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MeSH Review

Genes, p16

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Disease relevance of Genes, p16


High impact information on Genes, p16

  • High frequency of p16INK4A gene alterations in hepatocellular carcinoma [6].
  • The mts1 gene codes for a 101 amino acid protein which belongs to the subfamily of S100 Ca(2+)-binding proteins and is overexpressed in metastatic cancers as compared to their nonmetastatic counterparts [7].
  • It is closely linked to the P16 gene (MTS1) and is homozygously deleted in many tumor cell lines [8].
  • This suggests that p16INK4A gene alterations, inc contrast to p53, are not involved in the progression of STS [9].
  • Furthermore aberrant P15 protein expression was detected in 85% of patients analyzed with P15 gene abnormalities and abnormal P16 expression in 59% with P16 gene abnormalities [10].

Chemical compound and disease context of Genes, p16


Biological context of Genes, p16


Anatomical context of Genes, p16

  • The cyclin-dependent kinase 4 inhibitor (CDKN2) gene, which maps to 9p21, has been implicated by the finding of a high frequency of biallelic deletions in leukemic cell lines [16].
  • Frequent p16INK4 (MTS1) gene inactivation in testicular germ cell tumors [17].
  • The cyclin kinase inhibitor p16, encoded by the CDKN2A gene, suppresses the transformation of mouse embryonic fibroblasts by oncogenic RAS [18].
  • Our results demonstrated that: (1) the biallelic loss of p16INK4A gene is strictly related to a specific immunophenotype, namely ALL of T-cell lineage; (ii) no significant correlation exists between alterations at chromosome 9p level and the homozygous deletions of p16INK4A gene; and (iii) p18 gene was not deleted in the examined cases [19].
  • Establishment of a novel human B-cell line (OZ) with t(14;18)(q32;q21) and aberrant p53 expression was associated with the homozygous deletions of p15INK4B and p16INK4A genes [20].

Associations of Genes, p16 with chemical compounds


Gene context of Genes, p16

  • Analysis of CpG island hypermethylation in EAC has thus far been limited to the CDKN2A (p16) gene [24].
  • Two high-risk melanoma susceptibility genes-CDKN2A and CDK4-have been identified to date, with a third gene p14(ARF) also being suspected of playing a role [25].
  • Moreover, the absence of MTAPase activity seems to be a valuable marker of p16INK4A gene inactivation, thus indicating that the deleted chromosomal area on 9p21 very frequently involves the MTAPase gene [19].
  • On the other hand, genetic alterations of the cyclin D1 and p16INK4A genes were not so frequent, but appeared to be associated with the aggressive behavior of the tumor, which suggests that disruption of the cell cycle-related genes results in the progression of HCC [26].
  • Among the four CDK inhibitor genes, alterations of only the p16INK4A gene were found in 8 out of 34 (24%) cell lines, and all eight cell lines having a p16INK4A gene alteration had an alteration of either the K-ras of p53 gene [27].

Analytical, diagnostic and therapeutic context of Genes, p16

  • Sequence analyses of p16INK4A gene of six CLL cases with heterozygous deletion at this locus showed a 27-bp deletion at the splice acceptor site of intron 1 in one case and changes in the coding sequence in three other cases [28].
  • Adenovirus-mediated combined P16 gene and GM-CSF gene therapy for the treatment of established tumor and induction of antitumor immunity [29].
  • To increase the sensitivity of detection, a two-step methylation-specific PCR approach was used to analyze the methylation status of the promoter/exon 1 regions of both p14ARF and p16INK4A genes [30].


