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• W2017373957 abstract "No AccessJournal of UrologyInvestigative Urology1 May 1997Molecular Analysis of the INK4 Family of Genes in Prostate Carcinomas Dorothy J. Park, Sharon P. Wilczynski, Emily Y. Pham, Carl W. Miller, and H. Phillip Koeffler Dorothy J. ParkDorothy J. Park More articles by this author , Sharon P. WilczynskiSharon P. Wilczynski More articles by this author , Emily Y. PhamEmily Y. Pham More articles by this author , Carl W. MillerCarl W. Miller More articles by this author , and H. Phillip KoefflerH. Phillip Koeffler More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(01)64917-6AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: A newly recognized class of INK4 family of cyclin-dependent kinase inhibitors CDKIs) include its prototype, p16 (INK4A/MTS1/CDKN2), and three others, p15 (INK4B/MTS2), p18 (INK4C), and p19 (INK4D). The putative tumor suppressor gene, p16 is frequently altered in certain neoplasms and many cell lines. The potential role of INK4 CDKIs in pathogenesis of prostate carcinoma was studied. Materials and Methods: Thirty-two primary prostate cancer samples and two prostate cancer cell lines were examined for alterations of the p16, p15, p18, and p19 genes by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and Southern blot analysis. Results: Alteration of the p16 gene was found in one of 32 primary prostate cancer samples by PCR-SSCP. DNA sequencing of the sample showed a 24-basepair insertion in exon 1 of the p16 gene at codon 11. No other mutations were found in p15, p18, or p19 genes by PCR-SSCP. Furthermore, none of the p16, p15, p18, or p19 genes had alterations by Southern blot analysis. Conclusions: These results indicate that structural abnormalities of the INK4 CDKIs is a rare event in prostate carcinoma, and the loss of function of INK4 CDKIs by other mechanisms, such as methylation should be further explored. References 1 : Cancer statistics, 1996. CA Cancer J. Clin.1996; 46: 5. Google Scholar 2 : Role of the cyclin-dependent kinase inhibitors in the development of cancer. Blood1995; 86: 841. Google Scholar 3 : Cyclins and cancer II: cyclin D and CDK inhibitors come of age. Cell1994; 79: 573. Google Scholar 4 : How cells cycle toward cancer. Science1994; 263: 319. Google Scholar 5 : Joining the complex: cyclin-dependent kinase inhibitory proteins and the cell cycle. Cell1994; 79: 181. Google Scholar 6 : Mammalian G1 cyclins. Cell1993; 73: 1059. Google Scholar 7 : A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4. Nature1993; 366: 704. Google Scholar 8 : p15 sup INK4B is a potential effector of TGF-B-induced cell cycle arrest. Nature1994; 371: 257. Google Scholar 9 : Growth suppression by p18, a p16 sup INK4B/MTS1-and p14 sup INK4B/MTS2-related CDK6 inhibitor, correlate with wild-type pRb function. Genes Dev.1994; 8: 2939. Google Scholar 10 : Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6. Mol. Cell. Biol.1995; 15: 2672. Google Scholar 11 : Identification of human and mouse p19, a novel CDK4 and CDK6 inhibitor with homology to p16 INK4. Mol. Cell. Biol.1995; 15: 2682. Google Scholar 12 : WAF1, a potential mediator of p53 tumor suppression. Cell1993; 75: 817. Google Scholar 13 : Inhibition of CDK2 activity in vivo by an associated 20K regulatory subunit. Nature1993; 366: 257. Google Scholar 14 : The p21 Cdk-interacting protein Cip 1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell1993; 75: 805. Google Scholar 15 : Braking the cycle. Cell1993; 75: 839. Google Scholar 16 : p21 is a universal inhibitor of cyclin kinases. Nature1993; 366: 701. Google Scholar 17 : Cloning of p27 sup Kip 1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals. Cell1994; 78: 59. Google Scholar 18 : p27, a novel ingibitor of G1 cyclin-cdk protein kinase activity, is related to p21. Cell1994; 78: 67. Google Scholar 19 : Cloning of p57 sup KIIP2, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev.1995; 9: 639. Google Scholar 20 : Rates of p16 (MTS1) mutations in primary tumors with 9p loss. Science1994; 265: 415. Google Scholar 