Prognostic Significance of K-<i>ras</i> Codon 12 Mutations in Patients With Resected Stage I and II Non–Small-Cell Lung Cancer

Graziano, Stephen L.; Gamble, Gary P.; Newman, Nancy; Abbott, Lynn; Rooney, Michelle Nayahamui; Mookherjee, Sakti; Lamb, Melissa L.; Kohman, Leslie J.; Poiesz, Bernard J.

doi:10.1200/jco.1999.17.2.668

Cited by 182 publications

(67 citation statements)

References 23 publications

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“…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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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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“…According to the hypothesis that NSCLC-ND may share clinical behavior and therapy responsiveness with SCLC, which is the prototype of highly malignant and therapy-sensitive NE tumors of the lung, several studies 18 have correlated NSCLC-ND with shorter survival, more advanced disease stage, and/or increased chemosensitivity. 19 -31 Other investigators, however, have failed to show any correlation between NE differentiation and prognosis or susceptibility to the therapy 28,[32][33][34][35][36][37][38][39][40] or even have reported better survival rates for patients with NSCLC-ND. 24,37,38,41 Differences in tissue processing, techniques or markers used for highlighting NE differentiation, definitions of positive results, and study population selection may account for these contradictory results reported in the clinical meaning of NE differentiation in patients with NSCLC.…”

mentioning

confidence: 99%

Prognostic implications of neuroendocrine differentiation and hormone production in patients with Stage I nonsmall cell lung carcinoma

Pelosi

Pasini

Sonzogni

et al. 2003

Cancer

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Chiral dirhodium carboxylate complexes ([Rh2(S‐PTAD)4] or [Rh2(S‐PTTL)4], see scheme) efficiently catalyze asymmetric three‐component coupling reactions of α‐diazophosphonates, anilines, and electron‐deficient aldehydes to give α‐amino‐β‐hydroxyphosphonates. The high level of enantiocontrol provides evidence for the intermediacy of metal‐bound ammonium ylide in the product‐forming step.

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“…Currently, there are numerous immunomarkers used to detect bronchopulmonary neuroendocrine tumors, most commonly neuron-specific enolase, synaptophysin and chromogranin A, although each has a different sensitivity and specificity (9). Therefore, searching for the best panel of immunomarkers to detect the differentiation of neuroendocrine tumors is crucial.…”

Section: Discussionmentioning

confidence: 99%

RNAi targeting of hTERT gene expression induces apoptosis and inhibits the proliferation of lung cancer cells

Shao

Yang-de

et al. 2011

Oncology Letters

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Abstract. The present study aimed to investigate the effects of RNAi-mediated reduction in human telomerase reverse transcriptase (hTERT) expression on apoptosis and lung cancer cell proliferation. A number of cell lines, including 95D, were used. hTERT mRNA levels were detected, and the RNA concentration was calculated. MTT assay was used to detect the inhibition of cell proliferation. The siRNA with the highest suppression rate, siRNA-1, was transfected into 95D cells at three different concentrations (50, 80 and 100 nmol/l). The levels of hTERT mRNA in cells transfected with 50 nmol/l siRNA-1 were not significantly different from those of the negative controltransfected cells (P>0.05), whereas both 80 and 100 nmol/l siRNA-1 showed significant reductions in hTERT mRNA compared to the negative control cells (P<0.01). hTERT levels in the 80-and 100-nmol/l groups were not significantly different (P>0.05). Compared with the control cells, cells transfected with 50, 80 or 100 nmol/l siRNA-1 showed higher fractions of apoptotic cells 48 h post-transfection (P<0.01), although the apoptotic fraction in cells transfected with 50 nmol/l siRNA-1 was not significantly different compared to that in cells transfected with negative control siRNAs (P>0.05). Moreover, the 80-and 100-nmol/l-transfected cells showed significantly increased apoptotic indices (P<0.01). MTT results indicated a time-dependent inhibition of siRNA-1-transfected cell proliferation starting at 12 h and lasting through 48 h post-transfection; the inhibition was attenuated by 72 h post-transfection. The high levels of hTERT mRNA in all human lung cancer cell lines tested suggest that telomerase plays a role in lung carcinogenesis, and this hypothesis was strengthened by the data showing that the siRNA-mediated reduction in hTERT mRNA caused apoptosis and an inhibition of the proliferation of lung cancer cells.

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Prognostic Significance of K-ras Codon 12 Mutations in Patients With Resected Stage I and II Non–Small-Cell Lung Cancer

Cited by 182 publications

References 23 publications

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

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

Prognostic implications of neuroendocrine differentiation and hormone production in patients with Stage I nonsmall cell lung carcinoma

RNAi targeting of hTERT gene expression induces apoptosis and inhibits the proliferation of lung cancer cells

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