelopoiesis and to be able to induce or support myeloproliferation during chronic inflammation. Here, we studied the inflammatory myeloid-related proteins Si 00A4, S 100A8, S 100A9 and S100Al2 in myeloproliferative neoplasms (MPNs) in order to assess the involvement of chronic inflammation in the pathogenesis of MPN. Methods We analyzed the S100A4, S100A8, S100A9 and S100Al2 mRNA and protein levels in the bone marrow and circulation of 140 patients with MPN and 15 healthy controls using Western blotting, microarray-based mRNA expression profiling and ELISA assays, respectively. In addition we performed functional studies on the proliferation-related AKT and ERK1/2 signaling pathways in MPN-derived granulocytes using Western blotting and proteomic analyses. Results We found that the S100A mRNA levels were increased in MPN patient-derived circulatory CD34(+ )cells, and that their protein expression levels were also augmented in their granulocytes and bone marrow stroma cells, depending on the JAK2V617F mutation allele burden. We also found that calreticulin (CALR) mutations were related to reduced S100A8 plasma levels in primary myelofibrosis (PMF). The S100A8 plasma levels were found to be increased in MPN, the S100A9 plasma levels in PMF and essential thrombocythemia (ET), and the S100A12 plasma levels in polycythemia vera (PV). These 5100A plasma levels showed a positive correlation with the systemic inflammation marker IL-8, as well as with the numbers of leukocytes and thrombocytes, depending on the JAK2V617F mutation status. Additionally, we found that heterodimeric S100A8/9 can inhibit the AKT pathway in MPN-derived granulocytes mediated by the Toll-like receptor 4 (TLR4), depending on the CALR mutation status. Conversely, we found that blocking of the receptor for advanced glycation end products (RAGE) increased the S100A8/9-mediated inhibition of AKT signaling in the MPN-derived granulocytes. Moreover, we found that heterodimeric S100A8/9 generally induced TLR4-mediated ERK1/2 dephosphorylation proportionally to the JAK2V617F mutation allele burden. TLR4/RAGE blocking prevented the S100A8/9-mediated inhibition of ERK1/2 phosphorylation in PV. Conclusions From our data we conclude that the 5100A8 and S100A9 granulocyte and plasma levels are increased in MPN patients, along with inflammation markers, depending on their JAK2V617F mutation allele burden. We also found that SIO0A8/9-mediated inhibition of the proliferation-related AKT and ERK1/2 signaling pathways can be decreased by CALR mutationdependent TLR4 blocking and increased by RAGE inhibition in MPN.
PB  - Springer, Dordrecht
T2  - Cellular Oncology
T1  - TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms
EP  - 553
IS  - 5
SP  - 541
VL  - 41
DO  - 10.1007/s13402-018-0392-6
ER  - 

@article{
author = "Kovačić, Marijana and Mitrović-Ajtić, Olivera and Beleslin-Čokić, Bojana and Đikić, Dragoslava and Subotički, Tijana and Diklić, Miloš and Leković, Danijela and Gotić, Mirjana and Mossuz, Pascal and Čokić, Vladan",
year = "2018",
abstract = "Purpose Previously, the family of S 100A proteins has been found to be associated with inflammation and myelopoiesis and to be able to induce or support myeloproliferation during chronic inflammation. Here, we studied the inflammatory myeloid-related proteins Si 00A4, S 100A8, S 100A9 and S100Al2 in myeloproliferative neoplasms (MPNs) in order to assess the involvement of chronic inflammation in the pathogenesis of MPN. Methods We analyzed the S100A4, S100A8, S100A9 and S100Al2 mRNA and protein levels in the bone marrow and circulation of 140 patients with MPN and 15 healthy controls using Western blotting, microarray-based mRNA expression profiling and ELISA assays, respectively. In addition we performed functional studies on the proliferation-related AKT and ERK1/2 signaling pathways in MPN-derived granulocytes using Western blotting and proteomic analyses. Results We found that the S100A mRNA levels were increased in MPN patient-derived circulatory CD34(+ )cells, and that their protein expression levels were also augmented in their granulocytes and bone marrow stroma cells, depending on the JAK2V617F mutation allele burden. We also found that calreticulin (CALR) mutations were related to reduced S100A8 plasma levels in primary myelofibrosis (PMF). The S100A8 plasma levels were found to be increased in MPN, the S100A9 plasma levels in PMF and essential thrombocythemia (ET), and the S100A12 plasma levels in polycythemia vera (PV). These 5100A plasma levels showed a positive correlation with the systemic inflammation marker IL-8, as well as with the numbers of leukocytes and thrombocytes, depending on the JAK2V617F mutation status. Additionally, we found that heterodimeric S100A8/9 can inhibit the AKT pathway in MPN-derived granulocytes mediated by the Toll-like receptor 4 (TLR4), depending on the CALR mutation status. Conversely, we found that blocking of the receptor for advanced glycation end products (RAGE) increased the S100A8/9-mediated inhibition of AKT signaling in the MPN-derived granulocytes. Moreover, we found that heterodimeric S100A8/9 generally induced TLR4-mediated ERK1/2 dephosphorylation proportionally to the JAK2V617F mutation allele burden. TLR4/RAGE blocking prevented the S100A8/9-mediated inhibition of ERK1/2 phosphorylation in PV. Conclusions From our data we conclude that the 5100A8 and S100A9 granulocyte and plasma levels are increased in MPN patients, along with inflammation markers, depending on their JAK2V617F mutation allele burden. We also found that SIO0A8/9-mediated inhibition of the proliferation-related AKT and ERK1/2 signaling pathways can be decreased by CALR mutationdependent TLR4 blocking and increased by RAGE inhibition in MPN.",
publisher = "Springer, Dordrecht",
journal = "Cellular Oncology",
title = "TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms",
pages = "553-541",
number = "5",
volume = "41",
doi = "10.1007/s13402-018-0392-6"
}