  1. Chromosome 9p deletions in cutaneous malignant melanoma tumors: the minimal deleted region involves markers outside the p16 (CDKN2) gene. Puig, S., Ruiz, A., Lázaro, C., Castel, T., Lynch, M., Palou, J., Vilalta, A., Weissenbach, J., Mascaro, J.M., Estivill, X. Am. J. Hum. Genet. (1995) [Pubmed]
  2. Detection of homozygous deletions of the cyclin-dependent kinase 4 inhibitor (p16) gene in acute lymphoblastic leukemia and association with adverse prognostic features. Fizzotti, M., Cimino, G., Pisegna, S., Alimena, G., Quartarone, C., Mandelli, F., Pelicci, P.G., Lo Coco, F. Blood (1995) [Pubmed]
  3. Deletion map of chromosome 9 and p16 (CDKN2A) gene alterations in neuroblastoma. Takita, J., Hayashi, Y., Kohno, T., Yamaguchi, N., Hanada, R., Yamamoto, K., Yokota, J. Cancer Res. (1997) [Pubmed]
  4. Loss of p16 protein expression associated with methylation of the p16INK4A gene is a frequent finding in Hodgkin's disease. García, J.F., Villuendas, R., Algara, P., Sáez, A.I., Sánchez-Verde, L., Martínez-Montero, J.C., Martínez, P., Piris, M.A. Lab. Invest. (1999) [Pubmed]
  5. Alteration of p16 (CDKN2) gene is associated with interleukin-2-induced tumor cell growth in adult T-cell leukemia. Fujiwara, H., Arima, N., Hashimoto-Tamaoki, T., Matsushita, K., Ohtsubo, H., Arimura, K., Hidaka, S., Tei, C. Exp. Hematol. (1999) [Pubmed]
  6. High frequency of p16INK4A gene alterations in hepatocellular carcinoma. Liew, C.T., Li, H.M., Lo, K.W., Leow, C.K., Chan, J.Y., Hin, L.Y., Lau, W.Y., Lai, P.B., Lim, B.K., Huang, J., Leung, W.T., Wu, S., Lee, J.C. Oncogene (1999) [Pubmed]
  7. Interaction of metastasis associated Mts1 protein with nonmuscle myosin. Ford, H.L., Zain, S.B. Oncogene (1995) [Pubmed]
  8. Genomic structure, expression and mutational analysis of the P15 (MTS2) gene. Stone, S., Dayananth, P., Jiang, P., Weaver-Feldhaus, J.M., Tavtigian, S.V., Cannon-Albright, L., Kamb, A. Oncogene (1995) [Pubmed]
  9. No p16INK4A/CDKN2/MTS1 mutations independent of p53 status in soft tissue sarcomas. Meye, A., Würl, P., Hinze, R., Berger, D., Bache, M., Schmidt, H., Rath, F.W., Taubert, H. J. Pathol. (1998) [Pubmed]
  10. Frequent abnormalities of the p15 and p16 genes in mycosis fungoides and sezary syndrome. Scarisbrick, J.J., Woolford, A.J., Calonje, E., Photiou, A., Ferreira, S., Orchard, G., Russell-Jones, R., Whittaker, S.J. J. Invest. Dermatol. (2002) [Pubmed]
  11. Demethylation by 5-aza-2'-deoxycytidine (5-azadC) of p16INK4A gene results in downregulation of vascular endothelial growth factor expression in human lung cancer cell lines. Miki, K., Shimizu, E., Yano, S., Tani, K., Sone, S. Oncol. Res. (2000) [Pubmed]
  12. Risk of developing pancreatic cancer in families with familial atypical multiple mole melanoma associated with a specific 19 deletion of p16 (p16-Leiden). Vasen, H.F., Gruis, N.A., Frants, R.R., van Der Velden, P.A., Hille, E.T., Bergman, W. Int. J. Cancer (2000) [Pubmed]
  13. Analysis of G(1)/S checkpoint regulators in metastatic melanoma. Sauroja, I., Smeds, J., Vlaykova, T., Kumar, R., Talve, L., Hahka-Kemppinen, M., Punnonen, K., Jansèn, C.T., Hemminki, K., Pyrhönen, S. Genes Chromosomes Cancer (2000) [Pubmed]
  14. Alterations of the p16INK4A gene in human ovarian cancers. Kanuma, T., Nishida, J., Gima, T., Barrett, J.C., Wake, N. Mol. Carcinog. (1997) [Pubmed]
  15. Activation of RB tumor suppressor protein and growth suppression of small cell lung carcinoma cells by reintroduction of p16INK4A gene. Sumitomo, K., Shimizu, E., Shinohara, A., Yokota, J., Sone, S. Int. J. Oncol. (1999) [Pubmed]
