TY  - JOUR
AU  - Spasovski, Vesna
AU  - Tošić, Nataša
AU  - Kostić, Tatjana
AU  - Pavlović, Sonja
AU  - Čolović, Milica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/470
AB  - Uvod. Stečena somatska mutacija V617F u genu za Janus kinazu 2 (JAK2) uzrok je nekontrolisane proliferacije ćelija kod bolesnika s mijeloproliferativnim neoplazijama. Poznato je da do proliferacije ćelija mijeloidne loze dolazi i pod uticajem mutacija u drugim genima, kao što su mutacije u genu za tirozin-kinazni receptor FLT3, koji je najčešći mutirani gen u akutnim mijeloidnim leukemijama. Od posebnog je značaja to što mutirani protein FLT3 koristi isti signalni put kao protein JAK2. To je signalni put preko proteina STAT5, čija je aktivacija važna za samoobnavljanje matičnih ćelija hematopoeze. Cilj rada. Cilj istraživanja je bio da se otkrije mutacija V617F u genu za JAK2 kod bolesnika s mijeloproliferativnim neoplazijama. Ispitano je i istovremeno prisustvo mutacije FLT3-ITD kod ovih bolesnika radi rasvetljavanja hipoteze o sličnoj ulozi ova dva molekularnogenetička markera u hematološkim malignitetima. Metode rada. Metodom alel-specifičnog PCR (engl. polymerase chain reaction) analiziran je 61 bolesnik sa potvrđenom dijagnozom mijeloproliferativne neoplazije na mutaciju V617F u genu za JAK2 ili sumnjom na ovu dijagnozu. Kod bolesnika sa mutacijom u genu JAK2 je zatim ispitano postojanje mutacije FLT3-ITD metodom PCR. Rezultati. Kod 18 ispitanika je otkrivena mutacija V617F u genu za JAK2. Među njima je kod osam bolesnika dijagnostikovana policitemija vera, a kod deset esencijalna trombocitemija. Ni kod jednog ispitanika s mutacijom V617F u genu za JAK2 nije otkrivena mutacija FLT3-ITD. Zaključak. Rezultati ovog istraživanja podržavaju hipotezu da je za malignu transformaciju matične ćelije hematopoeze dovoljna jedna mutacija koja izaziva poremećaj proliferacije ćelije.
AB  - Introduction. An acquired somatic mutation V617F in Janus kinase 2 gene (JAK2) is the cause of uncontrolled proliferation in patients with myeloproliferative neoplasms. It is known that uncontrolled myeloid cell proliferation is also provoked by alteration in other genes, e.g. mutations in receptor tyrosine kinase FLT3 gene. FLT3 represents the most frequently mutated gene in acute myeloid leukaemia. Interestingly, mutated FLT3- ITD (internal tandem duplication) protein is a member of the same signalling pathway as JAK2 protein, the STAT5 signalling pathway. STAT5 activation is recognized as important for selfrenewal of haematopoetic stem cells. Objective. The aim of this study was the detection of JAK2- V617F mutation in patients with myeloproliferative neoplasms. Additionally, we investigated the presence of FLT3-ITD mutation in JAK2-V617F-positive patients in order to shed the light on the hypothesis of a similar role of these two molecular markers in haematological malignancies. Methods. Using allele-specific PCR, 61 patients with known or suspected diagnosis of myeloproliferative neoplasms were tested for the presence of JAK2-V617F mutation. Samples that were positive for JAK2 mutation were subsequently tested for the presence of FLT3-ITD mutation by PCR. Results. Eighteen of 61 analysed patients were positive for JAK2-V617F mutation. Among them, 8/18 samples were diagnosed as polycythaemia vera, and 10/18 as essential thrombocythaemia. None of JAK2-V617F-positive patient was positive for FLT3-ITD mutation. Conclusion. This study suggests that one activating mutation is sufficient for aberrant cell proliferation leading to malignant transformation of haematopoetic stem cell.
PB  - Srpsko lekarsko društvo, Beograd
T2  - Srpski arhiv za celokupno lekarstvo
T1  - Mutacija JAK2-V617F kod bolesnika s mijeloproliferativnim neoplazijama - veza sa mutacijom FLT3-ITD
T1  - JAK2-V617F mutation in patients with myeloproliferative neoplasms: Association with FLT3-ITD mutation
EP  - 618
IS  - 9-10
SP  - 614
VL  - 138
DO  - 10.2298/SARH1010614S
ER  - 

