The consensus molecular subtypes of colorectal cancer
Open accessAbstract
Colorectal cancer (CRC) is a frequently lethal disease with heterogeneous outcomes and drug responses. To resolve inconsistencies among the reported gene expression-based CRC classifications and facilitate clinical translation, we formed an international consortium dedicated to large-scale data sharing and analytics across expert groups. We show marked interconnectivity between six independent classification systems coalescing into four consensus molecular subtypes (CMSs) with distinguishing features: CMS1 (microsatellite instability immune, 14%), hypermutated, microsatellite unstable and strong immune activation; CMS2 (canonical, 37%), epithelial, marked WNT and MYC signaling activation; CMS3 (metabolic, 13%), epithelial and evident metabolic dysregulation; and CMS4 (mesenchymal, 23%), prominent transforming growth factor-β activation, stromal invasion and angiogenesis. Samples with mixed features (13%) possibly represent a transition phenotype or intratumoral heterogeneity. We consider the CMS groups the most robust classification system currently available for CRC-with clear biological interpretability-and the basis for future clinical stratification and subtype-based targeted interventions.
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CRC is characterized by extensive genomic heterogeneity and several defined subtypes based on mutational patterns, including partially overlapping subsets with distinct oncogenic alterations in KRAS, PIK3CA, BRAF and selected receptor tyrosine kinases.
“Finally, CRC is characterized by extensive genomic heterogeneity and several defined subtypes based on mutational patterns, including partially overlapping subsets with distinct oncogenic alterations in KRAS , PIK3CA, BRAF and selected receptor tyrosine kinases [29].”
From Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor (2022) · cites this paper as [29]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredCMS3 CRCs have the highest frequency (68%) of KRAS mutations, suggesting that this subtype may have a poorer response to KRAS inhibitors.
“Interestingly, CMS3 CRCs also have the highest frequency (68%) of KRAS mutations [84], suggesting that this subtype may have a poorer response to KRAS inhibitors.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [84]
The Results section on biological characterization says KRAS mutations are overrepresented in CMS3, supporting the comparative frequency claim. The passages in our copy do not give the stated 68% frequency; the suggestion about poorer response to KRAS inhibitors is not established by this source. (LLM, conf=0.85)
Experimental — accuracy not yet measuredCMS3 (metabolic, 13%) tumors are epithelial with evident metabolic deregulation and overrepresentation of KRAS mutations.
“CMS3 (metabolic, 13%) tumors are epithelial with evident metabolic deregulation and overrepresentation of KRAS mutations.”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [28]
The Results section (‘Biological characterization of the consensus molecular subtypes’; page unavailable) describes CMS3 as epithelial, reports pronounced enrichment of metabolism signatures, and says KRAS mutations are overrepresented. The eligible Results passages do not state that CMS3 accounts for 13% of tumors, so the percentage is not verified here. (LLM, conf=0.83)
Experimental — accuracy not yet measuredCMS2 (canonical, 37%) tumors are epithelial and have strong upregulation of Wnt and MYC signaling pathways and more frequent somatic copy number alterations (SCNA).
“CMS2 (canonical, 37%) tumors are epithelial and have strong upregulation of Wnt and MYC signaling pathways and more frequent somatic copy number alterations (SCNA).”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [28]
The Results section on biological characterization describes CMS2 as epithelial, with strong upregulation of WNT and MYC downstream targets. It also reports higher SCNA counts in CMS2–4 and more frequent oncogene copy-number gains and tumor-suppressor losses in CMS2 than in other subtypes. The 37% figure appears in the abstract, but the Results passages available here do not independently establish it. (LLM, conf=0.82)
Experimental — accuracy not yet measuredCMS4 (mesenchymal, 23%) tumors have prominent TGF-β activation, stromal infiltration and angiogenesis, and more frequent SCNA.
“CMS4 (mesenchymal, 23%) tumors have prominent TGF-β activation, stromal infiltration and angiogenesis, and more frequent SCNA.”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [28]
The Results (Biological characterization of the consensus molecular subtypes; page unavailable) describe CMS4-associated TGF-β signaling, stromal infiltration, angiogenesis and mesenchymal features. They also report higher SCNA counts for CMS2–4 than for CMS1, but do not establish that CMS4 has more SCNAs than every other subtype. The Results passages available do not state the 23% figure. (LLM, conf=0.84)
Experimental — accuracy not yet measured
CMS1 (MSI immune, 14%) tumors are hypermutated, microsatellite unstable, and have strong immune activation, with frequent occurrence of BRAF mutations.
