Publication:
Inactivation of p16INK4a by CpG hypermethylation is not a frequent event in colorectal cancer

dc.contributor.author Norrie, M en_US
dc.contributor.author Hawkins, Nicholas en_US
dc.contributor.author Todd, Alison en_US
dc.contributor.author Meagher, Alan en_US
dc.contributor.author O'Connor, Terence en_US
dc.contributor.author Ward, Robyn en_US
dc.date.accessioned 2021-11-25T13:30:14Z
dc.date.available 2021-11-25T13:30:14Z
dc.date.issued 2003 en_US
dc.description.abstract Backround and Objectives: Gene promoter hypermethylation is common in colorectal cancer and is associated with transcriptional silencing. However, the clinicopathological significance of p16INK4a gene silencing with hypermethylation is unknown. Therefore, the aim of this study was to analyze loss of p16 expression and its relationship to hypermethylation in sporadic colorectal cancer. Methods: Tissue from 426 colorectal cancers underwent histological analysis. Immunohistochemistry was performed for p16 expression. Fresh tumor DNA was analyzed for microsatellite instability (MSI) and the presence of K-ras mutations. In addition, DNA was bisulphite-modified and analyzed for p16INK4a promoter methylation by methylation-specific PCR. Results :There were 25% of tumors with p16INK4a promoter hypermethylation. These tumors were associated with older patients, right-sidedness, MSI and were poorly differentiated, mucinous, and had intraepithelial and peritumoral lymphocytes and a Crohn's-type lymphocytic reaction (P < 0.05). However, only right-sidedness was significant on multivariate analysis (P < 0.001). Only 8.1% of tumors did not express p16, and this was associated with hypermethylation (P < 0.05). Conclusion: p16INK4a promoter methylation, although common in colorectal cancer, does not result in a clinicopathologically distinct subgroup of tumors and infrequently results in transcriptional silencing. This suggests that p16INK4a gene inactivation does not have an important role in the pathogenesis of sporadic colorectal cancer. en_US
dc.identifier.issn 0022-4790 en_US
dc.identifier.uri http://hdl.handle.net/1959.4/39775
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/3.0/au/ en_US
dc.source Legacy MARC en_US
dc.title Inactivation of p16INK4a by CpG hypermethylation is not a frequent event in colorectal cancer en_US
dc.type Journal Article en
dcterms.accessRights metadata only access
dspace.entity.type Publication en_US
unsw.accessRights.uri http://purl.org/coar/access_right/c_14cb
unsw.identifier.doiPublisher http://dx.doi.org/10.1002/jso.10310 en_US
unsw.relation.faculty Medicine & Health
unsw.relation.ispartofjournal J Surg Oncol en_US
unsw.relation.ispartofpagefrompageto 143-150 en_US
unsw.relation.ispartofvolume 84 en_US
unsw.relation.originalPublicationAffiliation Norrie, M en_US
unsw.relation.originalPublicationAffiliation Hawkins, Nicholas, Medical Sciences, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Todd, Alison en_US
unsw.relation.originalPublicationAffiliation Meagher, Alan, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation O'Connor, Terence, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Ward, Robyn, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW en_US
unsw.relation.school School of Medical Sciences *
unsw.relation.school Clinical School St Vincents Hospital *
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