Colorectal premalignancy is associated with consensus molecular subtypes 1 and 2
Open accessAbstract
Background: Gene expression-based profiling of colorectal cancer (CRC) can be used to identify four molecularly homogeneous consensus molecular subtype (CMS) groups with unique biologic features. However, its applicability to colorectal premalignant lesions remains unknown. Patients and methods: We assembled the largest transcriptomic premalignancy dataset by integrating different public and proprietary cohorts of adenomatous and serrated polyps from sporadic (N = 311) and hereditary (N = 78) patient populations and carried out a comprehensive analysis of carcinogenesis pathways using the CMS random forest (RF) classifier. Results: Overall, transcriptomic subtyping of sporadic and hereditary polyps revealed CMS2 and CMS1 subgroups as the predominant molecular subtypes in premalignancy. Pathway enrichment analysis showed that adenomatous polyps from sporadic or hereditary cases (including Lynch syndrome) displayed a CMS2-like phenotype with WNT and MYC activation, whereas hyperplastic and serrated polyps with CMS1-like phenotype harbored prominent immune activation. Rare adenomas with CMS4-like phenotype showed significant enrichment for stromal signatures along with transforming growth factor-β activation. There was a strong association of CMS1-like polyps with serrated pathology, right-sided anatomic location and BRAF mutations. Conclusions: Based on our observations made in premalignancy, we propose a model of pathway activation associated with CMS classification in colorectal carcinogenesis. Specifically, while adenomatous polyps are largely CMS2, most hyperplastic and serrated polyps are CMS1 and may transition into other CMS groups during evolution into carcinomas. Our findings shed light on the transcriptional landscape of premalignant colonic polyps and may help guide the development of future biomarkers or preventive treatments for CRC.
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The CMS4 subtype is barely if not detected in adenomas and arises at the carcinoma stage, notably after transition from an indolent CMS3 subtype.
“A consensus that emerged from several studies is that the CMS4 subtype is barely if not detected in adenomas and arises at the carcinoma stage (17, 18), notably after transition from an indolent CMS3 subtype.”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [18]
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- Authors
- Chang, K., Willis, J. A., Reumers, J., Taggart, M. W., San Lucas, F. A., Thirumurthi, S., Kanth, P., Delker, D. A., Hagedorn, C. H., Lynch, P. M., Ellis, L. M., Hawk, E. T., Scheet, P. A., Kopetz, S., Arts, J., Guinney, J., Dienstmann, R., & Vilar, E.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Janssen (Belgium) (BE)
- University of Utah (US)
- Central Arkansas Veterans Healthcare System (US)
- Sage Bionetworks (US)
- Corresponding author
- Dienstmann, R.
- Vilar, E.
- ORCID
- Venue
- Annals of Oncology
- Publisher
- Elsevier BV
- Published
- 2018-10
- Volume
- 29
- Issue
- 10
- Pages
- 2061-2067
- ISSN
- 0923-7534 (ISSN-L)
- PMC
- PMC6225810
- OpenAlex
- W2888347846
- Cited by
- 51
- References
- 31
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 8 · 2023: 5 · 2022: 7 · 2021: 14 · 2020: 6 · 2019: 3 · 2018: 1
- FWCI
- 4.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Annals of Oncology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- US National Institutes of Health (R21 CA208461, National Cancer Institute)
- National Cancer Institute (P30 CA016672)
- The University of Texas MD Anderson Cancer Center Colorectal Cancer Moonshot Program
- Feinberg Family
- Cancer Prevention Educational Award (R25T CA057730)
- Research Training in Academic Medical Oncology T32 Award (CA009666-23)
- U.S. National Institutes of Health
- University of Texas Anderson Cancer Center
- Merck KGaA
- Grant for Oncology Innovation 2015
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Oncology › Colorectal Cancer Screening and Detection
- Keywords
- consensus molecular subtypes, colorectal cancer, colorectal adenoma, serrated polyps, hyperplastic polyps, Lynch syndrome, hereditary colorectal cancer, colorectal carcinogenesis, Wnt signaling, MYC activation, immune activation, BRAF mutation, TGF-beta, right-sided colon cancer
- MeSH terms
- Adenoma, Colonic Polyps, Female, Follow-Up Studies, Humans, Male, Middle Aged, Mutation, Neoplasm Staging, Phenotype, Precancerous Conditions, Predictive Value of Tests, Prognosis, Biomarkers, Tumor, Colorectal Neoplasms, Gene Expression Profiling, High-Throughput Nucleotide Sequencing, Transcriptome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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