Kovačić, M., Mitrović-Ajtić, O., Beleslin-Čokić, B., Đikić, D., Subotički, T., Diklić, M., Leković, D., Gotić, M., Mossuz, P.,& Čokić, V.. (2018). TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms. in Cellular Oncology
Springer, Dordrecht., 41(5), 541-553.
https://doi.org/10.1007/s13402-018-0392-6

Kovačić M, Mitrović-Ajtić O, Beleslin-Čokić B, Đikić D, Subotički T, Diklić M, Leković D, Gotić M, Mossuz P, Čokić V. TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms. in Cellular Oncology. 2018;41(5):541-553.
doi:10.1007/s13402-018-0392-6 .

Kovačić, Marijana, Mitrović-Ajtić, Olivera, Beleslin-Čokić, Bojana, Đikić, Dragoslava, Subotički, Tijana, Diklić, Miloš, Leković, Danijela, Gotić, Mirjana, Mossuz, Pascal, Čokić, Vladan, "TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms" in Cellular Oncology, 41, no. 5 (2018):541-553,
https://doi.org/10.1007/s13402-018-0392-6 . .

TY  - JOUR
AU  - Socoro-Yuste, Nuria
AU  - Čokić, Vladan
AU  - Mondet, Julie
AU  - Plo, Isabelle
AU  - Mossuz, Pascal
PY  - 2017
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/772
AB  - Apart from well-known genetic abnormalities, several studies have reported variations in protein expression in Philadelphianegative myeloproliferative neoplasm (MPN) patients that could contribute toward their clinical phenotype. In this context, a quantitative mass spectrometry proteomics protocol was used to identify differences in the granulocyte proteome with the goal to characterize the pathogenic role of aberrant protein expression in MPNs. LC/MS-MS (LTQ Orbitrap) coupled to iTRAQ labeling showed significant and quantitative differences in protein content among various MPN subtypes [polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF)], and according to the genetic status of JAK2 (JAK2V617F presence and JAK2V617F allele burden). A number of differentially expressed proteins were identified, with the most frequent being members of the RAS GTPase family and oxidative stress regulatory proteins. Subsequent analysis found that calreticulin (CALR), known to be involved in calcium homeostasis and apoptotic signaling, was overexpressed in JAK2V617F granulocytes compared with JAK2 wild type and independently of the JAK2V617F allele burden. Finally, it was demonstrated, in a Ba/F3 cell model, that increased calreticulin expression was directly linked to JAK2V617F and could be regulated by JAK2 kinase inhibitors. Implications: In conclusion, these results reveal proteome alterations in MPN granulocytes depending on the phenotype and genotype of patients, highlighting new oncogenic mechanisms associated with JAK2 mutations and overexpression of calreticulin.
PB  - Amer Assoc Cancer Research, Philadelphia
T2  - Molecular Cancer Research
T1  - Quantitative Proteome Heterogeneity in Myeloproliferative Neoplasm Subtypes and Association with JAK2 Mutation Status
EP  - 861
IS  - 7
SP  - 852
VL  - 15
DO  - 10.1158/1541-7786.MCR-16-0495
ER  - 

