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Published on: September 20, 2016
Integrated analysis of FHIT gene alterations in cancer
Lucía Simón-Carrasco1, Elena Pietrini1, Andrés J López-Contreras1
1Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), Consejo Superior de Investigaciones Científicas (CSIC) - Universidad de Sevilla - Universidad Pablo de Olavide, Seville, Spain.
Abstract:
The Fragile Histidine Triad Diadenosine Triphosphatase (FHIT) gene is located in the Common Fragile Site FRA3B and encodes an enzyme that hydrolyzes the dinucleotide Ap3A. Although FHIT loss is one of the most frequent copy number alterations in cancer, its relevance for cancer initiation and progression remains unclear. FHIT is frequently lost in cancers from the digestive tract, which is compatible with being a cancer driver event in these tissues. However, FHIT loss could also be a passenger event due to the inherent fragility of the FRA3B locus. Moreover, the physiological relevance of FHIT enzymatic activity and the levels of Ap3A is largely unclear. We have conducted here a systematic pan-cancer analysis of FHIT status in connection with other mutations and phenotypic alterations, and we have critically discussed our findings in connection with the literature to provide an overall view of FHIT implications in cancer.
Insights
The Fragile Histidine Triad (FHIT) gene
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The Fragile Histidine Triad (FHIT) gene, located at the FRA3B fragile site, encodes an enzyme hydrolyzing diadenosine triphosphatase (Ap3A).
- FHIT loss is a frequent event in cancer, particularly digestive tract cancers, but its role as a driver or passenger event is debated.
- The physiological significance of FHIT's enzymatic activity and Ap3A levels in cancer remains largely undetermined.
Purpose of the Study:
- To conduct a comprehensive pan-cancer analysis of FHIT gene status.
- To investigate the association between FHIT alterations and other mutations or phenotypic changes across various cancer types.
- To critically evaluate the implications of FHIT in cancer development and progression by integrating findings with existing literature.
Main Methods:
- Systematic pan-cancer analysis of FHIT gene status.
- Correlation analysis of FHIT alterations with other genomic mutations.
- Integration of phenotypic data with FHIT status.
- Literature review and critical discussion of findings.
Main Results:
- The study systematically analyzed FHIT gene status across multiple cancer types.
- Associations between FHIT alterations and other molecular/phenotypic features were explored.
- Findings were critically discussed in the context of existing literature to elucidate FHIT's role.
Conclusions:
- The study provides a comprehensive overview of FHIT gene alterations in cancer.
- It addresses the ambiguity surrounding FHIT's role as a cancer driver or passenger event.
- The research contributes to understanding the overall implications of FHIT in oncogenesis.
