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 . .