Loss of P16 in Esophageal Adenocarcinoma Detected by Fluorescence in situ Hybridization and Immunohistochemistry
By:
A. Kotzev and M. Kamenova
References
- 1. Hur C, Miller M, Kong CY, et al. Trends in esophageal adenocarcinoma incidence and mortality. Cancer. 2013;119:1149-1158.
- 2. Thrift AP, Whiteman DC. The incidence of esophageal adenocarcinoma continues to rise: analysis of period and birth cohort effects on recent trends. Ann Oncol. 2012;23:3155-3162.10.1093/annonc/mds181
- 3. Clemons NJ, Phillips WA, Lord RV. Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction. Cancer Biol Ther. 2013;14:782-795.10.4161/cbt.25362
- 4. Serrano M, Hannon GJ, Beach D. A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4. Nature. 1993;366:704-707.
- 5. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000;100:57-70.10.1016/S0092-8674(00)81683-9
- 6. Kamb A, Gruis NA, Weaver-Feldhaus J, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science. 1994;264:436-440.
- 7. Serrano M, Lee H, Chin L, Cordon-Cardo C, Beach D, De-Pinho RA. Role of the INK4a locus in tumor suppression and cell mortality. Cell. 1996;85:27-37.
- 8. Liggett WH Jr, Sidransky D. Role of the p16 tumor suppressor gene in cancer. J Clin Oncol. 1998;16:1197-1206.
- 9. Romagosa C, Simonetti S, López-Vicente L, et al. p16(Ink4a) overexpression in cancer: a tumor suppressor gene associated with senescence and high-grade tumors. Oncogene. 2011;30:2087-2097.10.1038/onc.2010.614
- 10. Nobori T, Miura K, Wu D, Lois A, Takabayashi K, Carson DA. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature. 1994;368:753-756.
- 11. Liu Q, Yan YX, McClure M, Nakagawa H, Fujimura F, Rustgi AK. MTS-1 (CDKN2) tumor suppressor gene deletions are a frequent event in esophagus squamous cancer and pancreatic adenocarcinoma cell lines. Oncogene. 1995;10:619-622.
- 12. Kamb A, Gruis NA, Weaver-Feldhaus J, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science. 1994;264:436-440.
- 13. Cairns P, Polascik TJ, Eby Y, et al. Frequency of homozygous deletion at p16/CDKN2 in primary human tumours. Nat Genet. 1995;11:210-212.10.1038/ng1095-210
- 14. Barrett MT, Sanchez CA, Galipeau PC, Neshat K, Emond M, Reid BJ. Allelic loss of 9p21 and mutation of the CDKN2/p16 gene develop as early lesions during neoplastic progression in Barrett’s esophagus. Oncogene. 1996;13:1867-1873.
- 15. González MV, Artímez ML, Rodrigo L, et al. Mutation analysis of the p53, APC, and p16 genes in the Barrett’s oesophagus, dysplasia, and adenocarcinoma. J Clin Pathol. 1997;50:212-217.
- 16. Lu Y, Zhang X, Zhang J. Inhibition of breast tumor cell growth by ectopic expression of p16/INK4A via combined effects of cell cycle arrest, senescence and apoptotic induction, and angiogenesis inhibition. J Cancer. 2012;3:333-344.10.7150/jca.4046
- 17. Hu H, Li Z, Chen J, et al. P16 reactivation induces anoikis and exhibits antitumour potency by downregulating Akt/survivin signalling in hepatocellular carcinoma cells. Gut. 2011;60:710-721.10.1136/gut.2010.220020
- 18. Allay JA, Steiner MS, Zhang Y, Reed CP, Cockroft J, Lu Y. Adenovirus p16 gene therapy for prostate cancer. World J Urol. 2000;18:111-120.10.1007/s003450050182
- 19. Schrump DS, Chen GA, Consuli U, Jin X, Roth JA. Inhibition of esophageal cancer proliferation by adenovirally mediated delivery of p16INK4. Cancer Gene Ther. 1996;3:357-364.
- 20. Xie SH, Lagergren J. A global assessment of the male predominance in esophageal adenocarcinoma. Oncotarget. 2016;7:38876-38883.
