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Inter‐ and intra‐tumoural heterogeneity in cancer‐associated fibroblasts of human pancreatic ductal adenocarcinoma
The Journal of pathology, 2019-05, Vol.248 (1), p.51-65
Neuzillet, Cindy
Tijeras‐Raballand, Annemilaï
Ragulan, Chanthirika
Cros, Jérôme
Patil, Yatish
Martinet, Matthieu
Erkan, Mert
Kleeff, Jörg
Wilson, Jeremy
Apte, Minoti
Tosolini, Marie
Wilson, Abigail S
Delvecchio, Francesca R
Bousquet, Corinne
Paradis, Valérie
Hammel, Pascal
Sadanandam, Anguraj
Kocher, Hemant M
2019
Details
Autor(en) / Beteiligte
Neuzillet, Cindy
Tijeras‐Raballand, Annemilaï
Ragulan, Chanthirika
Cros, Jérôme
Patil, Yatish
Martinet, Matthieu
Erkan, Mert
Kleeff, Jörg
Wilson, Jeremy
Apte, Minoti
Tosolini, Marie
Wilson, Abigail S
Delvecchio, Francesca R
Bousquet, Corinne
Paradis, Valérie
Hammel, Pascal
Sadanandam, Anguraj
Kocher, Hemant M
Titel
Inter‐ and intra‐tumoural heterogeneity in cancer‐associated fibroblasts of human pancreatic ductal adenocarcinoma
Ist Teil von
The Journal of pathology, 2019-05, Vol.248 (1), p.51-65
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2019
Link zum Volltext
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
Cancer‐associated fibroblasts (CAF) are orchestrators of the pancreatic ductal adenocarcinoma (PDAC) microenvironment. Stromal heterogeneity may explain differential pathophysiological roles of the stroma (pro‐ versus anti‐tumoural) in PDAC. We hypothesised that multiple CAF functional subtypes exist in PDAC, that contribute to stromal heterogeneity through interactions with cancer cells. Using molecular and functional analysis of patient‐derived CAF primary cultures, we demonstrated that human PDAC‐derived CAFs display a high level of inter‐ and intra‐tumour heterogeneity. We identified at least four subtypes of CAFs based on transcriptomic analysis, and propose a classification for human PDAC‐derived CAFs (pCAFassigner). Multiple CAF subtypes co‐existed in individual patient samples. The presence of these CAF subtypes in bulk tumours was confirmed using publicly available gene expression profiles, and immunostainings of CAF subtype markers. Each subtype displayed specific phenotypic features (matrix‐ and immune‐related signatures, vimentin and α‐smooth muscle actin expression, proliferation rate), and was associated with an assessable prognostic impact. A prolonged exposure of non‐tumoural pancreatic stellate cells to conditioned media from cancer cell lines (cancer education experiment) induced a CAF‐like phenotype, including loss of capacity to revert to quiescence and an increase in the expression of genes related to CAF subtypes B and C. This classification demonstrates molecular and functional inter‐ and intra‐tumoural heterogeneity of CAFs in human PDAC. Our subtypes overlap with those identified from single‐cell analyses in other cancers, and pave the way for the development of therapies targeting specific CAF subpopulations in PDAC. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.5224
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6492001
Format
–
Schlagworte
Actin
,
Adenocarcinoma
,
Cancer
,
Cancer-Associated Fibroblasts - pathology
,
Carcinoma, Pancreatic Ductal - genetics
,
Carcinoma, Pancreatic Ductal - pathology
,
Classification
,
Conditioning
,
Fibroblasts
,
Functional analysis
,
Gene expression
,
Gene Expression Profiling - methods
,
Gene Expression Regulation, Neoplastic
,
Genetic Heterogeneity
,
Heterogeneity
,
Humans
,
Kaplan-Meier Estimate
,
Muscles
,
Original Paper
,
Original Papers
,
Pancreas
,
Pancreatic cancer
,
Pancreatic Neoplasms - genetics
,
Pancreatic Neoplasms - pathology
,
pancreatic stellate cell
,
Pancreatic Stellate Cells - pathology
,
Phenotype
,
Phenotypes
,
Prognosis
,
Smooth muscle
,
Stellate cells
,
Stroma
,
Stromal Cells - pathology
,
Subpopulations
,
transcriptomics
,
Tumor cell lines
,
Tumor Cells, Cultured
,
Tumor Microenvironment
,
Tumors
,
tumour microenvironment
,
tumour‐stroma interactions
,
Vimentin
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