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

Pifarré, Alex; Rosell, Rafael; Monzó, Mariano; Anta, Javier; Moreno, Isabel; Sánchez, Juan Antonio Lascuraín; Ariza, Aurelio; Mate, JL; Martı́nez, Enrique; Sánchez, Miguel Ángel Goenaga

doi:10.1038/bjc.1997.31

Cited by 43 publications

(24 citation statements)

References 25 publications

(16 reference statements)

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“…Reports of the frequency of LOH can also differ for the same marker in the same type of tumor. For instance, D3S1284 (3p13-p14.1) was deleted in only 8% of NSCLC biopsies studied by Pifarre et al, 1997, but in 63% of the NSCLCs studied by Wistuba et al (2000). In contrast to this Tseng et al (1999) reported deletion of marker D3S1234 (3p14.2-p14.3) in NSCLC biopsies (stage I) in 58%, but Wistuba et al (2000) found this marker deleted in only 43% of NSCLC cell lines and in 52% of primary NSCLCs.…”

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confidence: 69%

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Zabarovsky¹,

2002

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Loss of heterozygosity (LOH) involving several chromosome 3p regions accompanied by chromosome 3p deletions are detected in almost 100% of small (SCLCs) and more than 90% of non-small (NSCLCs) cell lung cancers. In addition, these changes appear early in the pathogenesis of lung cancer and are found as clonal lesions in the smoking damaged respiratory epithelium including histologically normal epithelium as well as in epithelium showing histologic changes of preneoplasia. These 3p genetic alterations lead to the conclusion that the short arm of human chromosome 3 contains several tumor suppressor gene(s) (TSG(s)). Although the first data suggesting that 3p alterations were involved in lung carcinogenesis were published more than 10 years ago, only recently has significant progress been achieved in identifying the candidate TSGs and beginning to demonstrate their functional role in tumor pathogenesis. Some of the striking results of these findings has been the discovery of multiple 3p TSGs and the importance of tumor acquired promoter DNA methylation as an epigenetic mechanism for inactivating the expression of these genes in lung cancer. This progress, combined with the well known role of smoking as an environmental causative risk factor in lung cancer pathogenesis, is leading to the development of new diagnostic and therapeutic strategies which can be translated into the clinic to combat and prevent the lung cancer epidemic. It is clear now that genetic and epigenetic abnormalities of several genes residing in chromosome region 3p are important for the development of lung cancers but it is still obscure how many of them exist and which of the numerous candidate TSGs are the key players in lung cancer pathogenesis. We review herein our current knowledge and describe the most credible candidate genes.

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confidence: 69%

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Zabarovsky¹,

2002

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“…The reasons for noninclusion of a study into the meta-analysis were the lack of available survival results to calculate HR in 13 (Volm et al, 1993;Westra et al, 1993;Li et al, 1994;Kashii et al, 1995;Pifarré et al, 1997;Visscher et al, 1997;De Gregorio et al, 1998;Greatens et al, 1998;Fu et al, 1999;Miyake et al, 1999;Schneider et al, 2000;Andjelic et al, 2001;Broermann et al, 2002) and the lack of repartition of tumours according to RAS mutation/ expression in 1 (Ahrendt et al, 2002).…”

Section: Study Selection and Characteristicsmentioning

confidence: 99%

“…In total, 53 publications, published between 1990 and 2003, were found eligible for the systematic review (Rodenhuis et al, 1988(Rodenhuis et al, , 1997Slebos et al, 1990;Mitsudomi et al, 1991;Miyamoto et al, 1991;Harada et al, 1992;Sugio et al, 1992;Rosell et al, 1993Rosell et al, , 1995bRosell et al, , 1996Rosell et al, , 1997Volm et al, 1993Volm et al, , 2002Westra et al, 1993;Kern et al, 1994;Li et al, 1994;Silini et al, 1994;Fujino et al, 1995;Kashii et al, 1995;Keohavong et al, 1996Keohavong et al, , 1997Cho et al, 1997;Dosaka-Akita et al, 1997;Fukuyama et al, 1997;Komiya et al, 1997;Pifarré et al, 1997;Siegfried et al, 1997;Visscher et al, 1997;De Gregorio et al, 1998;Greatens et al, 1998;Huang et al, 1998;Kim et al, 1998;Kwiatkowski et al, 1998;Nemunaitis et al, 1998;Wang et al, 1998;Dingemans et al, 1999;Fu et al, 1999;Graziano et al, 1999;Miyake et al, 1999;Nelson et al, 1999;Hommura et al, 2000;…”