@article{
author = "Socoro-Yuste, Nuria and Čokić, Vladan and Mondet, Julie and Plo, Isabelle and Mossuz, Pascal",
year = "2017",
abstract = "Apart from well-known genetic abnormalities, several studies have reported variations in protein expression in Philadelphianegative myeloproliferative neoplasm (MPN) patients that could contribute toward their clinical phenotype. In this context, a quantitative mass spectrometry proteomics protocol was used to identify differences in the granulocyte proteome with the goal to characterize the pathogenic role of aberrant protein expression in MPNs. LC/MS-MS (LTQ Orbitrap) coupled to iTRAQ labeling showed significant and quantitative differences in protein content among various MPN subtypes [polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF)], and according to the genetic status of JAK2 (JAK2V617F presence and JAK2V617F allele burden). A number of differentially expressed proteins were identified, with the most frequent being members of the RAS GTPase family and oxidative stress regulatory proteins. Subsequent analysis found that calreticulin (CALR), known to be involved in calcium homeostasis and apoptotic signaling, was overexpressed in JAK2V617F granulocytes compared with JAK2 wild type and independently of the JAK2V617F allele burden. Finally, it was demonstrated, in a Ba/F3 cell model, that increased calreticulin expression was directly linked to JAK2V617F and could be regulated by JAK2 kinase inhibitors. Implications: In conclusion, these results reveal proteome alterations in MPN granulocytes depending on the phenotype and genotype of patients, highlighting new oncogenic mechanisms associated with JAK2 mutations and overexpression of calreticulin.",
publisher = "Amer Assoc Cancer Research, Philadelphia",
journal = "Molecular Cancer Research",
title = "Quantitative Proteome Heterogeneity in Myeloproliferative Neoplasm Subtypes and Association with JAK2 Mutation Status",
pages = "861-852",
number = "7",
volume = "15",
doi = "10.1158/1541-7786.MCR-16-0495"
}

Socoro-Yuste, N., Čokić, V., Mondet, J., Plo, I.,& Mossuz, P.. (2017). Quantitative Proteome Heterogeneity in Myeloproliferative Neoplasm Subtypes and Association with JAK2 Mutation Status. in Molecular Cancer Research
Amer Assoc Cancer Research, Philadelphia., 15(7), 852-861.
https://doi.org/10.1158/1541-7786.MCR-16-0495

Socoro-Yuste N, Čokić V, Mondet J, Plo I, Mossuz P. Quantitative Proteome Heterogeneity in Myeloproliferative Neoplasm Subtypes and Association with JAK2 Mutation Status. in Molecular Cancer Research. 2017;15(7):852-861.
doi:10.1158/1541-7786.MCR-16-0495 .

Socoro-Yuste, Nuria, Čokić, Vladan, Mondet, Julie, Plo, Isabelle, Mossuz, Pascal, "Quantitative Proteome Heterogeneity in Myeloproliferative Neoplasm Subtypes and Association with JAK2 Mutation Status" in Molecular Cancer Research, 15, no. 7 (2017):852-861,
https://doi.org/10.1158/1541-7786.MCR-16-0495 . .

TY  - CONF
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Puri, Raj K.
AU  - Beleslin-Čokić, Bojana
AU  - Mitrović-Ajtić, Olivera
AU  - Subotički, Tijana
AU  - Diklić, Miloš
AU  - Leković, Danijela
AU  - Gotić, Mirjana
PY  - 2015
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/616
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Gene and protein expression analyses of the mtor signaling pathway in myeloproliferative neoplasms
EP  - 528
SP  - 528
VL  - 100
UR  - https://hdl.handle.net/21.15107/rcub_rimi_616
ER  - 

@conference{
author = "Čokić, Vladan and Mossuz, Pascal and Puri, Raj K. and Beleslin-Čokić, Bojana and Mitrović-Ajtić, Olivera and Subotički, Tijana and Diklić, Miloš and Leković, Danijela and Gotić, Mirjana",
year = "2015",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Gene and protein expression analyses of the mtor signaling pathway in myeloproliferative neoplasms",
pages = "528-528",
volume = "100",
url = "https://hdl.handle.net/21.15107/rcub_rimi_616"
}

Čokić, V., Mossuz, P., Puri, R. K., Beleslin-Čokić, B., Mitrović-Ajtić, O., Subotički, T., Diklić, M., Leković, D.,& Gotić, M.. (2015). Gene and protein expression analyses of the mtor signaling pathway in myeloproliferative neoplasms. in Haematologica
Ferrata Storti Foundation, Pavia., 100, 528-528.
https://hdl.handle.net/21.15107/rcub_rimi_616

Čokić V, Mossuz P, Puri RK, Beleslin-Čokić B, Mitrović-Ajtić O, Subotički T, Diklić M, Leković D, Gotić M. Gene and protein expression analyses of the mtor signaling pathway in myeloproliferative neoplasms. in Haematologica. 2015;100:528-528.
https://hdl.handle.net/21.15107/rcub_rimi_616 .

