ArticleThe American journal of pathology1997
Frequent p16INK4 (MTS1) gene inactivation in testicular germ cell tumors.
Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 40 citations in OpenAlex.
- Epigenetic drugs and their molecular targets in testicular germ cell tumours.Nature reviews. Urology · 2019Review
- Loss of heterozygosity of CDKN2A (p16INK4a) and RB1 tumor suppressor genes in testicular germ cell tumors.Radiology and oncology · 2010Article
- Cancer stem cells and hepatocellular carcinoma.Cancer biology & therapy · 2009Review
- Article
- Frequent promoter hypermethylation of the O6-Methylguanine-DNA Methyltransferase (MGMT) gene in testicular cancer.Oncogene · 2002Article
- Lack of p19INK4d in human testicular germ-cell tumours contrasts with high expression during normal spermatogenesis.Oncogene · 2000Article
- Alterations of the p16-pRb pathway and the chromosome locus 9p21-22 in non-small-cell lung carcinomas: relationship with p53 and MDM2 protein expression.The American journal of pathology · 1998Article
- Alterations of p16-pRb pathway and chromosome locus 9p21-22 in sporadic invasive breast carcinomas.Molecular medicine (Cambridge, Mass.) · 1998Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms responsible for the development of testicular germ cell tumors (GCTs) have not as yet been elucidated. The aim of the present study was to determine whether genetic alterations of p16INK4 (MTS1) and/or cyclin-dependent kinase 4 (CDK4) occur in the genesis of these tumors. We have analyzed these two genes in 29 testicular GCTs, seminomas, and nonseminomas. None of the tumors showed either p16INK4 or CDK4 mutations. Only 1 of the 29 GCTs displayed loss of heterozygosity of the p16INK4 gene. No homozygous deletions of p16INK4 were detected. Evidence of hypermethylation of p16INK4 exon 1, however, was demonstrated in 13 of the 26 (50%) GCTs analyzed. Tumor samples having exon 1 of p16INK4 methylated expressed significantly lower levels of p16INK4 mRNA, as analyzed by reverse transcriptase polymerase chain reaction. These results suggest that p16INK4 inactivation plays a role in the genesis of GCTs.
Indexed as
Identifiers
9284835PMC1857830W70128731What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.