Abstract
Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with diverse functions, including matrix deposition and remodelling, extensive reciprocal signalling interactions with cancer cells and crosstalk with infiltrating leukocytes. As such, they are a potential target for optimizing therapeutic strategies against cancer. However, many challenges are present in ongoing attempts to modulate CAFs for therapeutic benefit. These include limitations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some antitumorigenic functions. On the basis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement our current knowledge and present a framework for advancing our understanding of this critical cell type within the tumour microenvironment.
| Original language | English |
|---|---|
| Pages (from-to) | 174-186 |
| Number of pages | 13 |
| Journal | Nature Reviews Cancer |
| Volume | 20 |
| Issue number | 3 |
| DOIs | |
| State | Published - 24 Jan 2020 |
All Science Journal Classification (ASJC) codes
- Oncology
- Cancer Research
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In: Nature Reviews Cancer, Vol. 20, No. 3, 24.01.2020, p. 174-186.
Research output: Contribution to journal › Review article › peer-review
TY - JOUR
T1 - A framework for advancing our understanding of cancer-associated fibroblasts
AU - Sahai, Erik
AU - Astsaturov, Igor
AU - Cukierman, Edna
AU - DeNardo, David G.
AU - Egeblad, Mikala
AU - Evans, Ronald M.
AU - Fearon, Douglas
AU - Greten, Florian R.
AU - Hingorani, Sunil R.
AU - Hunter, Tony
AU - Hynes, Richard O.
AU - Jain, Rakesh K.
AU - Janowitz, Tobias
AU - Jorgensen, Claus
AU - Kimmelman, Alec C.
AU - Kolonin, Mikhail G.
AU - Maki, Robert G.
AU - Powers, R. Scott
AU - Pure, Ellen
AU - Ramirez, Daniel C.
AU - Scherz-Shouval, Ruth
AU - Sherman, Mara H.
AU - Stewart, Sheila
AU - Tlsty, Thea D.
AU - Tuveson, David A.
AU - Watt, Fiona M.
AU - Weaver, Valerie
AU - Weeraratna, Ashani T.
AU - Werb, Zena
N1 - The Banbury Center meeting was supported financially by Cold Spring Harbor Laboratory and Northwell Health Affiliation. The authors thank R. Leshan for organizing this meeting. The funder had no involvement in the writing of this Consensus Statement. E.S. is financially supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001144), the UK Medical Research Council (FC001144) and the Wellcome Trust (FC001144) and receives additional research support from Cancer Research UK, EPSRC, AstraZeneca and BBSRC/GlaxoSmithKline. E.C. acknowledges funding from the Martin and Concetta Greenberg Pancreatic Cancer Institute, the In Vino Vita Institutional Pilot Award and the Translational Clinical Protocol Development Award at Fox Chase Cancer Center (Philadelphia, PA, USA); Pennsylvania’s Department of Health Health Research Formula Funds; the Greenfield Foundation; the Fifth District AHEPA Cancer Research Foundation; and US National Institutes of Health (NIH)/National Cancer Institute (NCI) grants R21-CA231252 and R01-CA232256 and Core Grant CA06927. D.D. acknowledges funding from NIH/NCI grants R01CA177670, R01CA203890, R01CA244938, P50CA196510 and U2CCA223303. M.E. acknowledges funding from the Thompson Family Foundation. R.M.E. is an investigator of the Howard Hughes Medical Institute at the Salk Institute and March of Dimes Chair in Molecular and Developmental Biology and is supported by a Stand Up To Cancer-Cancer Research UK-Lustgarten Foundation Pancreatic Cancer Dream Team Research Grant (Grant Number: SU2C-AACR-DT-20-16). F.R.G. is supported by institutional funds from the Georg-Speyer-Haus, the LOEWE Center Frankfurt Cancer Institute funded by the Hessen State Ministry for Higher Education, Research and the Arts [III L 5 - 519/03/03.001 - (0015)] and the Deutsche Forschungsgemeinschaft (FOR2438: Gr1916/11-1). S.R.H is supported by NCI grants U01CA224193, R01CA161112 and R01CA223483 and Pancreatic Cancer Action Network grant 17-85-HING. R.O.H. acknowledges funding from the US Department of Defense BCRP Investigator Award (W81XWH-14-1-0240) and the Starr Cancer Consortium (award no. I7-A718). R.K.J. is supported by grants from the National Cancer Institute (R35-CA197743, R01-CA208205, U01-CA224173), the National Foundation for Cancer Research, the Ludwig Center at Harvard Medical School, the Advanced Medical Research Foundation, the Ellison Foundation