Čokić, Vladan, Mossuz, Pascal, Puri, Raj K., Beleslin-Čokić, Bojana, Mitrović-Ajtić, Olivera, Subotički, Tijana, Diklić, Miloš, Leković, Danijela, Gotić, Mirjana, "Gene and protein expression analyses of the mtor signaling pathway in myeloproliferative neoplasms" in Haematologica, 100 (2015):528-528,
https://hdl.handle.net/21.15107/rcub_rimi_616 .

TY  - JOUR
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Han, Jing
AU  - Socoro, Nuria
AU  - Beleslin-Čokić, Bojana
AU  - Mitrović, Olivera
AU  - Subotički, Tijana
AU  - Diklić, Miloš
AU  - Leković, Danijela
AU  - Gotić, Mirjana
AU  - Puri, Raj K.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2015
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/670
AB  - The gene and protein expression profiles in myeloproliferative neoplasms (MPNs) may reveal gene and protein markers of a potential clinical relevance in diagnosis, treatment and prediction of response to therapy. Using cDNA microarray analysis of 25,100 unique genes, we studied the gene expression profile of CD34(+) cells and granulocytes obtained from peripheral blood of subjects with essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). The microarray analyses of the CD34(+) cells and granulocytes were performed from 20 de novo MPN subjects: JAK2 positive ET, PV, PMF subjects, and JAK2 negative ET/PMF subjects. The granulocytes for proteomic studies were pooled in 4 groups: PV with JAK2 mutant allele burden above 80%, ET with JAK2 mutation, PMF with JAK2 mutation and ET/PMF with no JAK2 mutation. The number of differentially regulated genes was about two fold larger in CD34(+) cells compared to granulocytes. Thirty-six genes (including RUNX1, TNFRSF19) were persistently highly expressed, while 42 genes (including FOXD4, PDE4A) were underexpressed both in CD34(+) cells and granulocytes. Using proteomic studies, significant up-regulation was observed for MAPK and PI3K/AKT signaling regulators that control myeloid cell apoptosis and proliferation: RAC2, MNDA, S100A8/9, CORO1A, and GNAI2. When the status of the mTOR signaling pathway related genes was analyzed, PI3K/AKT regulators were preferentially up-regulated in CD34(+) cells of MPNs, with down-regulated major components of the protein complex EIF4F. Molecular profiling of CD34(+) cells and granulocytes of MPN determined gene expression patterns beyond their recognized function in disease pathogenesis that included dominant up-regulation of PI3K/AKT signaling.
PB  - Public Library Science, San Francisco
T2  - PLoS One
T1  - Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway
IS  - 8
VL  - 10
DO  - 10.1371/journal.pone.0135463
ER  - 

@article{
author = "Čokić, Vladan and Mossuz, Pascal and Han, Jing and Socoro, Nuria and Beleslin-Čokić, Bojana and Mitrović, Olivera and Subotički, Tijana and Diklić, Miloš and Leković, Danijela and Gotić, Mirjana and Puri, Raj K. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2015",
abstract = "The gene and protein expression profiles in myeloproliferative neoplasms (MPNs) may reveal gene and protein markers of a potential clinical relevance in diagnosis, treatment and prediction of response to therapy. Using cDNA microarray analysis of 25,100 unique genes, we studied the gene expression profile of CD34(+) cells and granulocytes obtained from peripheral blood of subjects with essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). The microarray analyses of the CD34(+) cells and granulocytes were performed from 20 de novo MPN subjects: JAK2 positive ET, PV, PMF subjects, and JAK2 negative ET/PMF subjects. The granulocytes for proteomic studies were pooled in 4 groups: PV with JAK2 mutant allele burden above 80%, ET with JAK2 mutation, PMF with JAK2 mutation and ET/PMF with no JAK2 mutation. The number of differentially regulated genes was about two fold larger in CD34(+) cells compared to granulocytes. Thirty-six genes (including RUNX1, TNFRSF19) were persistently highly expressed, while 42 genes (including FOXD4, PDE4A) were underexpressed both in CD34(+) cells and granulocytes. Using proteomic studies, significant up-regulation was observed for MAPK and PI3K/AKT signaling regulators that control myeloid cell apoptosis and proliferation: RAC2, MNDA, S100A8/9, CORO1A, and GNAI2. When the status of the mTOR signaling pathway related genes was analyzed, PI3K/AKT regulators were preferentially up-regulated in CD34(+) cells of MPNs, with down-regulated major components of the protein complex EIF4F. Molecular profiling of CD34(+) cells and granulocytes of MPN determined gene expression patterns beyond their recognized function in disease pathogenesis that included dominant up-regulation of PI3K/AKT signaling.",
publisher = "Public Library Science, San Francisco",
journal = "PLoS One",
title = "Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway",
number = "8",
volume = "10",
doi = "10.1371/journal.pone.0135463"
}