@article{
author = "Spasovski, Vesna and Tošić, Nataša and Kostić, Tatjana and Pavlović, Sonja and Čolović, Milica",
year = "2010",
abstract = "Uvod. Stečena somatska mutacija V617F u genu za Janus kinazu 2 (JAK2) uzrok je nekontrolisane proliferacije ćelija kod bolesnika s mijeloproliferativnim neoplazijama. Poznato je da do proliferacije ćelija mijeloidne loze dolazi i pod uticajem mutacija u drugim genima, kao što su mutacije u genu za tirozin-kinazni receptor FLT3, koji je najčešći mutirani gen u akutnim mijeloidnim leukemijama. Od posebnog je značaja to što mutirani protein FLT3 koristi isti signalni put kao protein JAK2. To je signalni put preko proteina STAT5, čija je aktivacija važna za samoobnavljanje matičnih ćelija hematopoeze. Cilj rada. Cilj istraživanja je bio da se otkrije mutacija V617F u genu za JAK2 kod bolesnika s mijeloproliferativnim neoplazijama. Ispitano je i istovremeno prisustvo mutacije FLT3-ITD kod ovih bolesnika radi rasvetljavanja hipoteze o sličnoj ulozi ova dva molekularnogenetička markera u hematološkim malignitetima. Metode rada. Metodom alel-specifičnog PCR (engl. polymerase chain reaction) analiziran je 61 bolesnik sa potvrđenom dijagnozom mijeloproliferativne neoplazije na mutaciju V617F u genu za JAK2 ili sumnjom na ovu dijagnozu. Kod bolesnika sa mutacijom u genu JAK2 je zatim ispitano postojanje mutacije FLT3-ITD metodom PCR. Rezultati. Kod 18 ispitanika je otkrivena mutacija V617F u genu za JAK2. Među njima je kod osam bolesnika dijagnostikovana policitemija vera, a kod deset esencijalna trombocitemija. Ni kod jednog ispitanika s mutacijom V617F u genu za JAK2 nije otkrivena mutacija FLT3-ITD. Zaključak. Rezultati ovog istraživanja podržavaju hipotezu da je za malignu transformaciju matične ćelije hematopoeze dovoljna jedna mutacija koja izaziva poremećaj proliferacije ćelije., Introduction. An acquired somatic mutation V617F in Janus kinase 2 gene (JAK2) is the cause of uncontrolled proliferation in patients with myeloproliferative neoplasms. It is known that uncontrolled myeloid cell proliferation is also provoked by alteration in other genes, e.g. mutations in receptor tyrosine kinase FLT3 gene. FLT3 represents the most frequently mutated gene in acute myeloid leukaemia. Interestingly, mutated FLT3- ITD (internal tandem duplication) protein is a member of the same signalling pathway as JAK2 protein, the STAT5 signalling pathway. STAT5 activation is recognized as important for selfrenewal of haematopoetic stem cells. Objective. The aim of this study was the detection of JAK2- V617F mutation in patients with myeloproliferative neoplasms. Additionally, we investigated the presence of FLT3-ITD mutation in JAK2-V617F-positive patients in order to shed the light on the hypothesis of a similar role of these two molecular markers in haematological malignancies. Methods. Using allele-specific PCR, 61 patients with known or suspected diagnosis of myeloproliferative neoplasms were tested for the presence of JAK2-V617F mutation. Samples that were positive for JAK2 mutation were subsequently tested for the presence of FLT3-ITD mutation by PCR. Results. Eighteen of 61 analysed patients were positive for JAK2-V617F mutation. Among them, 8/18 samples were diagnosed as polycythaemia vera, and 10/18 as essential thrombocythaemia. None of JAK2-V617F-positive patient was positive for FLT3-ITD mutation. Conclusion. This study suggests that one activating mutation is sufficient for aberrant cell proliferation leading to malignant transformation of haematopoetic stem cell.",
publisher = "Srpsko lekarsko društvo, Beograd",
journal = "Srpski arhiv za celokupno lekarstvo",
title = "Mutacija JAK2-V617F kod bolesnika s mijeloproliferativnim neoplazijama - veza sa mutacijom FLT3-ITD, JAK2-V617F mutation in patients with myeloproliferative neoplasms: Association with FLT3-ITD mutation",
pages = "618-614",
number = "9-10",
volume = "138",
doi = "10.2298/SARH1010614S"
}

Spasovski, V., Tošić, N., Kostić, T., Pavlović, S.,& Čolović, M.. (2010). Mutacija JAK2-V617F kod bolesnika s mijeloproliferativnim neoplazijama - veza sa mutacijom FLT3-ITD. in Srpski arhiv za celokupno lekarstvo
Srpsko lekarsko društvo, Beograd., 138(9-10), 614-618.
https://doi.org/10.2298/SARH1010614S

Spasovski V, Tošić N, Kostić T, Pavlović S, Čolović M. Mutacija JAK2-V617F kod bolesnika s mijeloproliferativnim neoplazijama - veza sa mutacijom FLT3-ITD. in Srpski arhiv za celokupno lekarstvo. 2010;138(9-10):614-618.
doi:10.2298/SARH1010614S .

Spasovski, Vesna, Tošić, Nataša, Kostić, Tatjana, Pavlović, Sonja, Čolović, Milica, "Mutacija JAK2-V617F kod bolesnika s mijeloproliferativnim neoplazijama - veza sa mutacijom FLT3-ITD" in Srpski arhiv za celokupno lekarstvo, 138, no. 9-10 (2010):614-618,
https://doi.org/10.2298/SARH1010614S . .

TY  - CONF
AU  - Miljić, Predrag
AU  - Heylen, Evelien
AU  - Willemse, Johan
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
AU  - Colović, Milica
AU  - Elezović, Ivo
AU  - Hendriks, Dirk
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/426
AB  - Although the maintenance of precise balance between coagulation and fibrinolysis is of utmost importance for normal haemostasis, until recently these two systems were considered as completely separate mechanisms involved in the process of formation and dissolution of blood clot. Thrombin activatable fibrinolysis inhibitor (TAFI) is a recently described attenuator of the fibrinolytic rate and is considered to be the molecular link between coagulation and fibrinolysis. TAFI circulates in plasma as an inactive precursor and its conversion in active enzyme (TAFIa) occurs by the action of thrombin or plasmin, but most efficiently by thrombin in the presence of its cofactor thrombomodulin. Once generated, TAFI down-regulates fibrinolysis by removing C-terminal lysine residues from partially degraded fibrin; thereby preventing the upregulation of plasminogen binding and activation. Because TAFI is activated by thrombin on one side, and acts as the attenuator of fibrinolysis on another side, it enables fine synchronization between these two systems. The antifibrinolytic function of TAFI mostly depends on TAFI concentration, the rate of its activation and the half-life of TAFIa in plasma. Changes in thrombin generation can have a profound effect on the rate of TAFI activation, and consequently on the rate of fibrinolysis. Therefore, it has been hypothesized that increased thrombin generation seen in thrombophilia patients may enhance TAFI activation, leading to a hypofibrinolytic state, which may further contribute to the thrombotic tendency. However, the results of several studies, in which relation between TAFI level and the occurrence of thromboembolic complications in carriers of hereditary thrombophilia have been investigated, were not consistent.
PB  - Srpsko lekarsko društvo, Beograd
C3  - Srpski arhiv za celokupno lekarstvo
T1  - Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis
EP  - 78
SP  - 74
VL  - 138
DO  - 10.2298/SARH10S1074M
ER  - 

