English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Background  Tumor cell lines are commonly used as experimental tools in cancer research, but their relevance for the  in vivo  situation is debated. In a series of 11 microsatellite stable (MSS) and 9 microsatellite unstable (MSI) colon cancer cell lines and primary colon carcinomas (25 MSS and 28 MSI) with known ploidy stem line and  APC ,  KRAS , and  TP53  mutation status, we analyzed the promoter methylation of the following genes:  hMLH1 ,  MGMT ,  p16   INK4a   ( CDKN2A  α-transcript),  p14   ARF   ( CDKN2A  β-transcript),  APC , and  E-cadherin (CDH1) . We compared the DNA methylation profiles of the cell lines with those of the primary tumors. Finally, we examined if the epigenetic changes were associated with known genetic markers and/or clinicopathological variables.    Results  The cell lines and primary tumors generally showed similar overall distribution and frequencies of gene methylation. Among the cell lines, 15%, 50%, 75%, 65%, 20% and 15% showed promoter methylation for  hMLH1 ,  MGMT ,  p16   INK4a  ,  p14   ARF  ,  APC , and  E-cadherin , respectively, whereas 21%, 40%, 32%, 38%, 32%, and 40% of the primary tumors were methylated for the same genes.  hMLH1  and  p14   ARF   were significantly more often methylated in MSI than in MSS primary tumors, whereas the remaining four genes showed similar methylation frequencies in the two groups. Methylation of  p14   ARF  , which indirectly inactivates TP53, was seen more frequently in tumors with normal  TP53  than in mutated samples, but the difference was not statistically significant. Methylation of  p14   ARF   and  p16   INK4a   was often present in the same primary tumors, but association to diploidy, MSI, right-sided location and female gender was only significant for  p14   ARF  .  E-cadherin  was methylated in 14/34 tumors with altered  APC  further stimulating WNT signaling.    Conclusions  The present study shows that colon cancer cell lines are in general relevant  in vitro  models, comparable with the  in vivo  situation, as the cell lines display many of the same molecular alterations as do the primary carcinomas. The combined pattern of epigenetic and genetic aberrations in the primary carcinomas reveals associations between them as well as to clinicopathological variables, and may aid in the future molecular assisted classification of clinically distinct stages.

A CpG island hypermethylation profile of primary colorectal carcinomas and colon cancer cell lines.