Open AccessMutations in the signal transducer and activator of transcription family of genes in cancer
Author(s) -
Shahmarvand Nahid,
Nagy Alexandra,
Shahryari Jahanbanoo,
Ohgami Robert S.
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13525
Subject(s) - stat , stat protein , leukemia , cancer research , haematopoiesis , immunology , stat3 , biology , jak stat signaling pathway , lymphoma , stat4 , signal transduction , genetics , stem cell , tyrosine kinase
In recent years, it has become clear that members of the signal transducer and activator of transcription ( STAT ) family of genes play an important role in cancer. The STAT family consists of seven genes, STAT 1‐4 , STAT 5A, STAT 5B and STAT 6, that are involved in regulating cellular proliferation, apoptosis, angiogenesis and the immune system response. Constitutive activation of STAT 3 , via mutational changes, is important in oncogenesis in both solid and hematopoietic cancers. In the case of hematopoietic neoplasms, STAT 3 driver mutations have been described in T‐cell large granular lymphocytic (T‐ LGL ) leukemia and chronic natural killer lymphoproliferative disorders ( CLPD ‐ NK ) and are seen in 30%‐40% of T‐ LGL leukemia patients. STAT 5B is also mutated in T‐ LGL leukemia and CLPD ‐ NK , but in a much smaller proportion. Here we review past and current research on STAT genes in hematopoietic and solid cancers with emphasis on STAT3 and STAT5B and their roles in the pathogenesis of hematopoietic malignancies, particularly T‐LGL leukemia and CLPD‐NK.