Epigenetic inactivation of RASSF1A plays an important role in the progression of lung adenocarcinoma.

detection of aberrant promoter hypermethylation from smokers, lung cancer, and breast cancer patients

RASSF1 is a putative tumor suppressor in non-small cell lung cancer

There is a significant expression difference among the three RASSF1 transcripts in lung carcinoma. RASSF1A, closely associated with lymph metastasis and TNM stage of lung carcinoma, should be a new tumor suppressor gene.

there is an inverse relationship between Kras2 activation and RASSF1A promoter methylation in the majority of human lung adenocarcinomas and large cell carcinomas

the RASSF1A but not p16INK4a methylated promoter region has a role in progression of non-small cell lung cancer

Smoking under age 18 is an independent risk for RASSF1A hypermethylation, thus identifying a molecular alteration related to the epidemiologic effect of teenage smoking as a lung cancer risk.

Epigenetic inactivation of RASSF1A cannot be a prognostic marker of non-small cell lung cancer.

Hypermethylation of RASSF1A was commonly observed in primary tumors including lung, breast, pancreas, kidney, liver, cervix, nasopharyngeal, prostate, thyroid and other cancers.

RASSF1A exerts a tumor-suppressing effect by blocking oncogene-mediated JNK activation in lung cells.

Overexpression of RASSF1A diminished the ability of A549 non-small cell lung cancer cells to migrate either through a transwell filter or to close a wound.

Aberrant methylation of RASSF1A is associated with human non-small cell lung cancer

Isoenzymes may not be tumor suppressor genes but rather stimulates lung cancer cell proliferation.

Forty-two of 46 (91%) lung tumors with RASSF1A promoter methylation expressed DNMT3B4 compared with only 13 of 73 (18%) tumors without the promoter methylation.

results showed RASSF1A & DAPK genes' promoter methylation occurred frequently in lung tumors, although prevalence of this alteration in these genes was not associated with smoking status of the patients or occurrence of mutations in K-ras, p53 & EGFR

the hypermethylation of RASSF1A gene is a useful biomarker to predict the prognosis in non-small cell lung cancer

Results identified RASSF1 loci showing significant differential DNA methylation levels between tumor and non-tumor lung and highly significant hypermethylation in adenocarcinoma.

RASSF1A promoter polymorphisms affect RASSF1A expression, further contributing to the genetic susceptibility to lung cancer.

Hypermethylated RASSF1A promoter is frequently found in the serum DNA of non-small cell lung cancer patients.

role of deltaDNMT3B4/2 in regulating RASSF1A promoter-specific DNA methylation in non-small cell lung cancer.

Down-regulation of RBSP3/CTDSPL, NPRL2/G21, RASSF1A, ITGA9, HYAL1 and HYAL2 genes in non-small cell lung cancer

results show a high frequency of hypermethylation of the RASSF1A promoter and occurrence of Merkel Cell PolyoVirus infection in the tumour tissue of Small Cell lung cancer.

Hypermethylation of RASSF1 was significantly associated with shorter time to recurrence of nonsmall cell lung cancer.

RASSF1 Ala133Ser genotype increased the risk of lung cancer.

tumor suppressor genes RBSP3/CTDSPL, NPRL2/G21 and RASSF1A are downregulated in primary non-small cell lung cancer

Promoter hypermethylation of RASSF1A, p16, and DAPK genes was detected in lung cancer.

RASSF1 A/E is likely to act as a tumor suppressor gene in most pulmonary NET, and RASSF1 C as an oncogene in high-grade tumors.

RASSF1A promoter hypermethylation is associated with non-small cell lung carcinoma.

Findings suggest the role of RASSF1C/PIWIL1 proteins in initiation and progression of lung cancer.

Hypermethylation of RASSF1A was associated with non-small cell lung cancer.

RASSF1A promoter methylation is associated with non-small cell lung cancer.

GPR56, MT1G, and RASSF1 might be the potential methylation markers associated with acquired multidrug resistance of lung adenocarcinoma.

RASSF1A hypermethylation in sputum samples is elevated in lung cancer compared with controls.

This meta-analysis suggests, for the first time, that RASSF1A Ala133Ser polymorphism may contribute to cancer susceptibility, especially for lung cancer. [Meta-Analysis]

High methylation level of RASSF1A gene promoter region is associated with low drug sensitivity of non-small cell lung cancer.

The total frequency of FHIT, RASSF1A and RARbeta gene methylation was significantly higher in lung cancer.

RASSF1A gene hypermethylation is associated with lung cancer.

There was a significant relationship between RASSF1A promoter methylation and lung cancer risk. This relationship was stronger in NSCLC than in SCLC. [Meta-Analysis]

RASSF1A promoter gene methylation is highly associated with non-small cell lung cancer and disease progression.

Describe a novel interaction between Rheb and the tumor suppressor RASSF1A. This interaction may allow coordinate upregulation of Hippo while TOR is suppressed to modulate the balance of apoptosis and autophagy in lung tumor cells.

The present meta.analysis provides convincing evidence that the promoter methylation ratio of RASSF1A and p16 is associated with clinicopathological features in lung cancers, and could be used as effective biomarkers in early diagnosis in lung cancers.

High methylation in the RASSF1A promoter region is associated with lung cancer.

the methylation positive rates of SHOX2 with RASSF1A in stage III were both higher than the other stages of lung cancer

Circ_0078767 and RASSF1A were downregulated, while miR-330-3p was upregulated in non-small-cell lung cancer (NSCLC) than that in adjacent tissues. miR-330-3p had a binding relationship with circ_0078767 and RASSF1A. The overexpression of circ_0078767 and RASSF1A or the underexpression of miR-330-3p significantly suppressed NSCLC cell viability.

the sensitivity analysis indicated that RASSF1A methylation from lung cancer tissues was significantly associated with lower OS (HR = 1.24; 95% CI 1.04-1.45). Conclusion: RASSF1A methylation in lung cancer tissue can serve as a prognostic factor of NSCLC. More studies are needed to uncover the underlying mechanisms.

Results identify that high expression levels of RASSF1A can serve as a prognostic biomarker for lung adenocarcinoma patients. Loss or methylation of RASSF1A leads to constitutive YAP activity, which together with mechanical properties of extracellular matrix via P4HA2 drives cancer stem-like re-programming and metastatic progression in lung adenocarcinoma.

Predictive value of unmethylated RASSF1A on disease progression in non-small cell lung cancer patients receiving pemetrexed-based chemotherapy.

combined detection of RASSF1A and SHOX2 gene methylation was identified as an excellent method for the screening and surveillance of lung cancer that exhibits high sensitivity and specificity