21 : Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma. Nature Genet.1994; 8: 27. Google Scholar 22 : Distinct deletions of chromosome 9p associated with melanoma versus glioma, lung cancer, and leukemia. Cancer Res.1994; 54: 344. Google Scholar 23 : Homozygous deletions of human chromosome 9p21 in melanoma. Proc. Natl. Acad. Sci. USA1992; 89: 10557. Google Scholar 24 : Somatic mutations of the MTS (multiple tumor suppressor) 1/CDK4I (cyclin-dependent kinase-4 inhibitor) gene in human primary non-small cell lung carcinomas. Biochem. Biophys. Res. Commun.1994; 202: 1426. Google Scholar 25 : Germline p16 mutations in familial melanoma. Nature Genet.1994; 8: 15. Google Scholar 26 : A cell cycle regulator potentially involved in genesis of many tumor types. Science1994; 264: 436. Google Scholar 27 : Analysis of the p16 gene (CDKN2) as a candidate for the chromosome 9p melanoma susceptibility locus. Nature Genet.1994; 8: 22. Google Scholar 28 : Frequent somatic 1 mutation of the MTS1/CDK4I (multiple tumor suppressor/cyclin-dependent kinase 4 inhibitor) gene in esophageal squamous cell carcinoma. Cancer Res.1994; 54: 3396. Google Scholar 29 : Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature1994; 368: 753. Google Scholar 30 : p16 gene in uncultured tumors. Nature1994; 370: 183. Google Scholar 31 : Absence of p16 sup INK4 protein is restricted to the subset of lung cancer lines that retains wild type RB. Oncogene1994; 9: 3375. Google Scholar 32 : Candidate tumor-suppressor genes MTS1 (p16INK4A) and MTS2 (p15INK4B) display frequent homozygous deletions in primary cells from T- but not from B-cell lineage acute lymphoblastic leukemias. Blood1994; 84: 4038. Google Scholar 33 : Homozygous loss of the cyclin-dependent kinase 4-inhibitor (p16) gene in human leukemias. Blood1994; 84: 2431. Google Scholar 34 : p16 gene homozygous deletions in acute lymphoblastic leukemia. Blood1995; 85: 657. Google Scholar 35 : Analysis of a family of cyclin-dependent kinase inhibitors: p15/MTS1/INK4A, and p18 genes in acute lymphoblastic leukemia of childhood. Blood1995; 86: 755. Google Scholar 36 : Structural integrity of the cyclin-dependent kinase inhibitor genes, p15, p16 and p18 in myeloid leukaemias. Br. J. Haematol.1995; 91: 139. Google Scholar 37 : Molecular analysis of the cyclin-dependent kinase inhibitor p19INK4D in hematopoietic malignancies. J. Cancer Res. Clin. Oncol.1996; 1221: 559. Google Scholar 38 Spirin, K. S., Simpson, J. F., Miller, C. W. and Koeffler, H. P.: Molecular analysis of INK4 genes in breast carcinomas. Submitted. Google Scholar 39 : Current Protocols in Molecular Biology. New York: Greene Publishing Associates, Inc. and Wiley & Sons1993. Google Scholar 40 : Characterization of cDNA clones for human myeloperoxidase: predicted amino acid sequence and evidence for multiple mRNA species. Nucleic Acids Res.1987; 15: 2013. Google Scholar 41 : Rapid and sensitive detection of point mutations and genetic polymorphisms using polymerase chain reaction. Genomics1989; 5: 874. Google Scholar 42 : Molecular analysis of a family of cyclin-dependent kinase inhibitor genes (p15/MTS2/INK4B and p18/INK4C) in non-small cell lung cancers. Mol. Carcinogen.1995; 14: 263. Google Scholar 43 Miller, C. W., Yeon, C., Aslo, A., Mendoza, S., Aytac, U., Lampkin, B. C. and Koeffler, H. P.: The p19 cyclin dependent kinase inhibitor gene is mutated and rearranged in osteosarcoma. Submitted. Google Scholar 44 : Presence of ras oncogene mutations and human papilloma virus DNA in human prostate carcinoma. Cancer Res.1992; 52: 5991. Google Scholar 45 : Allelic loss of the retinoblastoma gene in primary human prostatic carcinoma. Prostate1995; 26: 35. Google Scholar 46 : p53 is mutated in a subset of advanced-stage prostate cancers. Cancer Res.1993; 53: 3369. Google Scholar 47 : Small subgroup of aggressive, highly proliferative prostatic carcinomas defined by p53 accumulation. J. Natl. Cancer Inst.1992; 84: 883. Google Scholar 48 : Mutational analysis of CDKN2 (CDK4I/MTS1) gene in tissues and cell lines of human prostate cancer. Jpn. J. Cancer Res.1995; 86: 