학술논문

Mutations in the signal transducer and activator of transcription family of genes in cancer
Document Type
article
Source
Cancer Science. 109(4)
Subject
Hematology
Rare Diseases
Cancer
Genetics
2.1 Biological and endogenous factors
Aetiology
Animals
Carcinogenesis
Hematologic Neoplasms
Humans
Leukemia
Large Granular Lymphocytic
Mutation
STAT Transcription Factors
CLPD-NK
JAK-STAT pathway
STAT3
STAT5B
T-LGL leukemia
Oncology and Carcinogenesis
Pharmacology and Pharmaceutical Sciences
Oncology & Carcinogenesis
Language
Abstract
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, STAT1-4, STAT5A, STAT5B and STAT6, that are involved in regulating cellular proliferation, apoptosis, angiogenesis and the immune system response. Constitutive activation of STAT3, via mutational changes, is important in oncogenesis in both solid and hematopoietic cancers. In the case of hematopoietic neoplasms, STAT3 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. STAT5B 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.