Fhit expression in non-small cell lung cancer (NSCLC)

K. M. Fong, J. Geradts, J. D. Minna, R. V. Zimmerman

Research output: Contribution to journalArticle

Abstract

Background: The FHIT gene is commonly is affected by translocations and deletions. Although FHIT alterations at the DNA and RNA level are frequent in many types of tumors, the biological and clinical significance of these changes is not clear. In this study we aimed at correlating loss of the FHIT protein with a variety of genetic and clinical parameters in a well-characterized cohort of NSCLCs. Method: Paraffin sections of 94 non- small cell carcinomas were reacted with an anti-FHIT polyclonal antibody in a standard immunohistochemical reaction. Abnormal cases were characterized by complete loss of cytoplasmic staining. The staining results were then correlated with previously obtained data: LOH at 3p14, LOH at other loci, K-ras mutations, p53 abnormalities, staining patterns for RB and p16, and with a number of clinical parameters, including survival. Results: 52 of 94 tumors (55%) lacked cytoplasmic staining, with preserved reactivity in adjacent normal cells. Lack of staining correlated with LOH at 3p14, but not at other loci on 3p. It was significantly more common in squamous cell carcinomas compared to bronchiolo-alveolar and adenocarcinomas. Absent FHIT expression was inversely correlated with mutations in codon 12 of the K-ras gene. Lack of FHIT expression tended to correlate with the number of pack years smoked. There was however no statistically significant association with abnormal tumor suppressor gene expression, stage of disease or survival. Conclusion: Loss of FHIT expression was observed in over half of all NSCLCs, and was markedly more common in squamous cell carcinomas. Correlation with LOH at 3p14 provides additional evidence that the FHIT gene may be an important 3p14 deletional target in lung cancer. However, aberrant expression of this gene may not be of prognostic relevance.

Original languageEnglish (US)
JournalRespirology
Volume4
Issue numberSUPPL. 1
StatePublished - 1999

Fingerprint

Non-Small Cell Lung Carcinoma
Staining and Labeling
Squamous Cell Carcinoma
Bronchiolo-Alveolar Adenocarcinoma
Gene Expression
Mutation
Small Cell Carcinoma
ras Genes
Tumor Suppressor Genes
Codon
Paraffin
Genes
Lung Neoplasms
Neoplasms
RNA
Antibodies
DNA

Keywords

  • FHIT gene
  • Immunohistochemistry
  • Lung cancer

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Fong, K. M., Geradts, J., Minna, J. D., & Zimmerman, R. V. (1999). Fhit expression in non-small cell lung cancer (NSCLC). Respirology, 4(SUPPL. 1).

Fhit expression in non-small cell lung cancer (NSCLC). / Fong, K. M.; Geradts, J.; Minna, J. D.; Zimmerman, R. V.

In: Respirology, Vol. 4, No. SUPPL. 1, 1999.

Research output: Contribution to journalArticle

Fong, KM, Geradts, J, Minna, JD & Zimmerman, RV 1999, 'Fhit expression in non-small cell lung cancer (NSCLC)', Respirology, vol. 4, no. SUPPL. 1.
Fong KM, Geradts J, Minna JD, Zimmerman RV. Fhit expression in non-small cell lung cancer (NSCLC). Respirology. 1999;4(SUPPL. 1).
Fong, K. M. ; Geradts, J. ; Minna, J. D. ; Zimmerman, R. V. / Fhit expression in non-small cell lung cancer (NSCLC). In: Respirology. 1999 ; Vol. 4, No. SUPPL. 1.
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abstract = "Background: The FHIT gene is commonly is affected by translocations and deletions. Although FHIT alterations at the DNA and RNA level are frequent in many types of tumors, the biological and clinical significance of these changes is not clear. In this study we aimed at correlating loss of the FHIT protein with a variety of genetic and clinical parameters in a well-characterized cohort of NSCLCs. Method: Paraffin sections of 94 non- small cell carcinomas were reacted with an anti-FHIT polyclonal antibody in a standard immunohistochemical reaction. Abnormal cases were characterized by complete loss of cytoplasmic staining. The staining results were then correlated with previously obtained data: LOH at 3p14, LOH at other loci, K-ras mutations, p53 abnormalities, staining patterns for RB and p16, and with a number of clinical parameters, including survival. Results: 52 of 94 tumors (55{\%}) lacked cytoplasmic staining, with preserved reactivity in adjacent normal cells. Lack of staining correlated with LOH at 3p14, but not at other loci on 3p. It was significantly more common in squamous cell carcinomas compared to bronchiolo-alveolar and adenocarcinomas. Absent FHIT expression was inversely correlated with mutations in codon 12 of the K-ras gene. Lack of FHIT expression tended to correlate with the number of pack years smoked. There was however no statistically significant association with abnormal tumor suppressor gene expression, stage of disease or survival. Conclusion: Loss of FHIT expression was observed in over half of all NSCLCs, and was markedly more common in squamous cell carcinomas. Correlation with LOH at 3p14 provides additional evidence that the FHIT gene may be an important 3p14 deletional target in lung cancer. However, aberrant expression of this gene may not be of prognostic relevance.",
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