“CMS1 (MSI immune, 14%) tumors are hypermutated, microsatellite unstable, and have strong immune activation, with frequent occurrence of BRAF mutations.”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [28]
The Results (Biological characterization of the consensus molecular subtypes; page unavailable) describe CMS1 as hypermutated, encompassing most MSI tumors, showing immune activation, and having frequent BRAF mutations. The Results text available in our copy does not state that CMS1 accounts for 14% of tumors, so that percentage is not supported by the admissible passages. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMany patient studies have documented that either CAF number or CAF function is linked to outcome.
“Many patient studies have documented how either CAF number or CAF function is linked to outcome140–142”
From A framework for advancing our understanding of cancer-associated fibroblasts (2020) · cites this paper as [141]
The Results (Biological characterization; no page provided) describe CMS4 colorectal tumors as having a gene-expression profile compatible with stromal infiltration. The Results (Clinical and prognostic associations; no page provided) link CMS4 to worse overall and relapse-free survival across patient cohorts. This supports a stromal-feature–outcome association, but the paper does not establish that CAF number or CAF function specifically is linked to outcome, or document many studies of those measures. (LLM, conf=0.82)
Experimental — accuracy not yet measuredBoth CMS1 (14%; defective DNA mismatched repair) and CMS3 (13%; metabolically deregulated) subtypes exhibit hyperactivated RTK and MAPK signaling.
“Both CMS1 (14%; defective DNA mismatched repair) and CMS3 (13%; metabolically deregulated) subtypes exhibit hyperactivated RTK and MAPK signaling [84, 85].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [84]
The Results section on biological characterization reports nearly universal genetic activation of RTK and MAPK pathways in CMS1 and CMS3. It also links CMS1 to defective DNA mismatch repair and CMS3 to pronounced metabolic signatures. The passages in our copy do not establish the stated subtype proportions of 14% and 13%. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAmong the four CRC subtypes, the CMS3 subtype has the highest frequency of KRAS mutations, along with PIK3CA mutations and PTEN deletions.
“Among the four CRC subtypes, the CMS3 subtype has the highest frequency of KRAS mutations, along with PIK3CA mutations and PTEN deletions [84].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [84]
The Results section (‘Biological characterization of the consensus molecular subtypes’; page unavailable) reports that KRAS mutations are overrepresented in CMS3. Our copy does not report that PIK3CA mutations or PTEN deletions are especially frequent in CMS3; the Online Methods mention measuring those alterations but give no subtype comparison for them. (LLM, conf=0.88)
Experimental — accuracy not yet measured87% of CRC samples analyzed could be assigned to one of four consensus molecular subtypes (CMS1-4), while the other 13% had mixed features.
“The authors determined that 87% of CRC samples analyzed could be assigned to one of four consensus molecular subtypes with distinguishing features (CMS1–4), while the other 13% had mixed features [28].”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [28]
An international consortium developed a gene expression-based classification system based on six different published CRC subtyping platforms to assign consensus molecular subtypes (CMS).
“To resolve inconsistencies among CRC subtype classifications, an international consortium formed across expert groups and developed a gene expression-based classification system based on six different published CRC subtyping platforms to systematically assign CRC consensus molecular subtypes (CMS) [28].”
From Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer (2025) · cites this paper as [28]
Several molecular classifiers in CRC have been built using global gene expression analysis, including CCS, Colorectal Cancer Assigner, colon cancer molecular subtype systems, and CRCSC.
“Several molecular classifiers in CRC have been built using global gene expression analysis, including colon cancer subtypes (CCS)13, the Colorectal Cancer Assigner14, colon cancer molecular subtype systems, and colorectal cancer subtyping consortium (CRCSC)15.”
From A tumor microenvironment-specific gene expression signature predicts chemotherapy resistance in colorectal cancer patients (2021) · cites this paper as [15]
A landmark 2015 study developed a bulk transcriptomic classification of primary colorectal cancer, the Consensus Molecular Subtypes (CMS), illustrating the profound impact of the tumour microenvironment on human colorectal cancer.
