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  3. Tumour budding is associated with the mesenchymal colon cancer subtype and RAS/RAF mutations: a study of 1320 colorectal cancers with Consensus Molecular Subgroup (CMS) data.
 

Tumour budding is associated with the mesenchymal colon cancer subtype and RAS/RAF mutations: a study of 1320 colorectal cancers with Consensus Molecular Subgroup (CMS) data.

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BORIS DOI
10.7892/boris.121735
Date of Publication
November 2018
Publication Type
Article
Division/Institute

Institut für Patholog...

Author
Trinh, Anne
Lädrach, Claudia
Dawson, Heather
Institut für Pathologie
Ten Hoorn, Sanne
Kuppen, Peter J K
Reimers, Marlies S
Koopman, Miriam
Punt, Cornelis J A
Lugli, Alessandroorcid-logo
Institut für Pathologie
Vermeulen, Louis
Zlobec, Intiorcid-logo
Institut für Pathologie
Subject(s)

500 - Science::570 - ...

600 - Technology::610...

Series
British journal of cancer
ISSN or ISBN (if monograph)
0007-0920
Publisher
Nature Publishing Group
Language
English
Publisher DOI
10.1038/s41416-018-0230-7
PubMed ID
30385823
Description
BACKGROUND

Tumour budding is an important prognostic factor in colorectal cancer (CRC). Molecular profiling of tumour buds suggests (partial) epithelial-mesenchymal transition and cancer stem-cell phenotype, similarly described in the "mesenchymal" Consensus Molecular Subtype 4 (CMS4), which identifies a particularly poor prognostic subgroup. Here, we determine the association of tumour budding with CMS classification, prognosis, and response to therapy.

METHODS

AMC-AJCCII-90 cohort (n = 76, stage II) was evaluated for peritumoural budding on H&E slides. LUMC (n = 270, stage I-IV), CAIRO (n = 504, metastatic CRC) and CAIRO2 (n = 472, metastatic CRC) cohorts were investigated for intratumoural budding using pan-cytokeratin-stained tissue microarrays. Budding was scored as count/area, then classified as <5 or ≥5 buds. For all cohorts, CMS classifications were available (gene-expression/immunohistochemistry-based classifiers).

RESULTS

High (≥5) budding predicted a worse outcome in multivariate analysis in AMC-AJCCII-90 (p = 0.018), LUMC (p < 0.0001), and CAIRO (p = 0.03), and in CAIRO2 (continuous variable, p = 0.02). Tumour budding counts were higher in CMS4 compared to epithelial CMS2/3 cancers (p < 0.01, all), and associated with KRAS/BRAF mutations (p < 0.01, AMC-AJCCII-90, CAIRO, CAIRO2).

CONCLUSION

Tumour budding is an adverse prognostic factor across all CRC stages and is associated with the mesenchymal CMS4 phenotype. KRAS/BRAF mutations are strongly correlated with tumour budding suggesting their involvement in the regulation of this process.
Handle
https://boris-portal.unibe.ch/handle/20.500.12422/60951
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s41416-018-0230-7.pdftextAdobe PDF1.53 MBpublisherpublished restricted
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