The historical relationship between meis1 and leukemia

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Küçük Resim

Tarih

2022

Dergi Başlığı

Dergi ISSN

Cilt Başlığı

Yayıncı

Springer

Erişim Hakkı

info:eu-repo/semantics/closedAccess

Araştırma projeleri

Organizasyon Birimleri

Dergi sayısı

Özet

Acute leukemia (AL) is a poor progressive resistant hematological disease, which has different subtypes and immunophenotypic properties according to leukemic blasts. AL is caused by genetic changes and associated with leukemia stem cells (LSCs), which determine its prognosis and endurance. LSCs are thought to be hematopoietic progenitor and stem cell (HPSCs)-like cells that underwent a malignant transformation. In addition to their low number, LSCs have the characteristics of self-renewal, resistance to chemotherapy, and relapse of leukemia. The myeloid ecotropic integration site-1 (MEIS1) protein is a member of the three-amino acid loop extension (TALE) family of homeodomain (HD) proteins that can bind to DNA sequence-specific manner. Studies have shown that overexpression of MEIS1 and associated cofactors involves tumorigenesis of numerous cancers. Historically, increased expression of Meis1 transcript as well as protein has been determined in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) patients. Moreover, resistance to conventional chemotherapy was observed in leukemic blast samples with high Meis1 content. In this review article, the molecular mechanism of the oncological role of the MEIS1 protein in leukemia and LSC is discussed. In addition, it was suggested that MEIS1 protein could be utilized as a possible treatment target in leukemia with an emphasis on the inhibition of MEIS1, which is overexpressed in LSC.

Açıklama

Anahtar Kelimeler

Leukemia, MEIS1, Leukemia Stem Cells

Kaynak

Advances in Experimental Medicine and Biology

WoS Q Değeri

Scopus Q Değeri

Q2

Cilt

1387

Sayı

Künye

Meriç, N. & Kocabaş, F. (2022). The Historical Relationship Between Meis1 and Leukemia. In: Turksen, K. (eds) Cell Biology and Translational Medicine, Volume 16. Advances in Experimental Medicine and Biology, 1387, 127-144. Springer, Cham. https://doi.org/10.1007/5584_2021_705