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000298342 1001_ $$0P:(DE-He78)f2f38d242b5d8cb3903e0ed098e8b554$$aVlachavas, Efstathios-Iason$$b0$$eFirst author$$udkfz
000298342 245__ $$aMolecular and functional profiling unravels targetable vulnerabilities in colorectal cancer.
000298342 260__ $$aHoboken, NJ$$bJohn Wiley & Sons, Inc.$$c2025
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000298342 500__ $$a#EA:B050#LA:B050# / 2025 Jun;19(6):1751-1774
000298342 520__ $$aColorectal cancer (CRC) patients with microsatellite-stable (MSS) tumors are mostly treated with chemotherapy. Clinical benefits of targeted therapies depend on mutational states and tumor location. Many tumors carry mutations in KRAS proto-oncogene, GTPase (KRAS) or B-Raf proto-oncogene, serine/threonine kinase (BRAF), rendering them more resistant to therapies. We performed whole-exome sequencing and RNA-Sequencing of 28 tumors of the Athens Comprehensive Cancer Center CRC cohort, and molecularly characterized CRC patients based on their microsatellite instability (MSI) status, single-nucleotide variations (SNVs)/copy number alterations (CNAs), and pathway/transcription factor activities at the individual patient level. Variants were classified using a computational score for integrative cancer variant annotation and prioritization. Complementing this with public multi-omics datasets, we identified activation of transforming growth factor beta (TGFβ) signaling to be more strongly activated in MSS patients, whereas Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and mitogen-activated protein kinase (MAPK) molecular cascades were activated specifically in MSI tumors. We unraveled mechanisms consistently perturbed in the transcriptional and mutational circuits and identified Runt-related transcription factors (RUNX transcription factors) as putative biomarkers in CRC, given their role in the regulation of pathways involved in tumor progression and immune evasion. Assessing the immunogenicity of CRC tumors in the context of RAS/RAF mutations and MSI/MSS status revealed a critical impact that KRAS mutations have on immunogenicity, particularly in the MSS patient subgroup, with implications for diagnosis and treatment.
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000298342 650_7 $$2Other$$aCRC
000298342 650_7 $$2Other$$aMSI status
000298342 650_7 $$2Other$$aRAS/RAF
000298342 650_7 $$2Other$$aSNVs/CNAs
000298342 650_7 $$2Other$$aWES/RNA‐sequencing
000298342 650_7 $$2Other$$apathway/TF activity
000298342 7001_ $$00000-0001-7163-7381$$aVoutetakis, Konstantinos$$b1
000298342 7001_ $$aKosmidou, Vivian$$b2
000298342 7001_ $$0P:(DE-He78)e2ea2ff7ded515543f890b6cb79dbee7$$aTsikalakis, Spyridon$$b3
000298342 7001_ $$aRoditis, Spyridon$$b4
000298342 7001_ $$aPateas, Konstantinos$$b5
000298342 7001_ $$aKim, Ryangguk$$b6
000298342 7001_ $$aPagel, Kymberleigh$$b7
000298342 7001_ $$0P:(DE-He78)1efb774993effe7a66a6ffc1b1cf9ccb$$aWolf, Stephan$$b8$$udkfz
000298342 7001_ $$0P:(DE-He78)13b64bdd8d9a2fdb2ab13cc480819130$$aWarsow, Gregor$$b9$$udkfz
000298342 7001_ $$0P:(DE-He78)b2df3652dfa3e19d5e96dfc53f44a992$$aDimitrakopoulou-Strauss, Antonia$$b10$$udkfz
000298342 7001_ $$aZografos, Georgios N$$b11
000298342 7001_ $$aPintzas, Alexander$$b12
000298342 7001_ $$0P:(DE-He78)68cbca3e3973d332ccc4c6e31a76b10c$$aBetge, Johannes$$b13$$udkfz
000298342 7001_ $$00000-0003-3896-4270$$aPapadodima, Olga$$b14
000298342 7001_ $$0P:(DE-He78)f6bebe05e7a748d3cbf9f59659567d52$$aWiemann, Stefan$$b15$$eLast author$$udkfz
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