@conference{
author = "Miljić, Predrag and Heylen, Evelien and Willemse, Johan and Đorđević, Valentina and Radojković, Dragica and Colović, Milica and Elezović, Ivo and Hendriks, Dirk",
year = "2010",
abstract = "Although the maintenance of precise balance between coagulation and fibrinolysis is of utmost importance for normal haemostasis, until recently these two systems were considered as completely separate mechanisms involved in the process of formation and dissolution of blood clot. Thrombin activatable fibrinolysis inhibitor (TAFI) is a recently described attenuator of the fibrinolytic rate and is considered to be the molecular link between coagulation and fibrinolysis. TAFI circulates in plasma as an inactive precursor and its conversion in active enzyme (TAFIa) occurs by the action of thrombin or plasmin, but most efficiently by thrombin in the presence of its cofactor thrombomodulin. Once generated, TAFI down-regulates fibrinolysis by removing C-terminal lysine residues from partially degraded fibrin; thereby preventing the upregulation of plasminogen binding and activation. Because TAFI is activated by thrombin on one side, and acts as the attenuator of fibrinolysis on another side, it enables fine synchronization between these two systems. The antifibrinolytic function of TAFI mostly depends on TAFI concentration, the rate of its activation and the half-life of TAFIa in plasma. Changes in thrombin generation can have a profound effect on the rate of TAFI activation, and consequently on the rate of fibrinolysis. Therefore, it has been hypothesized that increased thrombin generation seen in thrombophilia patients may enhance TAFI activation, leading to a hypofibrinolytic state, which may further contribute to the thrombotic tendency. However, the results of several studies, in which relation between TAFI level and the occurrence of thromboembolic complications in carriers of hereditary thrombophilia have been investigated, were not consistent.",
publisher = "Srpsko lekarsko društvo, Beograd",
journal = "Srpski arhiv za celokupno lekarstvo",
title = "Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis",
pages = "78-74",
volume = "138",
doi = "10.2298/SARH10S1074M"
}

Miljić, P., Heylen, E., Willemse, J., Đorđević, V., Radojković, D., Colović, M., Elezović, I.,& Hendriks, D.. (2010). Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis. in Srpski arhiv za celokupno lekarstvo
Srpsko lekarsko društvo, Beograd., 138, 74-78.
https://doi.org/10.2298/SARH10S1074M

Miljić P, Heylen E, Willemse J, Đorđević V, Radojković D, Colović M, Elezović I, Hendriks D. Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis. in Srpski arhiv za celokupno lekarstvo. 2010;138:74-78.
doi:10.2298/SARH10S1074M .

Miljić, Predrag, Heylen, Evelien, Willemse, Johan, Đorđević, Valentina, Radojković, Dragica, Colović, Milica, Elezović, Ivo, Hendriks, Dirk, "Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis" in Srpski arhiv za celokupno lekarstvo, 138 (2010):74-78,
https://doi.org/10.2298/SARH10S1074M . .

TY  - JOUR
AU  - Spasovski, Vesna
AU  - Tošić, Nataša
AU  - Kostić, Tatjana
AU  - Zukić, Branka
AU  - Stojiljković, Maja
AU  - Čolović, Milica
AU  - Pavlović, Sonja
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/450
AB  - Mijeloproliferativne neoplazije (MPN) su hematološki maligniteti koji se karakterišu nekontrolisanom ćelijskom proliferacijom i poremećajem u procesu apoptoze. Sistem FasR/FasL je uključen u kontrolu apoptoze u različitim tipovima ćelija. U ovom radu je izučavana uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija. Upoređena je ekspresija FasR i FasL između pacijenata sa MPN (24) i zdravih kontrola korišćenjem metode 'real-time' PCR. Detektovana je povećana ekspresija FasR kod pacijenata sa MPN. Nije utvrđena razlika u ekspresiji FasL. Mutacija B617F u JAK2 genu, karakteristična za MPN, je nađena kod 13 od 24 pacijenta. Pokazano je da ekspresija FasR i FasL nije povezana sa prisustvom B617F JAK2 mutacije.
AB  - Myeloproliferative neoplasms (MPN) are hematological malignancies characterized by uncontrolled cell proliferation and impaired apoptosis. The FasR/FasL system is involved in the control of apoptosis in different cell types. Here we have investigated the role of FasR/FasL in the pathogenesis of MPNs. We compared FasR/FasL expression between MPN patients (24) and healthy individuals using the real-time PCR assay. We found an increase of FasR expression in MPN patients. No difference was detected in FasL expression. Mutation V617F in the JAK2 gene, a hallmark of MPN, was detected in 13/24 patients. We found that neither FasR nor FasL expression were related to the presence of JAK2 V617F mutation.
PB  - Srpsko biološko društvo, Beograd, i dr.
T2  - Archives of Biological Sciences
T1  - Uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija
T1  - The role of FasR/FasL system in pathogenesis of myeloprolyferative neoplasms
EP  - 230
IS  - 2
SP  - 223
VL  - 62
DO  - 10.2298/ABS1002223S
ER  - 

@article{
author = "Spasovski, Vesna and Tošić, Nataša and Kostić, Tatjana and Zukić, Branka and Stojiljković, Maja and Čolović, Milica and Pavlović, Sonja",
year = "2010",
abstract = "Mijeloproliferativne neoplazije (MPN) su hematološki maligniteti koji se karakterišu nekontrolisanom ćelijskom proliferacijom i poremećajem u procesu apoptoze. Sistem FasR/FasL je uključen u kontrolu apoptoze u različitim tipovima ćelija. U ovom radu je izučavana uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija. Upoređena je ekspresija FasR i FasL između pacijenata sa MPN (24) i zdravih kontrola korišćenjem metode 'real-time' PCR. Detektovana je povećana ekspresija FasR kod pacijenata sa MPN. Nije utvrđena razlika u ekspresiji FasL. Mutacija B617F u JAK2 genu, karakteristična za MPN, je nađena kod 13 od 24 pacijenta. Pokazano je da ekspresija FasR i FasL nije povezana sa prisustvom B617F JAK2 mutacije., Myeloproliferative neoplasms (MPN) are hematological malignancies characterized by uncontrolled cell proliferation and impaired apoptosis. The FasR/FasL system is involved in the control of apoptosis in different cell types. Here we have investigated the role of FasR/FasL in the pathogenesis of MPNs. We compared FasR/FasL expression between MPN patients (24) and healthy individuals using the real-time PCR assay. We found an increase of FasR expression in MPN patients. No difference was detected in FasL expression. Mutation V617F in the JAK2 gene, a hallmark of MPN, was detected in 13/24 patients. We found that neither FasR nor FasL expression were related to the presence of JAK2 V617F mutation.",
publisher = "Srpsko biološko društvo, Beograd, i dr.",
journal = "Archives of Biological Sciences",
title = "Uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija, The role of FasR/FasL system in pathogenesis of myeloprolyferative neoplasms",
pages = "230-223",
number = "2",
volume = "62",
doi = "10.2298/ABS1002223S"
}

