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Methylation and expression of the tumour suppressor, PRDM5, in colorectal cancer and polyp subgroups

Overview of attention for article published in BMC Cancer, January 2015
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Title
Methylation and expression of the tumour suppressor, PRDM5, in colorectal cancer and polyp subgroups
Published in
BMC Cancer, January 2015
DOI 10.1186/s12885-015-1011-9
Pubmed ID
Authors

Catherine E Bond, Mark L Bettington, Sally-Ann Pearson, Diane M McKeone, Barbara A Leggett, Vicki LJ Whitehall

Abstract

Background PRDM5 is an epigenetic regulator that has been recognized as an important tumour suppressor gene. Silencing of PRDM5 by promoter hypermethylation has been demonstrated in several cancer types and PRDM5 loss results in upregulation of the Wnt pathway and increased cellular proliferation. PRDM5 has not been extensively investigated in specific subtypes of colorectal cancers. We hypothesized it would be more commonly methylated and inactivated in serrated pathway colorectal cancers that are hallmarked by a BRAF V600E mutation and a methylator phenotype, compared to traditional pathway cancers that are BRAF wild type.MethodsCancer (214 BRAF mutant, 122 BRAF wild type) and polyp (59 serrated polyps, 40 conventional adenomas) cohorts were analysed for PRDM5 promoter methylation using MethyLight technology. PRDM5 protein expression was assessed by immunohistochemistry in cancers and polyps. Mutation of PRDM5 was analysed using cBioPortal¿s publicly available database.Results BRAF mutant cancers had significantly more frequent PRDM5 promoter methylation than BRAF wild type cancers (77/214,36% vs 4/122,3%; p<0.0001). Serrated type polyps had a lower methylation rate than cancers but were more commonly methylated than conventional adenomas (6/59,10% vs 0/40,0%). PRDM5 methylation was associated with advanced stages of presentation (p<0.05) and the methylator phenotype (p=0.03). PRDM5 protein expression was substantially down-regulated in both BRAF mutant and wild type cancer cohorts (92/97,95% and 39/44,89%). The polyp subgroups showed less silencing than the cancers, but similar rates were found between the serrated and conventional polyp cohorts (29/59, 49%; 23/40, 58% respectively). Of 295 colorectal cancers, PRDM5 was mutated in only 6 (2%) cancers which were all BRAF wild type.ConclusionsSerrated pathway colorectal cancers demonstrated early and progressive PRDM5 methylation with advancing disease. Interestingly, PRDM5 protein expression was substantially reduced in all polyp types and more so in cancers which also indicates early and increasing PRDM5 down-regulation with disease progression. Methylation may be contributing to gene silencing in a proportion of BRAF mutant cancers, but the large extent of absent protein expression indicates other mechanisms are also responsible for this. These data suggest that PRDM5 is a relevant tumour suppressor gene that is frequently targeted in colorectal tumourigenesis.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 24 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 24 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 21%
Researcher 4 17%
Student > Doctoral Student 2 8%
Student > Postgraduate 2 8%
Student > Bachelor 1 4%
Other 3 13%
Unknown 7 29%
Readers by discipline Count As %
Medicine and Dentistry 8 33%
Biochemistry, Genetics and Molecular Biology 3 13%
Agricultural and Biological Sciences 3 13%
Nursing and Health Professions 1 4%
Engineering 1 4%
Other 0 0%
Unknown 8 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 24 January 2015.
All research outputs
#20,249,662
of 22,778,347 outputs
Outputs from BMC Cancer
#6,489
of 8,288 outputs
Outputs of similar age
#295,426
of 351,530 outputs
Outputs of similar age from BMC Cancer
#108
of 131 outputs
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