Common gene mutations in 103 authenticated colorectal cancer cell lines

Common gene mutations in 103 authenticated colorectal cancer cell lines | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Article Common gene mutations in 103 authenticated colorectal cancer cell lines Christian Kranjec, Ina Eilertsen, Luis Nunes, Seyed Moosavi, Kaja Berg, and 7 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6907318/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 27 Jan, 2026 Read the published version in Oncogenesis → Version 1 posted 9 You are reading this latest preprint version Abstract Colorectal cancer (CRC) cell lines represent the main molecular subtypes of tumors and are valuable models for preclinical investigations. However, cell lines can diverge over time and careful selection of models based on their molecular features is key. We have authenticated 103 commonly used CRC cell lines and present the mutation profiles of 20 CRC-relevant genes sequenced to an average depth of 575 times coverage. The cell lines reflected the distinct mutation patterns of hypermutation phenotypes associated with microsatellite instability and pathogenic POLE mutations. Hypermutated cell lines appeared to have a stronger mutational divergence and more frequent subclonal mutations, while mutations not associated with hypermutation were more frequently homozygous or hemizygous, predicted to be pathogenic, and subject to stronger selection pressure. Loss of heterozygosity at mutated loci was primarily observed in tumor suppressor genes. Genetic interactions based on co-occurring mutations identified cell lines representative of particularly aggressive subtypes of CRC, including concurrent BRAF p.V600 and truncating APC mutations, as well as APC / TP53 / RAS triple mutations with double hits of APC. This study provides a resource to guide the selection of cell lines for functional studies of CRC, and detailed mutation data including predictions of pathogenicity, variant allele frequencies and illustrations of the mutation distribution along the length of encoded proteins are included. Biological sciences/Cancer/Cancer models Biological sciences/Genetics/Mutation/Genomic instability Biological sciences/Genetics/Cancer genetics Biological sciences/Genetics/Mutation/Gene amplification Figures Figure 1 Figure 2 Figure 3 Full Text Additional Declarations There is NO conflict of interest to disclose. Table 1 is available in the Supplementary Files section. Supplementary Files Table1.xlsx Table 1 SupplementaryTables.xlsx Supplementary Tables SupplementaryFigures.pdf Supplementary Figures Cite Share Download PDF Status: Published Journal Publication published 27 Jan, 2026 Read the published version in Oncogenesis → Version 1 posted Editorial decision: revise 25 Sep, 2025 Review # 2 received at journal 24 Sep, 2025 Reviewer # 2 agreed at journal 11 Sep, 2025 Review # 1 received at journal 14 Jul, 2025 Reviewer # 1 agreed at journal 30 Jun, 2025 Reviewers invited by journal 26 Jun, 2025 Submission checks completed at journal 17 Jun, 2025 Editor assigned by journal 16 Jun, 2025 First submitted to journal 16 Jun, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6907318","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Article","associatedPublications":[],"authors":[{"id":476911035,"identity":"d5263c18-f562-4a44-862a-48774c3dca54","order_by":0,"name":"Christian Kranjec","email":"data:image/png;base64,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","orcid":"https://orcid.org/0000-0001-9713-7406","institution":"Oslo University Hospital","correspondingAuthor":true,"prefix":"","firstName":"Christian","middleName":"","lastName":"Kranjec","suffix":""},{"id":476911036,"identity":"70c9f916-139a-46c8-8d06-915dd903d4f6","order_by":1,"name":"Ina Eilertsen","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Ina","middleName":"","lastName":"Eilertsen","suffix":""},{"id":476911037,"identity":"1f3cc092-6247-428f-9923-da05076be824","order_by":2,"name":"Luis Nunes","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Luis","middleName":"","lastName":"Nunes","suffix":""},{"id":476911038,"identity":"0d7f215d-920a-4eb1-9f02-76d5ace9f81d","order_by":3,"name":"Seyed Moosavi","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Seyed","middleName":"","lastName":"Moosavi","suffix":""},{"id":476911039,"identity":"8e7bbd37-5c33-4611-98bf-1b26b0fe7ed2","order_by":4,"name":"Kaja Berg","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Kaja","middleName":"","lastName":"Berg","suffix":""},{"id":476911040,"identity":"ecc14589-fbab-4eec-8edb-f6376fc2bd6c","order_by":5,"name":"Mette Eknæs","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Mette","middleName":"","lastName":"Eknæs","suffix":""},{"id":476911041,"identity":"6b2b70e5-ee25-4663-909e-e55cda9e1701","order_by":6,"name":"Merete