  16. Deletions and rearrangement of CDKN2 in lymphoid malignancy. Stranks, G., Height, S.E., Mitchell, P., Jadayel, D., Yuille, M.A., De Lord, C., Clutterbuck, R.D., Treleaven, J.G., Powles, R.L., Nacheva, E. Blood (1995) [Pubmed]
  17. Frequent p16INK4 (MTS1) gene inactivation in testicular germ cell tumors. Chaubert, P., Guillou, L., Kurt, A.M., Bertholet, M.M., Metthez, G., Leisinger, H.J., Bosman, F., Shaw, P. Am. J. Pathol. (1997) [Pubmed]
  18. Codeletion of the JUN proto-oncogene and the CDKN2A tumor-suppressor gene in HRAS-transformed rat embryo fibroblast cell lines. Zhou, J.N., Ljungdahl, S., Röhme, D., Levan, G., Shoshan, M.C., Linder, S. Genes Chromosomes Cancer (1997) [Pubmed]
  19. P16INK4A gene homozygous deletions in human acute leukaemias with alterations of chromosome 9. Faienza, M.F., della Ragione, F., Basso, G., Coppola, B., Miraglia del Giudice, E., Schettini, F., Iolascon, A. Br. J. Haematol. (1996) [Pubmed]
  20. Establishment of a novel human B-cell line (OZ) with t(14;18)(q32;q21) and aberrant p53 expression was associated with the homozygous deletions of p15INK4B and p16INK4A genes. Nagai, M., Fujita, M., Ohmori, M., Matsubara, S., Taniwaki, M., Horiike, S., Tasaka, T., Koeffler, H.P., Takahara, J. Hematological oncology. (1997) [Pubmed]
  21. Increased expression of cyclin-dependent kinase inhibitor 2 (CDKN2A) gene product P16INK4A in ovarian cancer is associated with progression and unfavourable prognosis. Dong, Y., Walsh, M.D., McGuckin, M.A., Gabrielli, B.G., Cummings, M.C., Wright, R.G., Hurst, T., Khoo, S.K., Parsons, P.G. Int. J. Cancer (1997) [Pubmed]
  22. Growth inhibition and induction of apoptosis by flavopiridol in rat lung adenocarcinoma, osteosarcoma and malignant fibrous histiocytoma cell lines. Honoki, K., Yoshitani, K., Tsujiuchi, T., Mori, T., Tsutsumi, M., Morishita, T., Takakura, Y., Mii, Y. Oncol. Rep. (2004) [Pubmed]
  23. 5-Aza-2'-deoxycitydine induces demethylation and up-regulates transcription of p16INK4A gene in human gastric cancer cell lines. Fang, J.Y., Yang, L., Zhu, H.Y., Chen, Y.X., Lu, J., Lu, R., Cheng, Z.H., Xiao, S.D. Chin. Med. J. (2004) [Pubmed]
  24. Fields of aberrant CpG island hypermethylation in Barrett's esophagus and associated adenocarcinoma. Eads, C.A., Lord, R.V., Kurumboor, S.K., Wickramasinghe, K., Skinner, M.L., Long, T.I., Peters, J.H., DeMeester, T.R., Danenberg, K.D., Danenberg, P.V., Laird, P.W., Skinner, K.A. Cancer Res. (2000) [Pubmed]
  25. Genetic and environmental factors in cutaneous malignant melanoma. Bressac-de-Paillerets, B., Avril, M.F., Chompret, A., Demenais, F. Biochimie (2002) [Pubmed]
  26. Alteration of cell cycle-related genes in hepatocarcinogenesis. Nishida, N., Fukuda, Y., Ishizaki, K., Nakao, K. Histol. Histopathol. (1997) [Pubmed]
  27. Coincidental alterations of p16INK4A/CDKN2 and other genes in human lung cancer cell lines. Fujishita, T., Mizushima, Y., Kashii, T., Kobayashi, M. Anticancer Res. (1998) [Pubmed]
  28. p16INK4A and p15INK4B gene deletions in primary leukemias. Haidar, M.A., Cao, X.B., Manshouri, T., Chan, L.L., Glassman, A., Kantarjian, H.M., Keating, M.J., Beran, M.S., Albitar, M. Blood (1995) [Pubmed]
  29. Adenovirus-mediated combined P16 gene and GM-CSF gene therapy for the treatment of established tumor and induction of antitumor immunity. Wang, L., Qi, X., Sun, Y., Liang, L., Ju, D. Cancer Gene Ther. (2002) [Pubmed]
  30. Methylation of the INK4A/ARF locus in blood mononuclear cells. Deligezer, U., Erten, N., Akisik, E.E., Dalay, N. Ann. Hematol. (2006) [Pubmed]
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