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Asia Pac J Clin Oncol. 2018 Oct;14(5):e214-e223. doi: 10.1111/ajco.12868. Epub 2018 Mar 8.

Do FHIT gene alterations play a role in human solid tumors?

Author information

1
Research Laboratory in Pathology, Graduate Program in Pathology of the Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Brazil.
2
Department of Pathology, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Brazil.

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.

KEYWORDS:

FHIT gene; cancer; solid malignancies; tumor suppressor

PMID:
29516675
DOI:
10.1111/ajco.12868
[Indexed for MEDLINE]

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