Hektoen","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Merete","middleName":"","lastName":"Hektoen","suffix":""},{"id":476911042,"identity":"ec4f2967-b6f9-4c79-b249-263ad565b4bf","order_by":7,"name":"Barbara Niederdorfer","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Barbara","middleName":"","lastName":"Niederdorfer","suffix":""},{"id":476911043,"identity":"0f348e38-e317-45ae-9e32-cc189d88a338","order_by":8,"name":"Guro Lind","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Guro","middleName":"","lastName":"Lind","suffix":""},{"id":476911044,"identity":"5cd56244-23df-4c76-9797-0a3c9c737687","order_by":9,"name":"Rolf Skotheim","email":"","orcid":"https://orcid.org/0000-0002-5609-4048","institution":"Oslo university hospital-Radiumhospitalet","correspondingAuthor":false,"prefix":"","firstName":"Rolf","middleName":"","lastName":"Skotheim","suffix":""},{"id":476911045,"identity":"2e8ec6a6-6bb1-4c23-9e4a-2c550339ae42","order_by":10,"name":"Anita Sveen","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Anita","middleName":"","lastName":"Sveen","suffix":""},{"id":476911046,"identity":"ddb7608f-e5c4-4dfa-9dad-b6e83b3150b1","order_by":11,"name":"Ragnhild Lothe","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Ragnhild","middleName":"","lastName":"Lothe","suffix":""}],"badges":[],"createdAt":"2025-06-16 16:11:18","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6907318/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6907318/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1038/s41389-026-00599-0","type":"published","date":"2026-01-27T05:00:00+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":85713164,"identity":"b8d00845-1528-4d8a-8e55-0574cd6d7b31","added_by":"auto","created_at":"2025-07-01 03:14:32","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":123985,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eLandscape of SNVs and indels of CRC cell lines. A \u003c/strong\u003eOncoplot of non-synonymous SNVs and indels of 20 CRC-critical genes in 103 CRC cell lines (details in Supplementary Table 8). Genes (rows) and cell lines (columns) are ordered based on mutation frequency and MSI/\u003cem\u003ePOLE \u003c/em\u003estatus of the cell lines. Mutations are color-coded according to variant class. Multi-hit mutations (orange) indicate multiple mutations of the same gene in the same cell line. The bar plots on the right side and top represent the number of mutated samples per gene and mutated genes per sample, respectively. The sample annotation bars indicate the MSI/\u003cem\u003ePOLE \u003c/em\u003estatus and primary or metastatic tumor origin, and the gene class annotation indicates tumor-suppressors and oncogenes. Cell lines derived from the same patient (DLD-1:HCT 15, Isreco-1:Isreco-3, HT-29:WiDr, SW480:SW620) are marked by arrowheads of the same color. Cell lines derived from neuroendocrine tumors (COLO 329, HROC57, NCI-H716) are marked with black arrowheads. \u003cstrong\u003eB \u003c/strong\u003eSame plot as in panel \u003cstrong\u003eA\u003c/strong\u003e, including predicted pathogenic mutations only. MSI/MSS: microsatellite instable/stable; MSS-POLE: \u003cem\u003ePOLE \u003c/em\u003emutated samples. \u003cstrong\u003eC \u003c/strong\u003eLollipop plot of truncating multi-hit mutations of \u003cem\u003eAPC \u003c/em\u003eacross 42 cell lines (Supplementary Table 11). Mutations (lollipop circles) are colored according to whether they occur upstream (aa 1-1262 - black), within (MCR, aa 1263-1587 - red) or downstream (aa 1588-2843 - yellow) the MCR. Protein domains are color-coded and described according to Pfam nomenclature (Supplementary Table 10). Black and red asterisks mark the position of 15- and 20-aminoacids β-catenin binding sites, respectively.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1/1b280f1266d26738acef0a0b.png"},{"id":85713166,"identity":"ecb1acaf-4d33-4656-9077-629dc1d65747","added_by":"auto","created_at":"2025-07-01 03:14:32","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":113669,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eSomatic interactions of pathogenic mutations in gene pairs.