Prognostic Value of K-Ras 12 Genotypes in Patients With Advanced Nonsmall Cell Lung-Cancer Receiving Carboplatin With Either Intravenous or Chronic Oral Dose Etoposide

Rosell, R.; Li, Sr; Iniesta, Juan Antonio; Moreno, Irene; Martínez, Encarnación; Vadell, Catalina; Mate, JL; Ariza, Aurelio; Monzó, Mariano; Font, Albert; Molina, Francisco; Deanta, Jm; Pifarré, Alex

doi:10.3892/ijo.5.2.169

Cited by 3 publications

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“…The prevalence of K-ras mutations was not significantly different according to RER phenotype. However, in patients with stage I RER-positive tumours, there was a tendency to have aspartic and serine codon 12 K-ras mutations, which are said to confer more tumour aggressiveness (Rosell et al, 1994), while valine codon 12 mutations, which have less virulent behaviour, were linked to stage I RER-negative tumours, although the differences were not significant.…”

Section: Discussionmentioning

confidence: 90%

Prognostic value of replication errors on chromosomes 2p and 3p in non-small-cell lung cancer

Pifarré

Rosell²,

Monzó³

et al. 1997

Br J Cancer

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Section: Discussionmentioning

confidence: 90%

Prognostic value of replication errors on chromosomes 2p and 3p in non-small-cell lung cancer

Pifarré

Rosell²,

Monzó³

et al. 1997

Br J Cancer

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“…Second messengers allow transmition of the proliferation signal from the cell membrane to the nucleus. Of these second messengers, ras seems particularly useful for the early detection of adenocarcinoma [40][41][42][43][44][45][46][47]. Most ras mutations affect codon 12 of K-ras in 30% of adenocarcinomas in smokers and 5% in nonsmokers.…”

Section: Cpg Islandsmentioning

confidence: 99%

Early detection of lung cancer: role of biomarkers

Brambilla¹,

Fievet²,

Jeanmart³

et al. 2003

European Respiratory Journal

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Early detection of lung cancer requires none or few invasive techniques. Distal lung cancer (40% of the cases in most European countries) can be sensitively detected by spiral computed tomography. Theoretically, in 60% of cases, the proximal lesions (main to segmental bronchi, accessible by bronchoscopy) should be able to be detected by sputum cytology. Unfortunately, this very specific technique has a low sensitivity and is time consuming. Fluorescent bronchoscopy increases the detection rate of early or micro-invasive lesions and may be proposed in highly selected populations, but not as a screening test. Biomarkers in blood and sputum have not yet been clinically validated. However, the amount of data generated from studies first on resected tumours, then on early bronchial lesions and more recently on blood and sputum offer a wide field for investigation.Lung carcinogenesis is a multistep process characterised by the accumulation of successive molecular genetic and epigenetic abnormalities, resulting in selection of clonal cells with uncontrolled growth capacities throughout the whole respiratory tract (field cancerisation). Molecular lesions far precede morphological transformation of preneoplastic bronchial lesions (dysplasia) or alveolar lesions (atypical alveolar hyperplasia). Genetic and epigenetic abnormalities in the genes involved in cell cycle, senescence, apoptosis, repair, differentiation and cell migration control may be detected on bronchial biopsies, on respiratory cells from the sputum and even in the circulating deoxyribonucleic acid (DNA). The key genes involved include those in the P53-retinoblastoma (Rb) pathways.The balance between cyclin-dependent kinases and their inhibitors regulates the level of Rb phosphorylation and its function at G1-S transition; P53 plays at least two functions (cell cycle and apoptosis control). The balance of bax-bcl2 is important in the control of apoptosis as well as loss of fragile histidine triad expression. O(6)-methylguanine-DNA methyltransferase seems to be important in DNA repair control, the RARb receptor in differentiation, and cadherin H and E and different metalloproteases genes in cell migration.The demonstration of hyperexpression or silencing of these genes needs different validated techniques: immunohistochemistry on biopsies or cytological preparations, molecular biology techniques for mutations, loss of heterozygosity and aberrant methylation abnormalities. Automation and miniaturisation of these techniques will allow early detection and may be widely applied once clinically validated. Eur Respir J 2003; 21: Suppl. 39, 36s-44s. Lung cancer is the leading cause of cancer-related death, not only in males all around the world but also in females [1][2][3]. Despite the advances made in diagnosis and treatment in the last few decades, the prognosis of lung cancer is still very poor, with a 5-yr overall survival generally v10% in many countries. Lung cancer is detected by symptoms at a time when the local and moreover the metastasis extens...

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“…For example, p53 deletion and Bcl-2 expression render some tumour cells resistant to apoptosis following chemotherapy 4647 Expression of the k-Ras oncogene seems to produce a resistance to platinum based compounds and etoposide 48…”

Section: Implications For Treatmentmentioning

confidence: 99%

Genetics and pulmonary medicine bullet 7: Somatic mutations in the development of lung cancer

Roland¹,

Rudd²

1998

Thorax

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Prognostic Value of K-Ras 12 Genotypes in Patients With Advanced Nonsmall Cell Lung-Cancer Receiving Carboplatin With Either Intravenous or Chronic Oral Dose Etoposide

Cited by 3 publications

References 0 publications

Prognostic value of replication errors on chromosomes 2p and 3p in non-small-cell lung cancer

Prognostic value of replication errors on chromosomes 2p and 3p in non-small-cell lung cancer

Early detection of lung cancer: role of biomarkers

Genetics and pulmonary medicine bullet 7: Somatic mutations in the development of lung cancer

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