“The profound impact of the TME on human CRC was illustrated by a landmark study from 2015 that developed a bulk transcriptomic classification of primary CRC, the so-called ‘Consensus Molecular Subtypes’ (CMS).121”
From Current and emerging concepts for systemic treatment of metastatic colorectal cancer (2025) · cites this paper as [121]
CMS1 and CMS4 subtypes are characterised by pronounced activation of the tumour microenvironment.
“Two of these subtypes, CMS1 and CMS4, are characterised by a pronounced activation of the TME.”
From Current and emerging concepts for systemic treatment of metastatic colorectal cancer (2025) · cites this paper as [121]
The consensus molecular subtype CMS4 of colorectal cancer is associated with poor prognosis, including worse overall survival and relapse-free survival.
“the challenging consensus molecular subtype (CMS) CMS4 associated with poor prognosis”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
No genomic feature is specific to CMS4 tumors.
“no genomic feature is specific to CMS4 tumors (1).”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
CMS4 tumors exhibit a mesenchymal morphology.
“CMS4 tumors exhibit a mesenchymal morphology”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
CMS4 colorectal cancer is consistently associated with a dismal outcome, including at early stage.
“CMS4 colorectal cancer is consistently associated with a dismal outcome (1, 26), including at early stage (27).”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
The TGFβ pathway is enriched in CMS4 colorectal cancer.
“One of the most scrutinized pathways originally found to be enriched in CMS4 colorectal cancer is the TGFβ pathway (1).”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
YAP and TAZ expression is significantly increased in CMS4 tumors.
“YAP and TAZ, the main effectors of the Hippo pathway, whose expression was shown to be significantly increased in CMS4 tumors in reverse phase protein arrays (1).”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
Genetic alterations in SMAD4 and TGFBR2 are not overrepresented in the CMS4 subgroup.
“such genetic alterations are not overrepresented in the CMS4 subgroup (1)”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
CMS4 accounts for 20%-25% of colorectal cancer cases.
“While the CMS4 group globally accounts for 20%–25% of colorectal cancer cases (1)”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [1]
CMS1 marks highly microsatellite-instable (MSI-H) and hypermutated TSCs.
“CMS1 marks highly microsatelliteinstable (MSI-H) and hypermutated TSCs (Guinney et al., 2015).”
From Degradation of CCNK/CDK12 is a druggable vulnerability of colorectal cancer (2021) · cites this paper as Guinney et al., 2015
CMS4 is associated with particularly poor prognosis.
“CMS4 is associated with particularly poor prognosis (Guinney et al., 2015)”
From Degradation of CCNK/CDK12 is a druggable vulnerability of colorectal cancer (2021) · cites this paper as Guinney et al., 2015
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A Subset of Colorectal Cancers with Cross-Sensitivity to Olaparib and Oxaliplatin
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HLA class I loss in colorectal cancer: implications for immune escape and immunotherapy
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Self-citationAdipose stem cell niche reprograms the colorectal cancer stem cell metastatic machinery
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“The International CRC Subtyping Consortium has suggested that CRC can be divided into four subtypes with distinguished features: CMS1, CMS2, CMS3, and CMS4 [15].”
BackgroundGastric Cancer Genomics: Advances and Future Directions
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“…inconsistencies among CRC subtype classifications, an international consortium formed across expert groups and developed a gene expression-based classification system based on six different published CRC subtyping platforms to systematically assign CRC consensus molecular subtypes (CMS) [28].”
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Investigation of colorectal cancer in accordance with consensus molecular subtype classification
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- Authors
- Guinney, J., Dienstmann, R., Wang, X., de Reyniès, A., Schlicker, A., Soneson, C., Marisa, L., Roepman, P., Nyamundanda, G., Angelino, P., Bot, B. M., Morris, J. S., Simon, I. M., Gerster, S., Fessler, E., De Sousa E Melo, F., Missiaglia, E., Ramay, H., Barras, D., Homicsko, K., Maru, D., Manyam, G. C., Broom, B., Boige, V., Perez-Villamil, B., Laderas, T., Salazar, R., Gray, J. W., Hanahan, D., Tabernero, J., Bernards, R., Friend, S. H., Laurent-Puig, P., Medema, J. P., Sadanandam, A., Wessels, L., Delorenzi, M., Kopetz, S., Vermeulen, L., & Tejpar, S.