Spasovski, V., Tošić, N., Kostić, T., Zukić, B., Stojiljković, M., Čolović, M.,& Pavlović, S.. (2010). Uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija. in Archives of Biological Sciences
Srpsko biološko društvo, Beograd, i dr.., 62(2), 223-230.
https://doi.org/10.2298/ABS1002223S

Spasovski V, Tošić N, Kostić T, Zukić B, Stojiljković M, Čolović M, Pavlović S. Uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija. in Archives of Biological Sciences. 2010;62(2):223-230.
doi:10.2298/ABS1002223S .

Spasovski, Vesna, Tošić, Nataša, Kostić, Tatjana, Zukić, Branka, Stojiljković, Maja, Čolović, Milica, Pavlović, Sonja, "Uloga sistema FasR/FasL u patogenezi mijeloproliferativnih neoplazija" in Archives of Biological Sciences, 62, no. 2 (2010):223-230,
https://doi.org/10.2298/ABS1002223S . .

TY  - JOUR
AU  - Nagorni-Obradović, L. J.
AU  - Miljić, Predrag
AU  - Đorđević, Valentina
AU  - Pesut, D. P.
AU  - Jovanović, D.
AU  - Stojsić, J.
AU  - Stević, R.
AU  - Radojković, Dragica
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/372
AB  - Diagnosis of pulmonary thromboembolism (PTE) usually includes clinical pretest probability assessment, testing for specific degradation products of cross-linked fibrin (D-dimer) and imaging studies. Patients with radiological findings attributable to pulmonary infarction and normal D-dimer level, may present a diagnostic and therapeutic challenge. A 37-year-old Caucasian female had episodes of hemoptysis, and bilateral pulmonary nodular infiltrates on chest radiograph and computerized tomography. The plasma D-dimer level was normal, perfusion lung scan was not conclusive and histological examination of an open lung biopsy revealed recent thrombotic pulmonary infarction. She deteriorated and more perfusion defects were detected on perfusion lung scan. Genetic analysis revealed her to be a carrier of the prothrombin factor II (FII) G20210A mutation.
PB  - Macedonian Acad Sciences Arts, Skopje
T2  - Balkan Journal of Medical Genetics
T1  - The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products
EP  - 75
IS  - 2
SP  - 69
VL  - 12
DO  - 10.2478/v10034-010-0007-7
ER  - 

@article{
author = "Nagorni-Obradović, L. J. and Miljić, Predrag and Đorđević, Valentina and Pesut, D. P. and Jovanović, D. and Stojsić, J. and Stević, R. and Radojković, Dragica",
year = "2009",
abstract = "Diagnosis of pulmonary thromboembolism (PTE) usually includes clinical pretest probability assessment, testing for specific degradation products of cross-linked fibrin (D-dimer) and imaging studies. Patients with radiological findings attributable to pulmonary infarction and normal D-dimer level, may present a diagnostic and therapeutic challenge. A 37-year-old Caucasian female had episodes of hemoptysis, and bilateral pulmonary nodular infiltrates on chest radiograph and computerized tomography. The plasma D-dimer level was normal, perfusion lung scan was not conclusive and histological examination of an open lung biopsy revealed recent thrombotic pulmonary infarction. She deteriorated and more perfusion defects were detected on perfusion lung scan. Genetic analysis revealed her to be a carrier of the prothrombin factor II (FII) G20210A mutation.",
publisher = "Macedonian Acad Sciences Arts, Skopje",
journal = "Balkan Journal of Medical Genetics",
title = "The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products",
pages = "75-69",
number = "2",
volume = "12",
doi = "10.2478/v10034-010-0007-7"
}

Nagorni-Obradović, L. J., Miljić, P., Đorđević, V., Pesut, D. P., Jovanović, D., Stojsić, J., Stević, R.,& Radojković, D.. (2009). The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products. in Balkan Journal of Medical Genetics
Macedonian Acad Sciences Arts, Skopje., 12(2), 69-75.
https://doi.org/10.2478/v10034-010-0007-7

Nagorni-Obradović LJ, Miljić P, Đorđević V, Pesut DP, Jovanović D, Stojsić J, Stević R, Radojković D. The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products. in Balkan Journal of Medical Genetics. 2009;12(2):69-75.
doi:10.2478/v10034-010-0007-7 .

Nagorni-Obradović, L. J., Miljić, Predrag, Đorđević, Valentina, Pesut, D. P., Jovanović, D., Stojsić, J., Stević, R., Radojković, Dragica, "The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products" in Balkan Journal of Medical Genetics, 12, no. 2 (2009):69-75,
https://doi.org/10.2478/v10034-010-0007-7 . .

