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TGFβ signaling directs serrated adenomas to the mesenchymal colorectal cancer subtype
Open accessAbstract
The heterogeneous nature of colorectal cancer (CRC) complicates prognosis and is suggested to be a determining factor in the efficacy of adjuvant therapy for individual patients. Based on gene expression profiling, CRC is currently classified into four consensus molecular subtypes (CMSs), characterized by specific biological programs, thus suggesting the existence of unifying developmental drivers for each CMS. Using human organoid cultures, we investigated the role of such developmental drivers at the premalignant stage of distinct CRC subtypes and found that TGFβ plays an important role in the development of the mesenchymal CMS4, which is of special interest due to its association with dismal prognosis. We show that in tubular adenomas (TAs), which progress to classical CRCs, the dominating response to TGFβ is death by apoptosis. By contrast, induction of a mesenchymal phenotype upon TGFβ treatment prevails in a genetically engineered organoid culture carrying a BRAFV600E mutation, constituting a model system for sessile serrated adenomas (SSAs). Our data indicate that TGFβ signaling is already active in SSA precursor lesions and that TGFβ is a critical cue for directing SSAs to the mesenchymal, poor‐prognosis CMS4 of CRC. Sessile serrated adenomas (SSAs)—precursor lesions of the serrated neoplasia pathway to colorectal cancer (CRC)—are predicted to give rise to either the good‐ or the poor‐prognosis CRC consensus molecular subtype (CMS1 and CMS4, respectively). Sessile serrated adenomas (SSAs)—precursor lesions of the serrated neoplasia pathway to colorectal cancer (CRC)—are predicted to give rise to either the good‐ or the poor‐prognosis CRC consensus molecular subtype (CMS1 and CMS4, respectively).
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“Follow-up studies have documented that TGFβ can direct human organoid cultures to a CMS4 profile (20)”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [20]
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Metadata
- Authors
- Fessler, E., Drost, J., van Hooff, S. R., Linnekamp, J. F., Wang, X., Jansen, M., De Sousa E Melo, F., Prasetyanti, P. R., IJspeert, J. E., Franitza, M., Nürnberg, P., van Noesel, C. J., Dekker, E., Vermeulen, L., Clevers, H., & Medema, J. P.
- Affiliations
- Amsterdam UMC Location University of Amsterdam (NL)
- Royal Netherlands Academy of Arts and Sciences (NL)
- City University of Hong Kong (HK)
- University of Cologne (DE)
- Corresponding author
- Medema, Jan Paul
- ORCID
- Venue
- EMBO Molecular Medicine
- Published
- 2016-05-24
- Volume
- 8
- Issue
- 7
- Pages
- 745-760
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC4931289
- OpenAlex
- W2404590196
- Cited by
- 159
- References
- 69
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 16 · 2023: 12 · 2022: 16 · 2021: 20 · 2020: 25 · 2019: 13 · 2018: 16 · 2017: 14 · 2016: 4
- FWCI
- 8.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- EMBO Molecular Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, other-oa)
- KNAW Research Portal (The Royal Netherlands Academy of Arts and Sciences) (publishedVersion, other-oa)
- KNAW research portal (Royal Academy of Art and Sciences (KNAW)) (publishedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- CityU Scholars (submittedVersion, cc-by)
- Funders
- AMC Graduate School PhD Scholarship
- NWO‐ZonMw VENI (91614138)
- Dutch Cancer Society (UvA2013‐6331, UvA2014‐7245, UvA2015‐7587)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- TGF-beta signaling, colorectal cancer, consensus molecular subtypes, CMS4, mesenchymal subtype, sessile serrated adenoma, serrated neoplasia, tubular adenoma, BRAF V600E mutation, colorectal organoids, apoptosis, tumor progression, precursor lesions
- MeSH terms
- Adenoma, Humans, Organoids, Colorectal Neoplasms, Signal Transduction, Transforming Growth Factor beta, Carcinogenesis
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