- Affiliations
- Sage Bionetworks (US)
- Universitat Autònoma de Barcelona (ES)
- City University of Hong Kong (HK)
- The Netherlands Cancer Institute (NL)
- SIB Swiss Institute of Bioinformatics (CH)
- Agendia (Netherlands) (NL)
- Institute of Cancer Research (GB)
- The University of Texas MD Anderson Cancer Center (US)
- Amsterdam UMC Location University of Amsterdam (NL)
- Oregon Health & Science University (US)
- École Polytechnique Fédérale de Lausanne (CH)
- Universitair Ziekenhuis Leuven (BE)
- Corresponding author
- Guinney, Justin
- Vermeulen, Louis
- Tejpar, Sabine
- ORCID
- Guinney, Justin
- Dienstmann, Rodrigo
- Wang, Xin
- Schlicker, Andreas
- Soneson, Charlotte
- Roepman, Paul
- Angelino, Paolo
- Bot, Brian M
- Morris, Jeffrey S
- Gerster, Sarah
- Fessler, Evelyn
- Missiaglia, Edoardo
- Ramay, Hena
- Barras, David
- Manyam, Ganiraju C
- Broom, Bradley
- Laderas, Ted
- Gray, Joe W
- Hanahan, Douglas
- Tabernero, Josep
- Bernards, Rene
- Friend, Stephen H
- Medema, Jan Paul
- Sadanandam, Anguraj
- Wessels, Lodewyk
- Delorenzi, Mauro
- Kopetz, Scott
- Vermeulen, Louis
- Tejpar, Sabine
- Venue
- Nature Medicine
- Published
- 2015-10-12
- Volume
- 21
- Issue
- 11
- Pages
- 1350-1356
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4636487
- OpenAlex
- W1934094702
- Cited by
- 5,170
- References
- 75
- Citations by year
- 2026: 475 · 2025: 514 · 2024: 507 · 2023: 577 · 2022: 620 · 2021: 647 · 2020: 542 · 2019: 432 · 2018: 380 · 2017: 302 · 2016: 153 · 2015: 9 · 2014: 2 · 2013: 1
- FWCI
- 122.87
- Type
- journal article
- Language
- en
- Open access
- green
- pure.amsterdamumc.nl
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, other-oa)
- PubMed Central (acceptedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (acceptedVersion)
- RECERCAT (Consorci de Serveis Universitaris de Catalunya) (acceptedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- Dipòsit Digital de Documents de la UAB (Universitat Autònoma de Barcelona) (submittedVersion, public-domain)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- IRIS (submittedVersion)
- Lirias (KU Leuven) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, public-domain)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- SERVAL (Université de Lausanne) (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion)
- Funders
- Fonds Wetenschappelijk Onderzoek
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek
- KU Leuven (GOA/12/2106)
- Maag Lever Darm Stichting (MLDS-CDG 14-03)
- Vlaamse regering
- National Institutes of Health (UL1TR000371)
- National Cancer Institute (R01CA178744, R01CA184843, R01CA172670, U54CA149237, R01CA187238, P30CA016672)
- National Center for Advancing Translational Sciences
- H2020 European Research Council (638193)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gene expression and cancer classification
- Keywords
- colorectal cancer, consensus molecular subtypes, molecular classification, gene expression signatures, microsatellite instability, hypermutated tumors, Wnt signaling, MYC signaling, metabolic dysfunction, TGF-beta, stromal invasion, angiogenesis, intratumoral heterogeneity, immune activation, patient stratification
- MeSH terms
- Carcinoma, Humans, Mutation, Neovascularization, Pathologic, Phenotype, Proto-Oncogene Proteins, Colorectal Neoplasms, Gene Expression Regulation, Neoplastic, Transforming Growth Factor beta, Genes, myc, Proto-Oncogene Proteins p21(ras), ras Proteins, CpG Islands, DNA Methylation, Gene Expression Profiling, Consensus, Information Dissemination, Proto-Oncogene Proteins B-raf, Microsatellite Instability, DNA Copy Number Variations, Wnt Signaling Pathway
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