TY  - JOUR
AU  - Tošić, Nataša
AU  - Stojiljković, Maja
AU  - Čolović, Nataša
AU  - Colović, Milica
AU  - Pavlović, Sonja
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/358
AB  - The NUP98 gene at chromosome band 11p15 is known to be fused to a number of different partners in various hematological malignancies. The most frequently observed fusion partners of NUP98 are the homeobox family of transcriptional factors (HOX genes). We report a case of de novo AML M4 subtype, with a t(11;12)(p15;q13) translocation, generating a NUP98-HOXC13 chimeric transcript. Molecular analysis showed that the exon 16 of NUP98 was fused in frame with exon 2 of HOXC13. The patient was also positive for FLT3 internal tandem duplication (ITD), another molecular marker for the disease. Comparative study of data on the fusion of HOW cluster and NUP98 gene revealed that it is a rare event, found exclusively in AML patients. To our knowledge, this is the first case of t(11;12)(p15;q13) in de novo AML-M4 in association with FLT3 ITD mutation. Coexistence of NUP98-HOXC13 fusion and FLT3 ITD mutation is likely relevant in the process of leukemogenesis.
PB  - Elsevier Science Inc, New York
T2  - Cancer Genetics and Cytogenetics
T1  - Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review
EP  - 103
IS  - 2
SP  - 98
VL  - 193
DO  - 10.1016/j.cancergencyto.2009.03.007
ER  - 

@article{
author = "Tošić, Nataša and Stojiljković, Maja and Čolović, Nataša and Colović, Milica and Pavlović, Sonja",
year = "2009",
abstract = "The NUP98 gene at chromosome band 11p15 is known to be fused to a number of different partners in various hematological malignancies. The most frequently observed fusion partners of NUP98 are the homeobox family of transcriptional factors (HOX genes). We report a case of de novo AML M4 subtype, with a t(11;12)(p15;q13) translocation, generating a NUP98-HOXC13 chimeric transcript. Molecular analysis showed that the exon 16 of NUP98 was fused in frame with exon 2 of HOXC13. The patient was also positive for FLT3 internal tandem duplication (ITD), another molecular marker for the disease. Comparative study of data on the fusion of HOW cluster and NUP98 gene revealed that it is a rare event, found exclusively in AML patients. To our knowledge, this is the first case of t(11;12)(p15;q13) in de novo AML-M4 in association with FLT3 ITD mutation. Coexistence of NUP98-HOXC13 fusion and FLT3 ITD mutation is likely relevant in the process of leukemogenesis.",
publisher = "Elsevier Science Inc, New York",
journal = "Cancer Genetics and Cytogenetics",
title = "Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review",
pages = "103-98",
number = "2",
volume = "193",
doi = "10.1016/j.cancergencyto.2009.03.007"
}

Tošić, N., Stojiljković, M., Čolović, N., Colović, M.,& Pavlović, S.. (2009). Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review. in Cancer Genetics and Cytogenetics
Elsevier Science Inc, New York., 193(2), 98-103.
https://doi.org/10.1016/j.cancergencyto.2009.03.007

Tošić N, Stojiljković M, Čolović N, Colović M, Pavlović S. Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review. in Cancer Genetics and Cytogenetics. 2009;193(2):98-103.
doi:10.1016/j.cancergencyto.2009.03.007 .

Tošić, Nataša, Stojiljković, Maja, Čolović, Nataša, Colović, Milica, Pavlović, Sonja, "Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review" in Cancer Genetics and Cytogenetics, 193, no. 2 (2009):98-103,
https://doi.org/10.1016/j.cancergencyto.2009.03.007 . .

TY  - JOUR
AU  - Heylen, Evelien
AU  - Miljić, Predrag
AU  - Willemse, Johan
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
AU  - Colović, Milica
AU  - Elezović, Ivo
AU  - Hendriks, Dirk
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/399
AB  - Introduction: It is considered that high plasma levels of procarboxypeptidase U (proCPU or TAFI) can promote the development of thrombosis, but data comparing proCPU levels in thrombophilia carriers and healthy subjects are rather scarce. Moreover, the results of previous studies on the risk of thrombosis related to high proCPU concentration in this population were not consistent. Although the 325 polymorphism, of proCPU has a significant effect on the CPU half-life, it's influence on the risk of thrombosis or spontaneous pregnancy loss in carriers of hereditary thrombophilia is not clear. Materials and Methods: The study population consisted of 144 thrombophilic patients (94 heterozygous and 10 homozygous carriers of FV Leiden, 26 heterozygous carriers of the prothrombin G20210A variation and 14 double carriers of FV Leiden and FII variation) and 69 healthy controls. Results: The results show that patients with inherited thrombophilia have a tendency toward lower mean proCPU plasma levels compared to healthy controls, however, this difference was only significant in carriers of FII G20210A (p = 0.014). A higher frequency of the most stable Ile325Ile proCPU was seen among carriers of I'll G20210A mutation compared to the control group (19% vs 7%; p = 0.186). In the second part of the study proCPU as a risk factor for thrombosis was evaluated. In heterozygous carriers of FV Leiden or FII G20210A high levels of proCPU conferred to an almost 4-fold increased risk for spontaneous onset thrombosis. The more stable Ile325Ile proCPU seems to impose a higher risk for clinical manifestation of the thrombophilic condition. Finally, a significant positive correlation between F1 + 2 and proCPU concentration was seen. Conclusion: The increased risk of thrombosis in thrombophilia patients is not only ascribable to an increased thrombin generation, but also high levels of proCPU and the presence of the 325Ile genotype tip the balance towards thrombotic tendency even further.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Thrombosis Research
T1  - Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia
EP  - 432
IS  - 4
SP  - 427
VL  - 124
DO  - 10.1016/j.thromres.2009.01.005
ER  - 

