Clinical Sequencing Defines the Genomic Landscape of Metastatic Colorectal Cancer
Open accessAbstract
Metastatic colorectal cancers (mCRCs) are clinically heterogeneous, but the genomic basis of this variability remains poorly understood. We performed prospective targeted sequencing of 1,134 CRCs. We identified splice alterations in intronic regions of APC and large in-frame deletions in CTNNB1, increasing oncogenic WNT pathway alterations to 96% of CRCs. Right-sided primary site in microsatellite stable mCRC was associated with shorter survival, older age at diagnosis, increased mutations, and enrichment of oncogenic alterations in KRAS, BRAF, PIK3CA, AKT1, RNF43, and SMAD4 compared with left-sided primaries. Left-sided tumors frequently had no identifiable genetic alteration in mitogenic signaling, but exhibited higher mitogenic ligand expression. Our results suggest different pathways to tumorigenesis in right- and left-sided microsatellite stable CRC that may underlie clinical differences.
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PIK3CA mutations are enriched and occur in approximately 25% of KRAS mutated CRC and PTEN is mutated or lost in an additional 7% of tumors.
“In contrast, PIK3CA mutations are enriched and occur in approximately 25% of KRAS mutated CRC and PTEN is mutated or lost in an additional 7% of tumors [21].”
From Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor (2022) · cites this paper as [21]
The Results sections on recurrently mutated genes and clinical actionability report PIK3CA mutations in 18% of MSS CRC and PTEN oncogenic mutations in 5% of MSS versus 35% of MSI-H metastatic CRC (page numbers unavailable). They do not establish PIK3CA enrichment or an approximately 25% frequency specifically in KRAS-mutated CRC, or PTEN mutation or loss in an additional 7% of tumors. (LLM, conf=0.84)
Experimental — accuracy not yet measuredKRAS G12D mutations are most commonly observed in pancreatic ductal adenocarcinoma (36%) and colorectal cancers (12%) and are also found in lung, endometrial and other cancers.
“KRAS G12D mutations are most commonly observed in pancreatic ductal adenocarcinoma (36%, [20]) and colorectal cancers (12%, [21]) and are also found in lung, endometrial and other cancers.”
From Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor (2022) · cites this paper as [21]
The Results section on recurrently mutated genes in MSS colorectal cancer reports KRAS mutations in 44% of tumors, but does not identify G12D or give a 12% frequency. Searches for “G12D” and the claimed colorectal frequency found no passage in our copy that verifies the cited part of the sentence. (LLM, conf=0.72)
Experimental — accuracy not yet measuredKRAS-mutant colorectal cancer frequently exhibits strong dependency on EGFR-mediated feedback signaling, particularly after KRAS G12C inhibition.
“KRAS-mutant CRC frequently exhibits strong dependency on EGFR-mediated feedback signaling, particularly after KRAS G12C inhibition [26,27,28,32,33,56].”
From Precision Targeting of KRAS-Mutant Cancers: Beyond G12C Toward G12D and Pan-RAS Therapeutic Strategies (2026) · cites this paper as [56]
The Results (Clinical actionability of genomic alterations; page unavailable) discuss EGFR signaling in a subset of class 3 BRAF-mutant tumors without concurrent RAS-pathway alterations, not EGFR-mediated feedback dependency in KRAS-mutant CRC. Searches for KRAS G12C, EGFR feedback, and inhibitor-induced reactivation found no passage addressing the claimed effect after KRAS G12C inhibition. (LLM, conf=0.76)
Experimental — accuracy not yet measuredKRASG12D mutation accounts for approximately 10-12% of CRC cases.
“In particular, KRASG12D mutation is a more prevalent event, accounting for 10–12% of CRC cases [7]”
From Feedback activation of EGFR/wild-type RAS signaling axis limits KRASG12D inhibitor efficacy in KRASG12D-mutated colorectal cancer (2023) · cites this paper as [7]
The Results section on significantly recurrently mutated genes in MSS CRC reports KRAS mutations in 44% of tumors, but does not give a frequency for the G12D variant. Searches for “G12D” and variant-specific prevalence found no passage in our copy supporting the claimed 10–12% of CRC cases. (LLM, conf=0.72)
Experimental — accuracy not yet measuredBRAF mutations occur in ~8.5% of CRC cases with BRAFV600E, a class I BRAF mutation and the predominant mutation comprising two-thirds of all BRAF mutations in CRC.