622. Google Scholar 49 : Mutational effects on the p16 sup INK4a tumor suppressor protein. Cancer Res.1995; 55: 2503. Google Scholar 50 : Deletions of the cyclin-dependent kinase inhibitor genes p16 sup INK4A and p15 sup INK4B in non-Hodgkin's lymphomas. Blood1995; 86: 1534. Google Scholar 51 : Frequency of homozygous deletion at p16/CDKN2 in primary human tumors. Nature Genet.1995; 11: 210. Google Scholar 52 : Homozygous deletions of the p15 (MTS2) and p16 (CDKN2/MTS1) genes in adult T-cell leukemia. Blood1995; 85: 2699. Google Scholar 53 : Analysis of the INK4 family of genes in multiple myeloma. Br. J. Haematol.1997; 96: 98. Google Scholar 54 : Methylation and p16: suppressing the suppressor. Nature Med.1995; 1: 633. Google Scholar 55 : Inactivation of the CDKN2/p16/MTS1 gene is frequently associated with aberrant DNA methylation in all common human cancers. Cancer Res.1995; 55: 4525. Google Scholar 56 : Methylation of the 5′ CpG island of the p16/CDKN2 tumor suppressor gene in normal and transformed human tissues correlates with gene silencing. Cancer Res.1995; 55: 4531. Google Scholar 57 : 5′ CpG island methylation is associated with transcriptional silencing of the tumor suppressor p16/CDKN2/MTS1 in human cancers. Nature Med.1995; 1: 686. Google Scholar 58 : CDKN2 gene silencing in lung cancer by DNA hypermethylation and kinetics of p16INK4 protein induction by 5-aza 2′deoxycytidine. Oncogene1995; 11: 1211. Google Scholar 59 : Multiple mechanisms of p16 INK4A inactivation in non-small cell lung cancer cell lines. Cancer Res.1995; 55: 6200. Google Scholar From the Division of Hematology/Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, and the Department of Pathology, City of Hope National Medical Center, Duarte, California.© 1997 by American Urological Association, Inc.FiguresReferencesRelatedDetails Volume 157Issue 5May 1997Page: 1995-1999 Advertisement Copyright & Permissions© 1997 by American Urological Association, Inc.MetricsAuthor Information Dorothy J. Park More articles by this author Sharon P. Wilczynski More articles by this author Emily Y. Pham More articles by this author Carl W. Miller More articles by this author H. Phillip Koeffler More articles by this author Expand All Advertisement PDF downloadLoading ..." @default.
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• W2017373957 cites W1971512164 @default.
• W2017373957 cites W1974764716 @default.
• W2017373957 cites W1977299280 @default.
• W2017373957 cites W1977706798 @default.
• W2017373957 cites W1978881929 @default.
• W2017373957 cites W1982768428 @default.
• W2017373957 cites W1983348452 @default.
• W2017373957 cites W1994066190 @default.
• W2017373957 cites W1996027687 @default.
• W2017373957 cites W1996413533 @default.
• W2017373957 cites W1997073961 @default.
• W2017373957 cites W1998001782 @default.
• W2017373957 cites W2003907692 @default.
• W2017373957 cites W200461798 @default.
• W2017373957 cites W2015519364 @default.
• W2017373957 cites W2017689200 @default.
• W2017373957 cites W2020729244 @default.
• W2017373957 cites W2027558915 @default.
• W2017373957 cites W2033156691 @default.
• W2017373957 cites W2046577405 @default.
• W2017373957 cites W2048672429 @default.
• W2017373957 cites W2066657154 @default.
• W2017373957 cites W2066848701 @default.
• W2017373957 cites W2067795112 @default.
• W2017373957 cites W2070061120 @default.
• W2017373957 cites W2074067954 @default.
• W2017373957 cites W2083468823 @default.
• W2017373957 cites W2084023085 @default.
• W2017373957 cites W2086773265 @default.
• W2017373957 cites W2089218510 @default.
• W2017373957 cites W2089514388 @default.
• W2017373957 cites W2092104789 @default.
• W2017373957 cites W2092357174 @default.
• W2017373957 cites W2132580869 @default.
• W2017373957 cites W2138544437 @default.
• W2017373957 cites W2158350288 @default.
• W2017373957 cites W2161378573 @default.
• W2017373957 cites W2170331239 @default.
• W2017373957 cites W2272361594 @default.
• W2017373957 cites W2300127060 @default.
• W2017373957 cites W2301048882 @default.
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