@article{
author = "Heylen, Evelien and Miljić, Predrag and Willemse, Johan and Đorđević, Valentina and Radojković, Dragica and Colović, Milica and Elezović, Ivo and Hendriks, Dirk",
year = "2009",
abstract = "Introduction: It is considered that high plasma levels of procarboxypeptidase U (proCPU or TAFI) can promote the development of thrombosis, but data comparing proCPU levels in thrombophilia carriers and healthy subjects are rather scarce. Moreover, the results of previous studies on the risk of thrombosis related to high proCPU concentration in this population were not consistent. Although the 325 polymorphism, of proCPU has a significant effect on the CPU half-life, it's influence on the risk of thrombosis or spontaneous pregnancy loss in carriers of hereditary thrombophilia is not clear. Materials and Methods: The study population consisted of 144 thrombophilic patients (94 heterozygous and 10 homozygous carriers of FV Leiden, 26 heterozygous carriers of the prothrombin G20210A variation and 14 double carriers of FV Leiden and FII variation) and 69 healthy controls. Results: The results show that patients with inherited thrombophilia have a tendency toward lower mean proCPU plasma levels compared to healthy controls, however, this difference was only significant in carriers of FII G20210A (p = 0.014). A higher frequency of the most stable Ile325Ile proCPU was seen among carriers of I'll G20210A mutation compared to the control group (19% vs 7%; p = 0.186). In the second part of the study proCPU as a risk factor for thrombosis was evaluated. In heterozygous carriers of FV Leiden or FII G20210A high levels of proCPU conferred to an almost 4-fold increased risk for spontaneous onset thrombosis. The more stable Ile325Ile proCPU seems to impose a higher risk for clinical manifestation of the thrombophilic condition. Finally, a significant positive correlation between F1 + 2 and proCPU concentration was seen. Conclusion: The increased risk of thrombosis in thrombophilia patients is not only ascribable to an increased thrombin generation, but also high levels of proCPU and the presence of the 325Ile genotype tip the balance towards thrombotic tendency even further.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia",
pages = "432-427",
number = "4",
volume = "124",
doi = "10.1016/j.thromres.2009.01.005"
}

Heylen, E., Miljić, P., Willemse, J., Đorđević, V., Radojković, D., Colović, M., Elezović, I.,& Hendriks, D.. (2009). Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 124(4), 427-432.
https://doi.org/10.1016/j.thromres.2009.01.005

Heylen E, Miljić P, Willemse J, Đorđević V, Radojković D, Colović M, Elezović I, Hendriks D. Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia. in Thrombosis Research. 2009;124(4):427-432.
doi:10.1016/j.thromres.2009.01.005 .

Heylen, Evelien, Miljić, Predrag, Willemse, Johan, Đorđević, Valentina, Radojković, Dragica, Colović, Milica, Elezović, Ivo, Hendriks, Dirk, "Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia" in Thrombosis Research, 124, no. 4 (2009):427-432,
https://doi.org/10.1016/j.thromres.2009.01.005 . .

TY  - JOUR
AU  - Radojković, M.
AU  - Ristić, S.
AU  - Pavlović, Sonja
AU  - Colović, M.
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/388
AB  - An atypical case of Philadelphia (Ph) negative, e1a2 BCR-ABL transcript positive chronic myeloid leukemia (CML) characterized with cyclic periodic leukocytosis and spontaneous remissions is reported. The patient was treated with imatinib and good hematology response with molecular remission was achieved. So far, only few Ph positive CML patients expressing p190 BCR-ABL protein and different clinical characteristics and treatment have been described in the literature. This is the first report of Philadelphia negative, p190 BCR-ABL positive CML with cyclic spontaneous oscillation of white blood cell count (WBC), and excellent response to imatinib treatment.
T2  - Leukemia Research
T1  - Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis
EP  - e12
IS  - 6
SP  - e10
VL  - 33
DO  - 10.1016/j.leukres.2008.10.028
ER  - 

@article{
author = "Radojković, M. and Ristić, S. and Pavlović, Sonja and Colović, M.",
year = "2009",
abstract = "An atypical case of Philadelphia (Ph) negative, e1a2 BCR-ABL transcript positive chronic myeloid leukemia (CML) characterized with cyclic periodic leukocytosis and spontaneous remissions is reported. The patient was treated with imatinib and good hematology response with molecular remission was achieved. So far, only few Ph positive CML patients expressing p190 BCR-ABL protein and different clinical characteristics and treatment have been described in the literature. This is the first report of Philadelphia negative, p190 BCR-ABL positive CML with cyclic spontaneous oscillation of white blood cell count (WBC), and excellent response to imatinib treatment.",
journal = "Leukemia Research",
title = "Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis",
pages = "e12-e10",
number = "6",
volume = "33",
doi = "10.1016/j.leukres.2008.10.028"
}

Radojković, M., Ristić, S., Pavlović, S.,& Colović, M.. (2009). Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis. in Leukemia Research, 33(6), e10-e12.
https://doi.org/10.1016/j.leukres.2008.10.028

Radojković M, Ristić S, Pavlović S, Colović M. Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis. in Leukemia Research. 2009;33(6):e10-e12.
doi:10.1016/j.leukres.2008.10.028 .

Radojković, M., Ristić, S., Pavlović, Sonja, Colović, M., "Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis" in Leukemia Research, 33, no. 6 (2009):e10-e12,
https://doi.org/10.1016/j.leukres.2008.10.028 . .

TY  - JOUR
AU  - Jurisić, Vladimir
AU  - Pavlović, Sonja
AU  - Čolović, Nataša
AU  - Đorđević, Vesna
AU  - Bunjevacki, Vera
AU  - Janković, Gradimir
AU  - Colović, Milica
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/391
AB  - Patients with de novo acute myeloid leukemia (AML) and near-tetraploid or completely tetraploid karyotype at presentation are rare. We present four patients with near-tetraploidy/tetraploidy in a cohort of 426 consecutive AML patients (0.98%) in respect to their cytogenetic findings, immunophenotype pattern, response to chemotherapy, course of disease and molecular analyses including tyrosine kinase receptor FLT3 gene, NRAS gene, and tumour suppressor gene, p53. We have found FLT3/ITD mutation only in one patient among the four with near-tetraploidy. The main finding is that these patients had a variable clinical course, with two having a long period of remission (36 and 12 months) and two died, not having achieved remission.
PB  - Indian Acad Sciences, Bangalore
T2  - Journal of Genetics
T1  - Single institute study of FLT3 mutation in acute myeloid leukemia with near tetraploidy in Serbia
EP  - 152
IS  - 2
SP  - 149
VL  - 88
DO  - 10.1007/s12041-009-0022-1
ER  - 