Čokić, V., Mossuz, P., Han, J., Socoro, N., Beleslin-Čokić, B., Mitrović, O., Subotički, T., Diklić, M., Leković, D., Gotić, M., Puri, R. K., Noguchi, C. T.,& Schechter, A. N.. (2015). Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway. in PLoS One
Public Library Science, San Francisco., 10(8).
https://doi.org/10.1371/journal.pone.0135463

Čokić V, Mossuz P, Han J, Socoro N, Beleslin-Čokić B, Mitrović O, Subotički T, Diklić M, Leković D, Gotić M, Puri RK, Noguchi CT, Schechter AN. Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway. in PLoS One. 2015;10(8).
doi:10.1371/journal.pone.0135463 .

Čokić, Vladan, Mossuz, Pascal, Han, Jing, Socoro, Nuria, Beleslin-Čokić, Bojana, Mitrović, Olivera, Subotički, Tijana, Diklić, Miloš, Leković, Danijela, Gotić, Mirjana, Puri, Raj K., Noguchi, Constance T., Schechter, Alan N., "Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway" in PLoS One, 10, no. 8 (2015),
https://doi.org/10.1371/journal.pone.0135463 . .

TY  - CONF
AU  - Mitrović, Olivera
AU  - Mossuz, Pascal
AU  - Diklić, Miloš
AU  - Sefer, Dijana
AU  - Ilić, B.
AU  - Peruničić, Maja
AU  - Jovčić, Gordana
AU  - Čokić, Vladan
PY  - 2013
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/518
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Expression analysis of jak-stat dependent s100 calcium binding proteins a4 and a12 in myeloproliferative neoplasms
EP  - 616
SP  - 616
VL  - 98
UR  - https://hdl.handle.net/21.15107/rcub_rimi_518
ER  - 

@conference{
author = "Mitrović, Olivera and Mossuz, Pascal and Diklić, Miloš and Sefer, Dijana and Ilić, B. and Peruničić, Maja and Jovčić, Gordana and Čokić, Vladan",
year = "2013",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Expression analysis of jak-stat dependent s100 calcium binding proteins a4 and a12 in myeloproliferative neoplasms",
pages = "616-616",
volume = "98",
url = "https://hdl.handle.net/21.15107/rcub_rimi_518"
}

Mitrović, O., Mossuz, P., Diklić, M., Sefer, D., Ilić, B., Peruničić, M., Jovčić, G.,& Čokić, V.. (2013). Expression analysis of jak-stat dependent s100 calcium binding proteins a4 and a12 in myeloproliferative neoplasms. in Haematologica
Ferrata Storti Foundation, Pavia., 98, 616-616.
https://hdl.handle.net/21.15107/rcub_rimi_518

Mitrović O, Mossuz P, Diklić M, Sefer D, Ilić B, Peruničić M, Jovčić G, Čokić V. Expression analysis of jak-stat dependent s100 calcium binding proteins a4 and a12 in myeloproliferative neoplasms. in Haematologica. 2013;98:616-616.
https://hdl.handle.net/21.15107/rcub_rimi_518 .

