Geographical differences in non-small cell lung cancer K-ras mutations

Fong, K. M.; Zimmerman, PV; Smith, Peter J.

doi:10.1016/0169-5002(94)93805-9

Cited by 2 publications

(5 citation statements)

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“…It has been suggested that there may be a correlation between Fhit and p53 abnormalities in lung cancer (Burke et al, 1998;Marchetti et al, 1998b). In this series of NSCLCs, we had previously studied p53 abnormalities by PCR-SSCP (polymerase chain reaction single strand conformation polymorphism analysis) and immunohistochemical staining (Fong et al, 1995c;Geradts et al, 1999). While there was a correlation between Fhit negativity and LOH at 17p13, the chromosomal p53 locus, there was no correlation between loss of Fhit expression and mutational analysis of p53 exons 5-8 by PCR-SSCP or p53 overexpression by IHC (Table 3).…”

Section: Correlation Of Fhit Expression With P53 Rb and P16 Protein E...mentioning

confidence: 99%

“…Tumour blocks were obtained from 108 patients with primary NSCLC at The Prince Charles Hospital, Brisbane, Australia who had been treated with curative resectional surgery. This cohort of unselected patients had previously been investigated for molecular genetic changes at candidate chromosomal regions (Fong et al, 1994(Fong et al, , 1995a(Fong et al, , 1995b(Fong et al, , 1995c(Fong et al, , 1997. From this cohort, pathology review (by JG) identified 99 cases where adequate material remained for immunohistochemical evaluation.…”

Section: Patient Materialsmentioning

confidence: 99%

“…A detailed medical and smoking history was available and there were eight never/non-smokers and 91 smokers with mean pack years of 46 (range 1-150). This study is part of an ongoing research project and thus data on other molecular markers were available for analysis including: K-ras codon 12 mutations; p53 abnormalities; 3p14.2 LOH, LOH at other loci on 3p, and LOH at known or putative tumour suppressor gene loci on 1p,5q,8p,9p,11p,13q,17p,17q and 18q;and p53,RB and p16 expression by IHC (Fong et al, 1994(Fong et al, , 1995a(Fong et al, , 1995b(Fong et al, , 1995c(Fong et al, , 1998Geradts et al, 1999). As a positive external Fhit control, we used normal kidney.…”

Section: Patient Materialsmentioning

confidence: 99%

“…FHIT locus, as well as other allele loss at suspected tumour suppressor loci (Fong et al, 1994(Fong et al, , 1995a(Fong et al, , 1995b(Fong et al, , 1995c(Fong et al, , 1997. Our aims were to determine whether loss of heterozygosity (LOH) at the FHIT locus was associated with loss of protein expression, to determine the prognostic significance of Fhit down-regulation, to confirm the association between Fhit expression and tumour histology, and to probe for correlations with a variety of other genetic abnormalities in this cohort of well characterized NSCLCs.…”

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confidence: 99%

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Loss of Fhit expression in non-small-cell lung cancer: correlation with molecular genetic abnormalities and clinicopathological features

et al. 2000

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The FHIT gene is located at a chromosomal site (3p14.2) which is commonly affected by translocations and deletions in human neoplasia. Although FHIT alterations at the DNA and RNA level are frequent in many types of tumours, the biological and clinical significance of these changes is not clear. In this study we aimed at correlating loss of Fhit protein expression with a large number of molecular genetic and clinical parameters in a well-characterized cohort of non-small-cell lung cancers (NSCLCs). Paraffin sections of 99 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 Fhit staining. The Fhit staining results were then correlated with previously obtained clinical and molecular data. Fifty-two of 99 tumours lacked cytoplasmic Fhit staining, with preserved reactivity in adjacent normal cells. Lack of Fhit staining correlated with: loss of heterozygosity (LOH) at the FHIT 3p14.2 locus, but not at other loci on 3p; squamous histology; LOH at 17p13 and 5q but not with LOH at multiple other suspected tumour suppressor gene loci; and was inversely correlated with codon 12 mutations in K- ras. Fhit expression was not correlated overall with a variety of clinical parameters including survival and was not associated with abnormalities of immunohistochemical expression of p53, RB, and p16. All of these findings are consistent with loss of Fhit protein expression being as frequent an abnormality in lung cancer pathogenesis as are p53 and p16 protein abnormalities and that such loss occurs independently of the commitment to the metastatic state and of most other molecular abnormalities. © 2000 Cancer Research Campaign

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Section: Correlation Of Fhit Expression With P53 Rb and P16 Protein E...mentioning

confidence: 99%

Section: Patient Materialsmentioning

confidence: 99%

Section: Patient Materialsmentioning

confidence: 99%

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confidence: 99%

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Loss of Fhit expression in non-small-cell lung cancer: correlation with molecular genetic abnormalities and clinicopathological features

et al. 2000

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“…Current theories suggest that as many as 10 ± 20 events including alterations of oncogenes and tumor suppressor genes will have occurred by the time lung cancer is clinically evident (Minna et al, 1991). Tumor suppressor genes involved in NSCLC have been located on chromosome bands 3p, (Hung et al, 1995), 5q (Fong et al, 1995a), 9p (Kishimoto et al, 1995;Center et al, 1993), 11p (Tran andBepler and Garcia-Blanco, 1994), 11q (Rasio et al, 1995), and 17p and 17q (Fong et al, 1995b).…”

Section: Introductionmentioning

confidence: 99%

Novel regions of allelic deletion on chromosome 18p in tumors of the lung, brain and breast

et al. 1998

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Lung cancer is now the number one cause of cancer death for both men and women. An age-adjusted analysis over the past 25 years shows that in women specifically, lung cancer incidence is on the rise. It is estimated that 10-20 genetic events including the alteration of oncogenes and tumor suppressor genes will have occurred by the time a lung tumor becomes clinically evident. In an effort to identify regions containing novel cancer genes, chromosome 18p11, a band not previously implicated in disease, was examined for loss of heterozygosity (LOH). In this study, 50 matched normal and NSCLC tumor samples were examined using six 18p11 and one 18q12.3 PCR-based polymorphic markers. In addition, LOH was examined in 29 glioblastoma pairs and 14 paired breast carcinomas. This analysis has revealed potentially two regions of LOH in 18p11 in up to 38% of the tumor samples examined. The regions of LOH identified included a 2 cm area between markers D18S59 and D18S476, and a more proximal, 25 cm region of intermediate frequency between D18S452 and D18S453. These results provide evidence for the presence of one or more potential tumor suppressor genes on the short arm of chromosome 18 which may be involved in NSCLC, brain tumors and possibly breast carcinomas as well.

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Geographical differences in non-small cell lung cancer K-ras mutations

Cited by 2 publications

References 0 publications

Loss of Fhit expression in non-small-cell lung cancer: correlation with molecular genetic abnormalities and clinicopathological features

Loss of Fhit expression in non-small-cell lung cancer: correlation with molecular genetic abnormalities and clinicopathological features

Novel regions of allelic deletion on chromosome 18p in tumors of the lung, brain and breast

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