@article{
author = "Jurisić, Vladimir and Pavlović, Sonja and Čolović, Nataša and Đorđević, Vesna and Bunjevacki, Vera and Janković, Gradimir and Colović, Milica",
year = "2009",
abstract = "Patients with de novo acute myeloid leukemia (AML) and near-tetraploid or completely tetraploid karyotype at presentation are rare. We present four patients with near-tetraploidy/tetraploidy in a cohort of 426 consecutive AML patients (0.98%) in respect to their cytogenetic findings, immunophenotype pattern, response to chemotherapy, course of disease and molecular analyses including tyrosine kinase receptor FLT3 gene, NRAS gene, and tumour suppressor gene, p53. We have found FLT3/ITD mutation only in one patient among the four with near-tetraploidy. The main finding is that these patients had a variable clinical course, with two having a long period of remission (36 and 12 months) and two died, not having achieved remission.",
publisher = "Indian Acad Sciences, Bangalore",
journal = "Journal of Genetics",
title = "Single institute study of FLT3 mutation in acute myeloid leukemia with near tetraploidy in Serbia",
pages = "152-149",
number = "2",
volume = "88",
doi = "10.1007/s12041-009-0022-1"
}

Jurisić, V., Pavlović, S., Čolović, N., Đorđević, V., Bunjevacki, V., Janković, G.,& Colović, M.. (2009). Single institute study of FLT3 mutation in acute myeloid leukemia with near tetraploidy in Serbia. in Journal of Genetics
Indian Acad Sciences, Bangalore., 88(2), 149-152.
https://doi.org/10.1007/s12041-009-0022-1

Jurisić V, Pavlović S, Čolović N, Đorđević V, Bunjevacki V, Janković G, Colović M. Single institute study of FLT3 mutation in acute myeloid leukemia with near tetraploidy in Serbia. in Journal of Genetics. 2009;88(2):149-152.
doi:10.1007/s12041-009-0022-1 .

Jurisić, Vladimir, Pavlović, Sonja, Čolović, Nataša, Đorđević, Vesna, Bunjevacki, Vera, Janković, Gradimir, Colović, Milica, "Single institute study of FLT3 mutation in acute myeloid leukemia with near tetraploidy in Serbia" in Journal of Genetics, 88, no. 2 (2009):149-152,
https://doi.org/10.1007/s12041-009-0022-1 . .

TY  - JOUR
AU  - Jurisić, V.
AU  - Terzić, T.
AU  - Pavlović, Sonja
AU  - Čolović, Nataša
AU  - Colović, M.
PY  - 2008
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/315
AB  - Myelofibrosis is a clonal myeloproliferative disorder characterized by splenomegaly, abnormal deposition of collagen in the bone marrow, extramedullary hematopoiesis, dacriocytosis, and leukoerythroblastic blood smear. Development and maintenance of fibrosis are mediated by a complex network of several cytokines, including tumor necrosis factor-α (TNF-α). Osteosclerosis is the most frequently observed bone change in myelofibrosis. Based on this, we present an atypical case of leukemic transformation in myelofibrosis associated with diffuse osteolytic lesions and extremely elevated TNF-α and lactate dehydrogenase (LDH). Parathormone was not disturbed.
PB  - Elsevier GmbH
T2  - Pathology Research and Practice
T1  - Elevated TNF-α and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis
EP  - 132
IS  - 2
SP  - 129
VL  - 204
DO  - 10.1016/j.prp.2007.09.001
ER  - 

@article{
author = "Jurisić, V. and Terzić, T. and Pavlović, Sonja and Čolović, Nataša and Colović, M.",
year = "2008",
abstract = "Myelofibrosis is a clonal myeloproliferative disorder characterized by splenomegaly, abnormal deposition of collagen in the bone marrow, extramedullary hematopoiesis, dacriocytosis, and leukoerythroblastic blood smear. Development and maintenance of fibrosis are mediated by a complex network of several cytokines, including tumor necrosis factor-α (TNF-α). Osteosclerosis is the most frequently observed bone change in myelofibrosis. Based on this, we present an atypical case of leukemic transformation in myelofibrosis associated with diffuse osteolytic lesions and extremely elevated TNF-α and lactate dehydrogenase (LDH). Parathormone was not disturbed.",
publisher = "Elsevier GmbH",
journal = "Pathology Research and Practice",
title = "Elevated TNF-α and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis",
pages = "132-129",
number = "2",
volume = "204",
doi = "10.1016/j.prp.2007.09.001"
}

Jurisić, V., Terzić, T., Pavlović, S., Čolović, N.,& Colović, M.. (2008). Elevated TNF-α and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis. in Pathology Research and Practice
Elsevier GmbH., 204(2), 129-132.
https://doi.org/10.1016/j.prp.2007.09.001

Jurisić V, Terzić T, Pavlović S, Čolović N, Colović M. Elevated TNF-α and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis. in Pathology Research and Practice. 2008;204(2):129-132.
doi:10.1016/j.prp.2007.09.001 .

Jurisić, V., Terzić, T., Pavlović, Sonja, Čolović, Nataša, Colović, M., "Elevated TNF-α and LDH without parathormone disturbance is associated with diffuse osteolytic lesions in leukemic transformation of myelofibrosis" in Pathology Research and Practice, 204, no. 2 (2008):129-132,
https://doi.org/10.1016/j.prp.2007.09.001 . .

TY  - JOUR
AU  - Đorđević, Vesna
AU  - Denčić-Fekete, Marija
AU  - Jovanović, Jelica
AU  - Drakulić, Danijela
AU  - Stevanović, Milena
AU  - Janković, Gradimir
AU  - Gotić, Mirjana
PY  - 2008
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/322
AB  - An extra copy of 1q usually originates from the translocated unbalanced derivative chromosome, isochromosome, or "jumping translocation." We report a pattern of partial trisomies and unbalanced whole-arm translocations of 1q in 10 patients: 5 with myelodysplastic syndrome, 3 with acute myeloid leukemia, and a single patient with acute lymphoblastic leukemia and myeloproliferative syndrome. The trisomy of 1q was registered as the sole karyotype aberration in one patient, while it was accompanied by a limited number of additional chromosomal changes in nine patients. These patients are a subset of a larger group of 92 adults carrying a wide variety of chromosome 1 anomalies within a complex cytogenetic context observed over a period between 1994 and 2006 in a panel of 3,786 hematologic patients at the Institute of Hematology in Belgrade. Conventional cytogenetics was supplemented by fluorescence in situ hybridization with a probe specific for the paracentric region of 1q. Whole-arm 1q translocations involved chromosomes Y, 7, 14, 15, 16, and 19. This study suggests that gain of 1q as the sole cytogenetic abnormality may be sufficiently mutagenic to favor leukemogenesis and hematopoietic tissue degeneration (trilineage myelodysplasia).
PB  - Elsevier Science Inc, New York
T2  - Cancer Genetics and Cytogenetics
T1  - Pattern of trisomy 1q in hematological malignancies: a single institution experience
EP  - 18
IS  - 1
SP  - 12
VL  - 186
DO  - 10.1016/j.cancergencyto.2008.05.003
ER  - 