- 21. Bollschweiler E, Wolfgarten E, Gutschow C, Hölscher AH. Demographic variations in the rising incidence of esophageal adenocarcinoma in white males. Cancer. 2001;92:549-555.10.1002/1097-0142(20010801)92:3<;549::AID-CNCR1354>3.0.CO;2-L
- 22. Lagergren J, Lagergren P. Recent developments in esophageal adenocarcinoma. CA Cancer J Clin. 2013;63:232-248.10.3322/caac.21185
- 23. Duraiyan J, Govindarajan R, Kaliyappan K, Palanisamy M. Applications of immunohistochemistry. J Pharm Bioallied Sci. 2012;4(Suppl 2):S307-9.
- 24. Le Beau MM. Fluorescence in situ hybridization in cancer diagnosis. Important Adv Oncol. 1993;29-45.
- 25. Hu L, Ru K, Zhang L, et al. Fluorescence in situ hybridization (FISH): an increasingly demanded tool for biomarker research and personalized medicine. Biomark Res. 2014;2:3.
- 26. Trask BJ. Fluorescence in situ hybridization: applications in cytogenetics and gene mapping. Trends Genet. 1991;7:149-154.10.1016/0168-9525(91)90378-4
- 27. Waters JJ, Barlow AL, Gould CP. Demystified ... FISH. Mol Pathol. 1998;51:62-70.
- 28. Langer R, Von Rahden BH, Nahrig J, et al. Prognostic significance of expression patterns of c-erbB-2, p53, p16INK4A, p27KIP1, cyclin D1 and epidermal growth factor receptor in oesophageal adenocarcinoma: a tissue microarray study. J Clin Pathol. 2006;59:631-634.
- 29. Hardie LJ, Darnton SJ, Wallis YL, et al. p16 expression in Barrett’s esophagus and esophageal adenocarcinoma: association with genetic and epigenetic alterations. Cancer Lett. 2005;217:221-230.
- 30. Doak SH, Jenkins GJS, Parry EM, et al. Characterisation of p53 status at the gene, chromosomal and protein levels in oesophageal adenocarcinoma. Br J Cancer. 2003;89:1729-1735.
- 31. Zordan A. Fluorescence in situ hybridization on formalin-fixed, paraffin-embedded tissue sections. Methods Mol Biol. 2011;730:189-202.
- 32. Brankley SM, Wang KK, Harwood AR, et al. The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett’s esophagus. J Mol Diagn. 2006;8:260-267.
- 33. Fahmy M, Skacel M, Gramlich TL, et al. Chromosomal gains and genomic loss of p53 and p16 genes in Barrett’s esophagus detected by fluorescence in situ hybridization of cytology specimens. Mod Pathol. 2004;17:588-596.
- 34. Doak SH, Jenkins GJ, Parry EM, et al. Chromosome 4 hyperploidy represents an early genetic aberration in premalignant Barrett’s oesophagus. Gut. 2003;52:623-628.
- 35. Brankley SM, Fritcher EG, Smyrk TC, et al. Fluorescence in situ hybridization mapping of esophagectomy specimens from patients with Barrett’s esophagus with high-grade dysplasia or adenocarcinoma. Hum Pathol. 2012;43:172-179.10.1016/j.humpath.2011.04.018
- 36. Maley CC, Galipeau PC, Li X, Sanchez CA, Paulson TG, Reid BJ. Selectively advantageous mutations and hitchhikers in neoplasms: p16 lesions are selected in Barrett’s esophagus. Cancer Res. 2004;64:3414-3127.10.1158/0008-5472.CAN-03-3249
- 37. Wang JS, Guo M, Montgomery E, et al. DNA promoter hypermethylation of p16 and APC predicts neoplastic progression in Barrett’s esophagus. Am J Gastroenterol. 2009;104:2153-2160.
- 38. Klump B, Hsieh CJ, Holzmann K, Gregor M, Porschen R. Hypermethylation of the CDKN2/p16 promoter during neoplastic progression in Barrett’s esophagus. Gastroenterology. 1998;115:1381-1386.
- 39. Wong DJ, Barrett MT, Stöger R, Emond MJ, Reid BJ. p16INK4a promoter is hypermethylated at a high frequency in esophageal adenocarcinomas. Cancer Res. 1997;57:2619-2622.
Language: English
Page range: 14 - 19
Published on: Oct 23, 2017
Published by: Sofia Medical University
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© 2017 A. Kotzev, M. Kamenova, published by Sofia Medical University
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