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eHeatmap of significance levels for mutation interactions between gene pairs among \u003cstrong\u003eA \u003c/strong\u003enon-hypermutated (MSS; \u003cem\u003en \u003c/em\u003e= 76) and \u003cstrong\u003eB \u003c/strong\u003ehypermutated (MSI+MSS-POLE; \u003cem\u003en \u003c/em\u003e= 20) CRC cell lines. Co-occurrence versus mutually exclusivity is color-coded. p-values are from Fisher´s exact tests and plotted on log10-scale. Significant events are marked with asterisks (p \u0026lt; 0.01) and dots (p \u0026lt; 0.05) as indicated. Numbers next to the gene names correspond to the number of mutated samples. The \u003cem\u003eKRAS \u003c/em\u003eand \u003cem\u003eNRAS \u003c/em\u003egenes were grouped as \u003cem\u003eRAS \u003c/em\u003eand mutations targeting the \u003cem\u003eBRAF \u003c/em\u003eV600 hotspot (p.V600E/K) were grouped separately from other \u003cem\u003eBRAF \u003c/em\u003emutations. Cell lines derived from non-\u003c/p\u003e\n\u003cp\u003eunique patients (DLD-1, Isreco-3, SW620 and WiDr) and neuroendocrine cell lines (COLO 320, HROC57, NCI-H716) were excluded from the analysis. MSI/MSS: microsatellite instable/stable; MSS-POLE: \u003cem\u003ePOLE \u003c/em\u003emutated samples.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1/171d14d1fe59636d67f9a98f.png"},{"id":85713167,"identity":"143a04d1-6f67-46c7-9473-d27196252357","added_by":"auto","created_at":"2025-07-01 03:14:32","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":115606,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eGene amplifications and concurrent CNVs and SNVs/indels\u003c/strong\u003e\u003cem\u003e\u003cstrong\u003e. \u003c/strong\u003e\u003c/em\u003e\u003cstrong\u003eA \u003c/strong\u003eBarplot of amplifications and gains of \u003cem\u003eMYC\u003c/em\u003e, \u003cem\u003eCCND2\u003c/em\u003e, \u003cem\u003eMDM2\u003c/em\u003e, \u003cem\u003eEGFR \u003c/em\u003eand \u003cem\u003eERBB2. \u003c/em\u003eLow- and high-level amplifications are highlighted in red and magenta, respectively. Cell lines derived from the same patient (HT-29:WiDr, SW480:SW620) are marked by arrowheads of the same color. Cell lines derived from neuroendocrine tumors (COLO 329, HROC57, NCI-H716) are marked with black arrowheads. \u003cstrong\u003eB \u003c/strong\u003eBarplot of the proportion of different mutation types (CNVs and/or SNVs/indels) in each gene among non-hypermutated (MSS; left) and hypermutated (MSI+MSS-POLE; right) cell lines. MSI/MSS: microsatellite instable/stable; MSS-POLE: \u003cem\u003ePOLE \u003c/em\u003emutated samples; CN gain: copy number gain; CN loss: copy number loss; SNV: single nucleotide variant; Indel: insertion or deletion.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1/ed90d61b6c0ed3b0003b8cbf.png"},{"id":102575589,"identity":"2c1fb975-e14c-462e-8443-a61eaad094d6","added_by":"auto","created_at":"2026-02-13 08:11:50","extension":"pdf","order_by":1,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":821560,"visible":true,"origin":"","legend":"Article File","description":"","filename":"MainText.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1_covered_7d766367-61bd-48a3-8b1f-7e4121912d6b.pdf"},{"id":85713489,"identity":"1a7d1e4f-e4d7-4a2a-bec9-70152eac921b","added_by":"auto","created_at":"2025-07-01 03:22:32","extension":"xlsx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":10738,"visible":true,"origin":"","legend":"Table 1","description":"","filename":"Table1.xlsx","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1/913133ff01aefaad3287c0e6.xlsx"},{"id":85713168,"identity":"9c12f00e-4d9b-475c-b853-b3dd84d2123e","added_by":"auto","created_at":"2025-07-01 03:14:32","extension":"xlsx","order_by":2,"title":"","display":"","copyAsset":false,"role":"supplement","size":995934,"visible":true,"origin":"","legend":"Supplementary Tables","description":"","filename":"SupplementaryTables.xlsx","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1/c670d694dd92a922fd87f249.xlsx"},{"id":85713175,"identity":"8a7123e2-d24b-451b-a229-f256d13f5134","added_by":"auto","created_at":"2025-07-01 03:14:33","extension":"pdf","order_by":3,"title":"","display":"","copyAsset":false,"role":"supplement","size":24356292,"visible":true,"origin":"","legend":"Supplementary Figures","description":"","filename":"SupplementaryFigures.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6907318/v1/5edf7129c96e95c8b0c08354.pdf"}],"financialInterests":"\u003cp\u003eThere is \u003cstrong\u003eNO\u003c/strong\u003e conflict of interest to disclose.\u003c/p\u003e\n\u003cp\u003eTable 1 is available in the Supplementary Files section.