Mitrović, Olivera, Mossuz, Pascal, Diklić, Miloš, Sefer, Dijana, Ilić, B., Peruničić, Maja, Jovčić, Gordana, Čokić, Vladan, "Expression analysis of jak-stat dependent s100 calcium binding proteins a4 and a12 in myeloproliferative neoplasms" in Haematologica, 98 (2013):616-616,
https://hdl.handle.net/21.15107/rcub_rimi_518 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Sefer, Dijana
AU  - Diklić, Miloš
AU  - Breković, Tijana
AU  - Vignjević, Sanja
AU  - Ilić, B.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2012
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/436
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica
T1  - Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies
EP  - 380
SP  - 380
VL  - 97
UR  - https://hdl.handle.net/21.15107/rcub_rimi_436
ER  - 

@conference{
author = "Čokić, Vladan and Mossuz, Pascal and Sefer, Dijana and Diklić, Miloš and Breković, Tijana and Vignjević, Sanja and Ilić, B. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2012",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica",
title = "Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies",
pages = "380-380",
volume = "97",
url = "https://hdl.handle.net/21.15107/rcub_rimi_436"
}

Čokić, V., Mossuz, P., Sefer, D., Diklić, M., Breković, T., Vignjević, S., Ilić, B., Noguchi, C. T.,& Schechter, A. N.. (2012). Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies. in Haematologica
Ferrata Storti Foundation, Pavia., 97, 380-380.
https://hdl.handle.net/21.15107/rcub_rimi_436

Čokić V, Mossuz P, Sefer D, Diklić M, Breković T, Vignjević S, Ilić B, Noguchi CT, Schechter AN. Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies. in Haematologica. 2012;97:380-380.
https://hdl.handle.net/21.15107/rcub_rimi_436 .

Čokić, Vladan, Mossuz, Pascal, Sefer, Dijana, Diklić, Miloš, Breković, Tijana, Vignjević, Sanja, Ilić, B., Noguchi, Constance T., Schechter, Alan N., "Expression analysis of s100 proteins in myeloproliferative neoplasm by microarray and proteomic studies" in Haematologica, 97 (2012):380-380,
https://hdl.handle.net/21.15107/rcub_rimi_436 .

TY  - CONF
AU  - Čokić, Vladan
AU  - Mossuz, Pascal
AU  - Han, Jing
AU  - Diklić, Miloš
AU  - Budeč, Mirela
AU  - Sefer, Dijana
AU  - Leković, Danijela
AU  - Antić, Darko
AU  - Breković, Tijana
AU  - Mojsilović, Sonja
AU  - Puri, Raj K.
AU  - Noguchi, Constance T.
AU  - Schechter, Alan N.
PY  - 2011
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/348
PB  - Amer Soc Hematology, Washington
C3  - Blood
T1  - Microarray and Proteomic Analysis of Myeloproliferative Neoplasms
EP  - 1649
IS  - 21
SP  - 1649
VL  - 118
UR  - https://hdl.handle.net/21.15107/rcub_rimi_348
ER  - 

@conference{
author = "Čokić, Vladan and Mossuz, Pascal and Han, Jing and Diklić, Miloš and Budeč, Mirela and Sefer, Dijana and Leković, Danijela and Antić, Darko and Breković, Tijana and Mojsilović, Sonja and Puri, Raj K. and Noguchi, Constance T. and Schechter, Alan N.",
year = "2011",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "Microarray and Proteomic Analysis of Myeloproliferative Neoplasms",
pages = "1649-1649",
number = "21",
volume = "118",
url = "https://hdl.handle.net/21.15107/rcub_rimi_348"
}

Čokić, V., Mossuz, P., Han, J., Diklić, M., Budeč, M., Sefer, D., Leković, D., Antić, D., Breković, T., Mojsilović, S., Puri, R. K., Noguchi, C. T.,& Schechter, A. N.. (2011). Microarray and Proteomic Analysis of Myeloproliferative Neoplasms. in Blood
Amer Soc Hematology, Washington., 118(21), 1649-1649.
https://hdl.handle.net/21.15107/rcub_rimi_348

Čokić V, Mossuz P, Han J, Diklić M, Budeč M, Sefer D, Leković D, Antić D, Breković T, Mojsilović S, Puri RK, Noguchi CT, Schechter AN. Microarray and Proteomic Analysis of Myeloproliferative Neoplasms. in Blood. 2011;118(21):1649-1649.
https://hdl.handle.net/21.15107/rcub_rimi_348 .

Čokić, Vladan, Mossuz, Pascal, Han, Jing, Diklić, Miloš, Budeč, Mirela, Sefer, Dijana, Leković, Danijela, Antić, Darko, Breković, Tijana, Mojsilović, Sonja, Puri, Raj K., Noguchi, Constance T., Schechter, Alan N., "Microarray and Proteomic Analysis of Myeloproliferative Neoplasms" in Blood, 118, no. 21 (2011):1649-1649,
https://hdl.handle.net/21.15107/rcub_rimi_348 .