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The FHIT gene 3p14.2 is abnormal in lung cancer

G Sozzi1, M L Veronese, M Negrini

  • 1Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA.

Cell
|April 5, 1996
PubMed

Insights

The FHIT gene plays a crucial role in lung cancer development. Abnormalities in FHIT gene transcripts and loss of FHIT alleles were frequently observed in both small cell and non-small cell lung tumors, indicating its significance in lung carcinogenesis.

Area of Science:

  • Molecular biology
  • Cancer genetics
  • Oncology

Background:

  • The FHIT (Fragile Histidine Triad) gene, located at the 3p14.2 fragile site, is a potential tumor suppressor.
  • Alterations in the FHIT gene have been implicated in various human cancers, but its specific role in lung carcinogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role of the FHIT gene in the development of lung cancer.
  • To analyze FHIT gene alterations in both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).

Main Methods:

  • Analysis of FHIT messenger RNA (mRNA) transcripts using reverse transcription-polymerase chain reaction (RT-PCR) and sequencing.
  • Evaluation of FHIT gene allelic loss via microsatellite polymorphism analysis.
  • Detection of genomic alterations using complementary DNA (cDNA) and genomic probes, including Southern blotting.

Main Results:

  • Abnormal FHIT mRNA transcripts were detected in 80% of SCLC and 40% of NSCLC tumors.
  • Loss of FHIT alleles was observed in 76% of the analyzed lung tumors.
  • Abnormal transcripts often lacked two or more exons, and SCLC samples showed rearranged FHIT gene fragments.

Conclusions:

  • The FHIT gene is frequently altered in lung tumors, suggesting its critical involvement in lung carcinogenesis.
  • FHIT gene abnormalities, including transcript and allelic alterations, are significant in the pathogenesis of both SCLC and NSCLC.

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