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Do FHIT gene alterations play a role in human solid tumors?
Author(s) -
Silveira Zavalhia Lisiane,
Weber Medeiros Aline,
Oliveira Silva Andrew,
Vial Roehe Adriana
Publication year - 2018
Publication title -
asia‐pacific journal of clinical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 29
eISSN - 1743-7563
pISSN - 1743-7555
DOI - 10.1111/ajco.12868
Subject(s) - fhit , loss of heterozygosity , carcinogenesis , cancer research , tumor suppressor gene , biology , chromosomal fragile site , epigenetics , gene , tumor progression , genetics , allele , chromosome
Abstract The fragile histidine triad ( FHIT ) gene encloses an active common chromosomal fragile site, FRA3B. This gene is known to be associated with genomic instability, apoptosis and DNA damage. FHIT disturbances have been related to carcinogenesis in different types of human tumor. Despite this, there are some controversies about the exact role of the FHIT gene in relation to tumor biology. Several pieces of evidence support the hypothesis that FHIT acts as a tumor suppressor gene. A loss or decrease in the Fhit protein expression appears to be related to tumor progression, poor prognostic factors and lower survival rates. The most frequent causes of FHIT expression changes are gene mutations, epigenetic alteration and loss of heterozygosity. This literature review aims to clarify the involvement of the FHIT gene in carcinogenesis, tumor progression and clinical outcome in prevalent solid malignancies, such as breast, lung, cervical, esophageal, gastric and colorectal cancers.