mice with a heterozygous deficiency for the A/J Cdkn2a allele were significantly more susceptible to lung tumor progression than mice with a heterozygous deficiency for a BALB/cJ Cdkn2a allele, when compared to their respective wild type mice

Perturbations of the Ink4a/Arf gene locus in aflatoxin B1-induced mouse lung tumors.

lung tumors, which can arise in the presence of functional p19(Arf), rarely display p19(Arf) induction. In contrast, sarcomas always show robust activation, suggesting that loss of the p19(Arf)-p53 pathway is a requisite event for sarcomagenesis.

loss of P16 protein by promoter methylation results in non small cell lung tumorigenesis

Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells.

aberrant CDKN2A promoter methylation is associated with preinvasive bronchial lesions in lung carcinoma

MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmonary fibrosis

Pathogenetic and biologic significance of TP14ARF alterations in nonsmall cell lung carcinoma.

Aberrant p16 promoter methylation is associated with smokers and former smokers with nonsmall cell lung cancer

p16 inactivation by promoter methylation has different effects in non-small cell lung and colorectal cancer: clinical implications

p16-Leiden germline mutation may be involved in susceptibility to lung cancer and oral squamous cell carcinomas development in some patients

E-cadherin and p16INK4a are commonly methylated in non-small cell lung cancer

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

Frequent p16INK4a promoter hypermethylation is associated with human papillomavirus-infected female lung cancer

The frequency of p16INK4A or CDH13 hypermethylation in patient serum and the total lack of methylation in serum from healthy individuals, offer a promising tool for non invasive early detection of lung cancer.

tobacco smoking may be associated with an increased incidence of aberrant promoter methylation of the p16 and MGMT genes in non-small cell lung cancer

aberrant methylation of p16(INK4a) is seen in in chromate workers with lung cancer

Effects of exogenous p16(ink4a) gene on biological behavior of human lung cancer cells are reported.

study of EGFR, HER2, TP53& KRAS mutations of p14arf expression of non-small cell lung cancers in relation to smoking

In summary, p16 methylation is very frequent among non-small cell lung carcinoma patients, and correlates with heavy cigarette consumption only in disease-free smokers.

Loss of heterozygosity (LOH) of the hDMP1 gene was detectable in approximately 35% of human lung carcinomas, which was found in mutually exclusive fashion with LOH of INK4a/ARF or that of P53. DMP1 is a pivotal tumor suppressor for human lung cancers.

Results identified CDKN2A EX2 loci showing significant differential DNA methylation levels between tumor and non-tumor lung and highly significant hypermethylation in adenocarcinoma.

Despite the fact that p16 is important in non-small cell lung cancer carcinogenesis, the data obtained do not allow the prognostic impact of this biological marker to be established.

Inactivation of p16 gene in histologically normal bronchi could aid the identification of individuals at risk of developing squamous cell carcinoma of the lung.

Evaluation of p16 and ESR1 promoter methylation in blood using real-time PCR appears to be very useful for lung cancer diagnosis

aberrant methylation is more frequent in invasive lung adenocarcinomas than in noninvasive tumors

p16 is a useful marker for the discrimination between cervical and pulmonary squamous cell carcinomas.

This study suggests that P16/CDKN2A gene inactivation in asbestos-exposed non-small-cell lung cancer cases mainly occurs via deletion.

p16INK4A, DAPK1, PTEN and MT1G genes were not frequently methylated in the stage I non-small cell lung cancer in China.

Numerical aberrations of chromosome 9 and p16 gene deletion are common findings in all subtypes of non-small cell lung cancer.

There is over-expression of E2F-1 gene and deletion of p14(ARF) gene in the tumorigenesis of the lung cancer in Gejiu and Xuanwei regions in Yunnan Province.

simultaneous detection of p53, Rb, p16, and EGFR in a suspension microarray facilitates rapid diagnosis of lung cancer

Loss of p16 is associated with lung cancer.

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

Loss of p16 and increased incidence of autosomal aneuploidy and chromatid breaks, along with other chromosomal alterations, can contribute to the progression of lung cancer.

Low CDKN2A is associated with lung cancer .

Combined effects of cigarette smoke and hypermethylations of p16 are associated with non small cell lung cancer.

Loss of p16Ink4a by promoter hypermethylation is associated with lung adenocarcinoma.