\u003c/p\u003e","formattedTitle":"Common gene mutations in 103 authenticated colorectal cancer cell lines","fulltext":[],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":false,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":true,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":true,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"oncogenesis","isNatureJournal":false,"hasQc":false,"allowDirectSubmit":false,"externalIdentity":"oncsis","sideBox":"Learn more about [Oncogenesis](http://www.nature.com/oncsis/)","snPcode":"41389","submissionUrl":"https://mts-oncsis.nature.com/cgi-bin/main.plex","title":"Oncogenesis","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"ejp","reportingPortfolio":"Nature AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"","lastPublishedDoi":"10.21203/rs.3.rs-6907318/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6907318/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"Colorectal cancer (CRC) cell lines represent the main molecular subtypes of tumors and are valuable models for preclinical investigations. However, cell lines can diverge over time and careful selection of models based on their molecular features is key. We have authenticated 103 commonly used CRC cell lines and present the mutation profiles of 20 CRC-relevant genes sequenced to an average depth of 575 times coverage. The cell lines reflected the distinct mutation patterns of hypermutation phenotypes associated with microsatellite instability and pathogenic \u003ci\u003ePOLE\u003c/i\u003e mutations. Hypermutated cell lines appeared to have a stronger mutational divergence and more frequent subclonal mutations, while mutations not associated with hypermutation were more frequently homozygous or hemizygous, predicted to be pathogenic, and subject to stronger selection pressure. Loss of heterozygosity at mutated loci was primarily observed in tumor suppressor genes. Genetic interactions based on co-occurring mutations identified cell lines representative of particularly aggressive subtypes of CRC, including concurrent \u003ci\u003eBRAF\u003c/i\u003e p.V600 and truncating \u003ci\u003eAPC\u003c/i\u003e mutations, as well as \u003ci\u003eAPC\u003c/i\u003e/\u003ci\u003eTP53\u003c/i\u003e/\u003ci\u003eRAS\u003c/i\u003e triple mutations with double hits of APC. This study provides a resource to guide the selection of cell lines for functional studies of CRC, and detailed mutation data including predictions of pathogenicity, variant allele frequencies and illustrations of the mutation distribution along the length of encoded proteins are included.","manuscriptTitle":"Common gene mutations in 103 authenticated colorectal cancer cell lines","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-07-01 03:14:27","doi":"10.21203/rs.3.rs-6907318/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"revise","date":"2025-09-25T14:06:08+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"This content is not available.","date":"2025-09-24T12:59:17+00:00","index":2,"fulltext":"This content is not available."},{"type":"reviewerAgreed","content":"This content is not available.","date":"2025-09-11T07:05:19+00:00","index":2,"fulltext":"This content is not available."},{"type":"editorInvitedReview","content":"This content is not available.","date":"2025-07-14T14:16:40+00:00","index":1,"fulltext":"This content is not available."},{"type":"reviewerAgreed","content":"This content is not available.","date":"2025-06-30T08:38:13+00:00","index":1,"fulltext":"This content is not available."},{"type":"reviewersInvited","content":"","date":"2025-06-26T13:54:11+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-06-17T14:30:10+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-06-16T16:08:38+00:00","index":"","fulltext":""},{"type":"submitted","content":"Oncogenesis","date":"2025-06-16T16:08:37+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"oncogenesis","isNatureJournal":false,"hasQc":false,"allowDirectSubmit":false,"externalIdentity":"oncsis","sideBox":"Learn more about [Oncogenesis](http://www.nature.com/oncsis/)","snPcode":"41389","submissionUrl":"https://mts-oncsis.nature.com/cgi-bin/main.plex","title":"Oncogenesis","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"ejp","reportingPortfolio":"Nature AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"9bee518f-1c81-4333-8af2-1ad62eb3b0ea","owner":[],"postedDate":"July 1st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[{"id":50644053,"name":"Biological sciences/Cancer/Cancer models"},{"id":50644054,"name":"Biological sciences/Genetics/Mutation/Genomic instability"},{"id":50644055,"name":"Biological sciences/Genetics/Cancer genetics"},{"id":50644056,"name":"Biological sciences/Genetics/Mutation/Gene amplification"}],"tags":[],"updatedAt":"2026-02-13T08:11:37+00:00","versionOfRecord":{"articleIdentity":"rs-6907318","link":"https://doi.org/10.1038/s41389-026-00599-0","journal":{"identity":"oncogenesis","isVorOnly":false,"title":"Oncogenesis"},"publishedOn":"2026-01-27 05:00:00","publishedOnDateReadable":"January 27th, 2026"},"versionCreatedAt":"2025-07-01 03:14:27","video":"","vorDoi":"10.1038/s41389-026-00599-0","vorDoiUrl":"https://doi.org/10.1038/s41389-026-00599-0","workflowStages":[]},"version":"v1","identity":"rs-6907318","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6907318","identity":"rs-6907318","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}