“BRAF mutations occur in ~8.5% of CRC cases [88] with BRAFV600E, a class I BRAF mutation and the predominant mutation comprising two-thirds of all BRAF mutations in CRC.”
From Recent Advances in Therapeutic Strategies to Improve Colorectal Cancer Treatment (2024) · cites this paper as [88]
KRAS mutations are enriched in microsatellite stable (MSS) tumors relative to microsatellite instability-high (MSI-H) tumors and rarely cooccur with actionable oncogenic drivers for which approved immunotherapy and targeted therapy options exist.
“As observed in large genomic studies (36), KRAS mutations are enriched in microsatellite stable (MSS) tumors relative to microsatellite instability-high (MSI-H) tumors and rarely cooccur with actionable oncogenic drivers for which approved immunotherapy and targeted therapy options exist.”
From Efficacy and Safety of Adagrasib plus Cetuximab in Patients with <i>KRAS</i> G12C-Mutated Metastatic Colorectal Cancer (2024) · cites this paper as [36]
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“In particular, KRAS mutation is a more prevalent event, accounting for 10–12% of CRC cases [7] and is significantly associated with an increased risk of metastasis and a worse prognosis [8].”
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Identification of four novel hub genes as monitoring biomarkers for colorectal cancer
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- Authors
- Yaeger, R., Chatila, W. K., Lipsyc, M. D., Hechtman, J. F., Cercek, A., Sanchez-Vega, F., Jayakumaran, G., Middha, S., Zehir, A., Donoghue, M. T. A., You, D., Viale, A., Kemeny, N., Segal, N. H., Stadler, Z. K., Varghese, A. M., Kundra, R., Gao, J., Syed, A., Hyman, D. M., Vakiani, E., Rosen, N., Taylor, B. S., Ladanyi, M., Berger, M. F., Solit, D. B., Shia, J., Saltz, L., & Schultz, N.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Schultz, Nikolaus
- ORCID
- Yaeger, Rona
- Chatila, Walid K.
- Hechtman, Jaclyn F.
- Cercek, Andrea
- Jayakumaran, Gowtham
- Middha, Sumit
- Zehir, Ahmet
- Donoghue, Mark T.A.
- You, Daoqi
- Viale, Agnes
- Kemeny, Nancy
- Segal, Neil H.
- Stadler, Zsofia K.
- Varghese, Anna M.
- Kundra, Ritika
- Gao, Jianjiong
- Syed, Aijazuddin
- Hyman, David M.
- Vakiani, Efsevia
- Rosen, Neal
- Taylor, Barry S.
- Ladanyi, Marc
- Berger, Michael F.
- Solit, David B.
- Shia, Jinru
- Saltz, Leonard
- Schultz, Nikolaus
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2018-01
- Volume
- 33
- Issue
- 1
- Pages
- 125-136.e3
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC5765991
- OpenAlex
- W2783494975
- Cited by
- 858
- References
- 36
- Citations by year
- 2026: 82 · 2025: 101 · 2024: 101 · 2023: 106 · 2022: 138 · 2021: 116 · 2020: 112 · 2019: 65 · 2018: 31
- FWCI
- 30.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Marie-Josée and Henry R. Kravis Center for Molecular Oncology
- NCI Cancer Center Core (P30-CA008748)
- Robertson Foundation
- Stand Up To Cancer Colorectal Cancer Dream Team Translational Research (SU2C-AACR-DT22-17)
- Amgen
- Loxo Oncology
- AstraZeneca
- Puma Biotechnology
- 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 › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- metastatic colorectal cancer, tumor genomic landscape, microsatellite stable tumors, right-sided primary tumor, KRAS mutation, BRAF mutation, PIK3CA, AKT1, RNF43, SMAD4, mitogenic signaling
- MeSH terms
- Adult, Aged, Colonic Neoplasms, Female, Humans, Male, Middle Aged, Mutation, Colorectal Neoplasms, Phosphatidylinositol 3-Kinases, Genomics, Proto-Oncogene Proteins B-raf, Microsatellite Instability, Carcinogenesis
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