The p16, DAPK and RAR beta genes methylation are strongly associated with clinical data of non-small cell lung cancer, and methylation of p16 and DAPK genes are associated with tobacco smoking.

expression status is an independent prognostic factor in non-small cell lung cancer; meta-analysis

p16 is not a reliable indicator of high-risk human papillomavirus infection in squamous cell carcinomas of the lung, skin, and esophagus.

Loss of p16 due to hypermethylation of the promoter region is associated with non-small cell lung carcinomas.

Report p16 methylation analysis in induced sputum from patients with lung cancer and non malignant disease.

TP53 mutation and CDKN2A methylation specifically interact to promote lung tumorigenesis in subjects with CYP1A1 risk genotype.

Cigarette smoking is positively correlated to p16(INK4alpha) gene hypermethylation in non-small cell lung carcinoma patients.

p16 hypermethylation is associated with lung tumours from ever-smokers.

Results identify a link between the p14(ARF) and EGFR pathways and suggest that EGFR L858R counteracts the pro-apoptotic function of p14(ARF) by downregulating its expression to promote carcinogenesis in the lung.

The lower rate of TP16 somatic mutations in lung adenocarcinomas are characteristic of the Kujukuri cohort as compared to Caucasians.

aberrant p16 alterations directly correlated with altered those in PTEN in non-small cell lung cancer.

CDKN2A (p16) promoter hypermethylation influences the outcome in young lung cancer patients.

16INK4a promoter methylation plays an important role in carcinogenesis of non-small cell lung cancer

In 22 lung cancer patients with negative histology and cytology at initial bronchoscopy, FHIT and p16 mRNA loss was detected in 40.9% (9/22) and 36.4% (8/22) cases, respectively.

Positive association between p16 promoter methylation and smoking is seen in non-small-cell lung carcinoma.

patients with non-small cell lung cancer had a significant higher level of anti-p16 IgG antibody than control subjects

Hypermethylation of p14ARF promoter is associated with lung cancer.

promoter methylation is a biomarker for diagnosis of non-small cell lung cancer

The presence of individual and multiple alterations of p53, p16 and PTEN were compared in in non-small cell lung carcinoma (NSCLC), glioma and breast carcinoma.

p14(ARF) and p16(INK4a) gene methylation in peripheral blood mononuclear cells may be used for screening and warning lung cancer in coke oven workers

MTAP expression is an independent prognostic factor and has greater prognostic significance than p16 expression in non-small cell lung cancer and concordant loss of MTAP and p16 expression indicates poor outcomes in lung cancer patients.

Melanoma-prone families with mutations in CDKN2A have an increased prevalence of cancers including lung, pancreatic, and breast cancer & this information should be included in genetic counseling and cancer prevention for CDKN2A mutation carriers

Loss of p16 expression is associated with lymph node metastasis in lung adenocarcinoma

protein pairs significantly correlated with an increased risk of death in non-small cell lung cancer: c-Myc with p16, mSin3A with p16

These results indicate that the loss of RB1 and CDKN2A function induces distinctively different signaling cascades in non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma

High serum p16 gene promoter methylation is associated with non-small cell lung cancer.

P16INK4A gene promoter methylation is associated with lung cancer.

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 p16 promoter region is associated with lung cancer.

E6AP (UBE3A) abundance is down-regulated in a proportion of NSCLC (non-small cell lung cancer) patients, and this correlates with low p16INK4a in tumors and worse overall survival.

These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma. Our results provide an alternative mechanism for etoposide in lung carcinoma and suggest NMI has a critical role in suppressing lung carcinoma progression.

Results provide evidence that P16(INK4a) gene promoter methylation detection in serum or bronchoalveolar fluid/sputum may be a potential biomarker for non-small cell lung cancer diagnosis.

Results provide evidence that the abnormal methylation of the p14ARF promoter region plays an important role in the development of lung cancer cells.

p16 and p53 were detected in 50.7 and 57.3% of lung adenocarcinomas (ADCs; n = 75), and 35.2 and 63.6% of lung squamous cell carcinomas (n = 88). In ADCs, p16 positive tumors demonstrated a favorable median overall survival time of 60.9 months, compared with p16 negative tumors of 46.9 months (p < 0.05).

Biomarker-driven phase 2 umbrella trial study for patients with recurrent small cell lung cancer failing platinum-based chemotherapy.

Clinical Significance of P16 Gene Methylation in lung cancer.

Survival of lung cancer Patients Dependent on the LOH Status for DMP1, ARF, and p53.