Section: Study Selection and Characteristicsmentioning

confidence: 99%

The role of RAS oncogene in survival of patients with lung cancer: a systematic review of the literature with meta-analysis

et al. 2004

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The proto-oncogene RAS, coding for a 21 kDa protein (p21), is mutated in 20% of lung cancer. However, the literature remains controversial on its prognostic significance for survival in lung cancer. We performed a systematic review of the literature with metaanalysis to assess its possible prognostic value on survival. Published studies on lung cancer assessing prognostic value of RAS mutation or p21 overexpression on survival were identified by an electronic search. After a methodological assessment, we estimated individual hazard ratios (HR) estimating RAS protein alteration or RAS mutation effect on survival and combined them using metaanalytic methods. In total, 53 studies were found eligible, with 10 concerning the same cohorts of patients. Among the 43 remaining studies, the revelation method was immunohistochemistry (IHC) in nine and polymerase chain reaction (PCR) in 34. Results in terms of survival were significantly pejorative, significantly favourable, not significant and not conclusive in 9, 1, 31, 2, respectively. In total, 29 studies were evaluable for meta-analysis but we aggregated only the 28 dealing with non-small-cell lung cancer (NSCLC) and not the only one dealing with small-cell-lung cancer (SCLC). The quality scores were not statistically significantly different between studies with or without significant results in terms of survival, allowing us to perform a quantitative aggregation. The combined HR was 1.35 (95% CI: 1.16 -1.56), showing a worse survival for NSCLC with KRAS2 mutations or p21 overexpression and, particularly, in adenocarcinomas (ADC) (HR 1.59; 95% CI 1.26 -2.02) and in studies using PCR (HR 1.40; 95% CI 1.18 -1.65) but not in studies using IHC (HR 1.08; 95% CI 0.86 -1.34). RAS appears to be a pejorative prognostic factor in terms of survival in NSCLC globally, in ADC and when it is studied by PCR.

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“…The other form of genomic instability is microsatellite instability (MIN) or (MSI); also referred to as microsatellite alterations (MA) or replication errors (RER), representing replication and DNA repair infidelity. The high incidence of genomic instability in lung tumours has been well established [96][97][98][99][100] and in some cases it has been associated with prognosis [101][102][103]. The present authors have recently demonstrated genetic alterations in 97.6% of lung tumours examined by a panel of 12 microsatellite markers selected at specific locations [104], and have calculated the threshold of LOH detection to 23% by assessing the interassay variation.…”

Section: Genomic Instabilitymentioning

confidence: 99%

The Liverpool Lung Project: a molecular epidemiological study of early lung cancer detection

Field¹,

Youngson²

2002

Eur Respir J

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Lung cancer is the major cause of death from neoplastic disease in the world, and even with politically-motivated smoking cessation campaigns throughout Europe, the disease remains the major cause of death. The development of molecular epidemiological population-based research into early lung cancer detection, such as the Liverpool Lung Project (LLP), may provide a way forward. This is the first major molecular epidemiological study of detection of early lung cancer.The use of molecular epidemiological risk assessments prior to clinical diagnosis and markers of preclinical carcinogenesis in patients with a high risk of developing lung cancer will reduce the incidence of clinically-detectable lung cancer, given the appropriate intervention strategies.The aims are as follows: 1) to prepare a molecular genetic and epidemiological risk assessment model based on environmental exposures and genetic predisposition; 2) to develop an archive of specimens relating to at-risk individuals and those with lung cancer; 3) to redefine lung cancer based on molecular pathology using the fields of expression profiling, genetic instability and molecular cytogenetics; 4) to identify and assess novel markers of precarcinogenesis in high-risk populations; and 5) to facilitate the development of new treatment strategies (e.g. chemoprevention programmes and targeted drug therapies).The LLP has two components: 1) a case-controlled study of newly-diagnosed cases of lung cancer that will provide a baseline, risk assessment; and 2) a prospective cohort study to be carried out over a 10-yr period that will identify markers of preclinical carcinogenesis. In-depth interviews are carried out using structured and semi-structured questionnaires. Sputum, blood and tumour specimens are collected and will be assessed for specific molecular markers (e.g. genetic instability, mutation and expression profiling, and methylation status).Conclusions from The Liverpool Lung Project will be based around molecularepidemiological and genotyping risk assessment models, as well as redefining the disease, and ultimately contributing to the development of new early lung cancer detection and treatment strategies.

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

Cited by 43 publications

References 25 publications

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

The role of RAS oncogene in survival of patients with lung cancer: a systematic review of the literature with meta-analysis

The Liverpool Lung Project: a molecular epidemiological study of early lung cancer detection

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