K-ras gene point mutation: a stable tumor marker in non-small cell lung carcinoma

Li, Shanrong; Rosell, Rafael; Urban, A; Font, Albert; Ariza, Aurelio; Armengol, P; Abad, Albert; Navas, JoséJ.; Monzó, Mariano

doi:10.1016/0169-5002(94)90279-8

Cited by 28 publications

(17 citation statements)

References 16 publications

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“…Several studies have reported an incidence of 15-33% of activated K-ras gene in lung carcinomas, while more recent studies have revealed a higher incidence of more than 50% (42)(43)(44). In the current study we found K-ras codon 12 point mutations in 18% of the specimens examined.…”

Section: Discussionsupporting

confidence: 64%

“…In the current study we found K-ras codon 12 point mutations in 18% of the specimens examined. In cases of squamous cell carcinomas the incidence of K-ras mutations was higher than in other studies (24,42), propably due to the more sensitive assay used. Activation of the K-ras gene was examined, since point mutations of this member of the ras family are found more commonly in lung cancer and occur predominantly at codon 12.…”

Section: Discussioncontrasting

confidence: 39%

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Detection of human papilloma virus (HPV) and K-ras mutations in human lung carcinomas

Noutsou¹,

Koffa²,

Ergazaki³

et al. 1996

Int J Oncol

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Abstract. The purpose of our study was to assess the prevalence and prognostic significance of HPV infection as well as K-ras codon 12 point mutations in lung cancer. Patients diagnosed with lung carcinoma between 1988 and 1992 (N=99) were selected. HPV detection and typing was performed by PCR from paraffin-embedded tissues, while mutations in codon 12 of K-ras gene were detected using the restriction fragment length polymorphism (RFLP) analysis. The prevalence of HPV infection was 15%, while K-ras codon 12 point mutations were found in 18% of the specimens examined.

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Section: Discussionsupporting

confidence: 64%

Section: Discussioncontrasting

confidence: 39%

Detection of human papilloma virus (HPV) and K-ras mutations in human lung carcinomas

Noutsou¹,

Koffa²,

Ergazaki³

et al. 1996

Int J Oncol

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“…A similar phenomenon was also reported in patients with colorectal cancer (Tortola et al, 2001). Although K-RAS mutations seem to be associated with the early development of NSCLC, it cannot be excluded that K-RAS mutations are lost later during tumour progression (Burmer and Loeb, 1989;Li et al, 1994). This may, in part, explain the discordance in the K-RAS mutation status between primary tumours and metachronous metastases.…”

Section: Discussionmentioning

confidence: 68%

Comparison of EGFR and K-RAS gene status between primary tumours and corresponding metastases in NSCLC

et al. 2008

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In non-small-cell lung cancer (NSCLC), epidermal growth factor receptor (EGFR) and K-RAS mutations of the primary tumour are associated with responsiveness and resistance to tyrosine kinase inhibitors (TKIs), respectively. However, the EGFR and K-RAS mutation status in metastases is not well studied. We compared the mutation status of these genes between the primary tumours and the corresponding metastases of 25 patients. Epidermal growth factor receptor and K-RAS mutation status was different between primary tumours and corresponding metastases in 7 (28%) and 6 (24%) of the 25 patients, respectively. Among the 25 primary tumours, three 'hotspot' and two non-classical EGFR mutations were found; none of the corresponding metastases had the same mutation pattern. Among the five (20%) K-RAS mutations detected in the primary tumours, two were maintained in the corresponding metastasis. Epidermal growth factor receptor and K-RAS mutations were detected in the metastatic tumours of three (12%) and five (20%) patients, respectively. The expressions of EGFR and phosphorylated EGFR showed 10 and 50% discordance, in that order. We conclude that there is substantial discordance in EGFR and K-RAS mutational status between the primary tumours and corresponding metastases in patients with NSCLC and this might have therapeutic implications when treatment with TKIs is considered.

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“…For example, ras mutations are detected in 40-50% of colon carcinomas (Perucho et al, 1981;Vogelstein et al, 1988;Burmer et al, 1991;Wang et al, 1993); 80% of pancreatic carcinomas (Mariyama et al, 1989;Shibata et al, 1990;Burmer et al, 1991;Pinto et al, 1997); and 30-50% of lung adenocarcinomas (Rodenhuis et al, 1988;Suzuki et al, 1990, Reynolds et al, 1991Li et al, 1994;Mills et al, 1995). Kras2 mutations account for >90% of the activating ras mutations observed in these tumor types.…”

Section: Introductionmentioning

confidence: 99%

LOH of chromosome 12p correlates with Kras2 mutation in non-small cell lung cancer

Zhang

Dai

et al. 2003

Oncogene

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Previous observation has shown that the wild-type Kras2 allele is a suppressor of lung cancer in mice. Here we report that loss of heterozygosity (LOH) of chromosome 12p was detected in B50% of human lung adenocarcinomas and large cell carcinomas, and Kras2 mutations were detected at codon 12 in B40% of adenocarcinomas and large cell carcinomas. Interestingly, all of the lung adenocarcinomas and large cell carcinomas containing a Kras2 mutation exhibited allelic loss of the wild-type Kras2 allele when a correlation between LOH of the region on chromosome 12p and Kras2 mutation was made. These results from human lung cancer tissues provide a strong evidence in support of our previous observation in mouse models that the wild-type Kras2 is a tumor suppressor of lung cancer.

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K-ras gene point mutation: a stable tumor marker in non-small cell lung carcinoma

Cited by 28 publications

References 16 publications

Detection of human papilloma virus (HPV) and K-ras mutations in human lung carcinomas

Detection of human papilloma virus (HPV) and K-ras mutations in human lung carcinomas

Comparison of EGFR and K-RAS gene status between primary tumours and corresponding metastases in NSCLC

LOH of chromosome 12p correlates with Kras2 mutation in non-small cell lung cancer

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