@article{
author = "Đorđević, Vesna and Denčić-Fekete, Marija and Jovanović, Jelica and Drakulić, Danijela and Stevanović, Milena and Janković, Gradimir and Gotić, Mirjana",
year = "2008",
abstract = "An extra copy of 1q usually originates from the translocated unbalanced derivative chromosome, isochromosome, or "jumping translocation." We report a pattern of partial trisomies and unbalanced whole-arm translocations of 1q in 10 patients: 5 with myelodysplastic syndrome, 3 with acute myeloid leukemia, and a single patient with acute lymphoblastic leukemia and myeloproliferative syndrome. The trisomy of 1q was registered as the sole karyotype aberration in one patient, while it was accompanied by a limited number of additional chromosomal changes in nine patients. These patients are a subset of a larger group of 92 adults carrying a wide variety of chromosome 1 anomalies within a complex cytogenetic context observed over a period between 1994 and 2006 in a panel of 3,786 hematologic patients at the Institute of Hematology in Belgrade. Conventional cytogenetics was supplemented by fluorescence in situ hybridization with a probe specific for the paracentric region of 1q. Whole-arm 1q translocations involved chromosomes Y, 7, 14, 15, 16, and 19. This study suggests that gain of 1q as the sole cytogenetic abnormality may be sufficiently mutagenic to favor leukemogenesis and hematopoietic tissue degeneration (trilineage myelodysplasia).",
publisher = "Elsevier Science Inc, New York",
journal = "Cancer Genetics and Cytogenetics",
title = "Pattern of trisomy 1q in hematological malignancies: a single institution experience",
pages = "18-12",
number = "1",
volume = "186",
doi = "10.1016/j.cancergencyto.2008.05.003"
}

Đorđević, V., Denčić-Fekete, M., Jovanović, J., Drakulić, D., Stevanović, M., Janković, G.,& Gotić, M.. (2008). Pattern of trisomy 1q in hematological malignancies: a single institution experience. in Cancer Genetics and Cytogenetics
Elsevier Science Inc, New York., 186(1), 12-18.
https://doi.org/10.1016/j.cancergencyto.2008.05.003

Đorđević V, Denčić-Fekete M, Jovanović J, Drakulić D, Stevanović M, Janković G, Gotić M. Pattern of trisomy 1q in hematological malignancies: a single institution experience. in Cancer Genetics and Cytogenetics. 2008;186(1):12-18.
doi:10.1016/j.cancergencyto.2008.05.003 .

Đorđević, Vesna, Denčić-Fekete, Marija, Jovanović, Jelica, Drakulić, Danijela, Stevanović, Milena, Janković, Gradimir, Gotić, Mirjana, "Pattern of trisomy 1q in hematological malignancies: a single institution experience" in Cancer Genetics and Cytogenetics, 186, no. 1 (2008):12-18,
https://doi.org/10.1016/j.cancergencyto.2008.05.003 . .

TY  - JOUR
AU  - Bakrac, Milena
AU  - Jurisić, Vladimir
AU  - Kostić, Tatjana
AU  - Popović, Vera
AU  - Pekić, Sandra
AU  - Kraguljac, Nada
AU  - Colović, Milica
PY  - 2007
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/269
PB  - BMJ Publishing Group, London
T2  - Journal of Clinical Pathology
T1  - Pure red cell aplasia associated with type I autoimmune polyglandular syndrome - successful response to treatment with mycophenolate mofetil: case report and review of literature
EP  - 720
IS  - 6
SP  - 717
VL  - 60
DO  - 10.1136/jcp.2006.042671
ER  - 

@article{
author = "Bakrac, Milena and Jurisić, Vladimir and Kostić, Tatjana and Popović, Vera and Pekić, Sandra and Kraguljac, Nada and Colović, Milica",
year = "2007",
publisher = "BMJ Publishing Group, London",
journal = "Journal of Clinical Pathology",
title = "Pure red cell aplasia associated with type I autoimmune polyglandular syndrome - successful response to treatment with mycophenolate mofetil: case report and review of literature",
pages = "720-717",
number = "6",
volume = "60",
doi = "10.1136/jcp.2006.042671"
}

Bakrac, M., Jurisić, V., Kostić, T., Popović, V., Pekić, S., Kraguljac, N.,& Colović, M.. (2007). Pure red cell aplasia associated with type I autoimmune polyglandular syndrome - successful response to treatment with mycophenolate mofetil: case report and review of literature. in Journal of Clinical Pathology
BMJ Publishing Group, London., 60(6), 717-720.
https://doi.org/10.1136/jcp.2006.042671

Bakrac M, Jurisić V, Kostić T, Popović V, Pekić S, Kraguljac N, Colović M. Pure red cell aplasia associated with type I autoimmune polyglandular syndrome - successful response to treatment with mycophenolate mofetil: case report and review of literature. in Journal of Clinical Pathology. 2007;60(6):717-720.
doi:10.1136/jcp.2006.042671 .

Bakrac, Milena, Jurisić, Vladimir, Kostić, Tatjana, Popović, Vera, Pekić, Sandra, Kraguljac, Nada, Colović, Milica, "Pure red cell aplasia associated with type I autoimmune polyglandular syndrome - successful response to treatment with mycophenolate mofetil: case report and review of literature" in Journal of Clinical Pathology, 60, no. 6 (2007):717-720,
https://doi.org/10.1136/jcp.2006.042671 . .