HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Mascaux, C. Articles by Sculier, J.P. Search for Related Content PubMed PubMed Citation Articles by Mascaux, C. Articles by Sculier, J.P.

Fragile histidine triad protein expression in nonsmall cell lung cancer and correlation with Ki-67 and with p53

Depts of ¹ Internal Medicine and Laboratory of Clinical Investigation and Experimental Oncology, and ² Pathology, Jules Bordet Institute, ³ Dept of Chest Medicine, St Peter University Hospital, Free Univerisity of Brussels and ⁴ Fond National de la Recherche Scientifique, Brussels, Belgium

CORRESPONDENCE: J.P. Sculier, Service de Médecine, Jules Bordet Institute, 1, rue Héger Bordet, B-1000 Brussels, Belgium. Fax: 32 25343756. E-mail: sculier@bordet.be

Keywords: fragile histidine triad, Ki-67, lung neoplasms, nonsmall cell lung cancer

Received: October 2, 2002
Accepted January 10, 2003

This study was supported by La foundation Vésale. B. Martin and A.P Meert received a fellowship from Fonds National pour la Recherche Scientifique (FNRS), Télévie Bruxelles (grant n°7.4512.98 and n°3.4579.02).

Fragile histidine triad (FHIT) is a tumour suppressor gene, which is altered in a variety of epithelial tumours, including lung cancer. Biochemical and functional pathways of its tumourigenicity are not yet understood. Its role in tumour proliferation is particularly controversial. The purpose of this study was to correlate the expression of FHIT protein in nonsmall cell lung cancer (NSCLC) with tumour proliferation as estimated by Ki-67 antigen and with p53, a suppressor gene.

FHIT, Ki-67 and p53 expression were evaluated by immunohistochemistry in 119 resected NSCLC.

Altogether, 58 tumours were negative (expression <10%) for FHIT. The median expression in tumours was 15% positive cells, in comparison with 100% in normal matched lung tissue. The expression was as strong as in normal tissue in only 19 cases. FHIT expression was significantly lower in squamous cell carcinoma (SCC) (5%) than in adenocarcinoma (ADC) (64%). The median expression of Ki-67 was 20% and 69% of tumours were positives (expression >10%). Ki-67 expression was significantly higher in SCC (33.3%) than in ADC (10%). The loss of FHIT protein was not correlated with the expression of p53 (median: 7.5%, 58% of positive tumours for a cut-off of 10% of positive cells) or Ki-67. But percentage of labelled cells for p53 and Ki-67 were significantly correlated.

The results suggest that for fragile histidine triad, the pathway of tumourigenesis is independent of p53 and of tumoural proliferation, as reported previously in vitro.

This article has been cited by other articles:

				J. S. Kim, J. W. Kim, J. Han, Y. M. Shim, J. Park, and D.-H. Kim Cohypermethylation of p16 and FHIT Promoters as a Prognostic Factor of Recurrence in Surgically Resected Stage I Non-Small Cell Lung Cancer. Cancer Res., April 15, 2006; 66(8): 4049 - 4054. [Abstract] [Full Text] [PDF]

				J. S. Kim, H. Kim, Y. M. Shim, J. Han, J. Park, and D.-H. Kim Aberrant methylation of the FHIT gene in chronic smokers with early stage squamous cell carcinoma of the lung Carcinogenesis, November 1, 2004; 25(11): 2165 - 2171. [Abstract] [Full Text] [PDF]