ArticleNature communications2022
BRCA mutational status shapes the stromal microenvironment of pancreatic cancer linking clusterin expression in cancer associated fibroblasts with HSF1 signaling.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- A systematic review on the culture methods and applications of 3D tumoroids for cancer research and personalized medicine.Cellular oncology (Dordrecht, Netherlands) · 2025Pooled it
- ALKBH5 in Cancer-Associated Fibroblasts Governs an Epitranscriptomic Axis That Drives Pancreatic Cancer Metastasis.Cancer research · 2026Article
- Multi-stromal organoid co-culture modelling reveals epithelial-fibroblast heterogeneity in pancreatic cancer and pancreatitis.Nature cell biology · 2026Article
- The dual immune landscape of homologous recombination-deficient tumors: mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- Post-Translational Modifications in Pancreatic Cancer: Mechanisms to Clinical Applications.Journal of gastroenterology and hepatology · 2026Review
- ATM Deficiency Induces TGFβ-Mediated Stromal Programming in Pancreatic Cancer.Cancer research · 2026Article
- Molecular phenotypes and spatial archetypes: A new framework for cancer-associated fibroblasts.Cancer cell · 2026Review
- Heterogeneity and plasticity of cancer-associated fibroblasts.Nature cancer · 2026Review
- Heterocellular crosstalk and architecture of the pancreatic tumour microenvironment.Nature reviews. Cancer · 2026Review
- Implications of Homologous Recombination Deficiency for Neoadjuvant Platinum-Based Chemotherapy in Pancreatic Cancer: A Narrative Review.Annals of surgical oncology · 2026Review
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- The research advances of crosstalk between cancer-associated fibroblasts and tumor cells using co-culture organoids.Cell death & disease · 2026Review
- Transgelin defines pro-tumorigenic cancer-associated fibroblasts in pancreatic cancer.British journal of cancer · 2026Article
- Emerging therapeutic advancements in pancreatic cancer: a contemporary review.Discover oncology · 2025Review
- Oncolytic herpes simplex virus reprograms cancer-associated fibroblasts to enhance antitumor immunity in pancreatic cancer.Molecular therapy. Oncology · 2025Article
- Plasticity and Functional Heterogeneity of Cancer-Associated Fibroblasts.Cancer research · 2025Review
- HSF2 drives breast cancer progression by acting as a stage-specific switch between proliferation and invasion.Science advances · 2025Article
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- Case Report: Atypical Nodular Dermatofibrosis and Renal Cysts in a Bichon Frise with a BRCA2 Mutation and No FLCN Mutation.Animals : an open access journal from MDPI · 2025Article
- Proteomics in pancreatic cancer.Biomarker research · 2025Review
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Authors and funding
29 authors at 9 institutions in 4 countries.
Funding
Abstract
Tumors initiate by mutations in cancer cells, and progress through interactions of the cancer cells with non-malignant cells of the tumor microenvironment. Major players in the tumor microenvironment are cancer-associated fibroblasts (CAFs), which support tumor malignancy, and comprise up to 90% of the tumor mass in pancreatic cancer. CAFs are transcriptionally rewired by cancer cells. Whether this rewiring is differentially affected by different mutations in cancer cells is largely unknown. Here we address this question by dissecting the stromal landscape of BRCA-mutated and BRCA Wild-type pancreatic ductal adenocarcinoma. We comprehensively analyze pancreatic cancer samples from 42 patients, revealing different CAF subtype compositions in germline BRCA-mutated vs. BRCA Wild-type tumors. In particular, we detect an increase in a subset of immune-regulatory clusterin-positive CAFs in BRCA-mutated tumors. Using cancer organoids and mouse models we show that this process is mediated through activation of heat-shock factor 1, the transcriptional regulator of clusterin. Our findings unravel a dimension of stromal heterogeneity influenced by germline mutations in cancer cells, with direct implications for clinical research.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.