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The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

Molecular pathological classification of colorectal cancer

Open access
Müller, Mike F., Ibrahim, Ashraf E. K., Arends, Mark J.·2016·Virchows Archiv

Abstract

Colorectal cancer (CRC) shows variable underlying molecular changes with two major mechanisms of genetic instability: chromosomal instability and microsatellite instability. This review aims to delineate the different pathways of colorectal carcinogenesis and provide an overview of the most recent advances in molecular pathological classification systems for colorectal cancer. Two molecular pathological classification systems for CRC have recently been proposed. Integrated molecular analysis by The Cancer Genome Atlas project is based on a wide-ranging genomic and transcriptomic characterisation study of CRC using array-based and sequencing technologies. This approach classified CRC into two major groups consistent with previous classification systems: (1) ∼16 % hypermutated cancers with either microsatellite instability (MSI) due to defective mismatch repair (∼13 %) or ultramutated cancers with DNA polymerase epsilon proofreading mutations (∼3 %); and (2) ∼84 % non-hypermutated, microsatellite stable (MSS) cancers with a high frequency of DNA somatic copy number alterations, which showed common mutations in APC, TP53, KRAS, SMAD4, and PIK3CA. The recent Consensus Molecular Subtypes (CMS) Consortium analysing CRC expression profiling data from multiple studies described four CMS groups: almost all hypermutated MSI cancers fell into the first category CMS1 (MSI-immune, 14 %) with the remaining MSS cancers subcategorised into three groups of CMS2 (canonical, 37 %), CMS3 (metabolic, 13 %) and CMS4 (mesenchymal, 23 %), with a residual unclassified group (mixed features, 13 %). Although further research is required to validate these two systems, they may be useful for clinical trial designs and future post-surgical adjuvant treatment decisions, particularly for tumours with aggressive features or predicted responsiveness to immune checkpoint blockade.

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Research works printed but not linked: 3

  1. Toft NJ, Curtis LJ, Sansom OJ, Leitch AL, Wyllie AH, te Riele H, Arends MJ, Clarke AR (2002) Heterozygosity for p53 promotes microsatellite instability and tumorigenesis on a Msh2 deficient background. Oncogene 21(41):6299–6306 · doi:10.1038/sj.onc.1205727
  2. Berg M, Hagland HR, Søreide K (2014) Comparison of CpG island methylator phenotype (CIMP) frequency in colon cancer using different probe-and gene-specific scoring alternatives on recommended multi-gene panels. PLoS One 9(1), e86657
  3. Chetty R, Bateman AC, Torlakovic E, Wang LM, Gill P, Al-Badri A, Arends M, Biddlestone L, Burroughs S, Carey F (2014) A pathologist’s survey on the reporting of sessile serrated adenomas/polyps. J Clin Pathol 67(5):426–430 · doi:10.1136/jclinpath-2013-202128

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Metadata

Authors
Müller, M. F., Ibrahim, A. E. K., & Arends, M. J.
Venue
Virchows Archiv
Published
2016-06-20
Volume
469
Issue
2
Pages
125-134
ISSN
  • 0945-6317 (ISSN-L)
  • 1432-2307
OpenAlex
W2467345490
Cited by
432
References
54
FWCI
25.80
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Molecular pathological classification of colorectal cancer. https://app.cochat.ai/papers/10.1007/s00428-016-1956-3
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Müller, M. F., Ibrahim, A. E. K., & Arends, M. J. (2016). Molecular pathological classification of colorectal cancer. Virchows Archiv. https://doi.org/10.1007/s00428-016-1956-3

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