and the Jane’s Trust Foundation. T.J. acknowledges funding from National Cancer Institute Cold Spring Harbor Laboratory Cancer Center support grant P30CA045508. C.J. acknowledges funding from Cancer Research UK Institute Award A19258. A.C.K is supported by NCI grants R01CA157490, R01CA188048, P01CA117969 and R35CA232124, NIH grant R01GM095567, the Lustgarten Foundation and SU2C. M.G.K. acknowledges funding from the NIH (grants R01CA195659 and 1R21CA216745). R.G.M. acknowledges funding from the Liddy Shriver Sarcoma Alliance (ImmunoSarc grant), the Sarcoma Alliance for Research through Collaboration (SARC) and Fondazione Enrico Pallazzo (18-MSSM-0302). E.P. acknowledges funding from NIH P01 CA217805 ‘Extending Chimeric Antigen (CAR) T Cell Therapy to Thoracic Cancers’ (project leader S. Albelda; co-principal investigator project 2 E.P.). R.S-S. is the incumbent Ernst and Kaethe Ascher Career Development Chair in Life Sciences and is supported by the Israel Science Foundation (grants 401/17 and 1384/1), the European Research Council (grant agreement 754320), the Laura Gurwin Flug Family Fund, the Peter and Patricia Gruber Awards, the Comisaroff Family Trust, the Estate of Annice Anzelewitz and the Estate of Mordecai M. Roshwal. M.H.S. acknowledges funding from American Cancer Society Research Scholar Grant 132898-RSG-18-142-01-CSM. S.S. acknowledges funding from NIH grant R01 CA130919 and the US Army Medical Research Acquisition Activity, supported in part by the Office of the Assistant Secretary of Defense for Health Affairs, through the Breast Cancer Research Program, under award no. W81XWH-16-1-0728. T.D.T. acknowledges support by the American Foundation for Urological Disease and Pfizer Pharmaceuticals Groups, NIH grants DK45861, DK52708, CA64872, CA59831 and DK52721, a CaPCURE award, NIH/NCI PO1 CA107584 (under LBNL contract no. DE-AC02-05CH11231), California Breast Cancer Research Program grant 14OB-0165 and NIH/NCI U54 CA143803. D.A.T is supported by the Cold Spring Harbor Laboratory Association, the V Foundation, and the NIH (grants 5P30CA45508, 5P50CA101955, P20CA192996, 1U10CA180944, U01CA224013, U01CA210240-01A1, 1R01CA188134 and 1R01CA190092). F.M.W. acknowledges funding from the UK Medical Research Council (MR/PO18823/1), Cancer Research UK (C219/A23522), Guy’s and St Thomas’ NHS Foundation Trust Biomedical Research Centre (IS-BRC-1215-20006) and the Wellcome Trust (206439/Z/17/Z). A.T.W. acknowledges funding from NIH grants R01CA232256 and R01CA174746. Z.W. acknowledges funding from NIH/NCI U01 CA199315-04 ‘Integrative Approach to Heterogeneity in Breast Cancer Metastasis’.
PY - 2020/1/24
Y1 - 2020/1/24
N2 - Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with diverse functions, including matrix deposition and remodelling, extensive reciprocal signalling interactions with cancer cells and crosstalk with infiltrating leukocytes. As such, they are a potential target for optimizing therapeutic strategies against cancer. However, many challenges are present in ongoing attempts to modulate CAFs for therapeutic benefit. These include limitations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some antitumorigenic functions. On the basis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement our current knowledge and present a framework for advancing our understanding of this critical cell type within the tumour microenvironment.
AB - Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with diverse functions, including matrix deposition and remodelling, extensive reciprocal signalling interactions with cancer cells and crosstalk with infiltrating leukocytes. As such, they are a potential target for optimizing therapeutic strategies against cancer. However, many challenges are present in ongoing attempts to modulate CAFs for therapeutic benefit. These include limitations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some antitumorigenic functions. On the basis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement our current knowledge and present a framework for advancing our understanding of this critical cell type within the tumour microenvironment.
UR - http://www.scopus.com/inward/record.url?scp=85078418124&partnerID=8YFLogxK
U2 - https://doi.org/10.1038/s41568-019-0238-1
DO - https://doi.org/10.1038/s41568-019-0238-1
M3 - مقالة مرجعية
C2 - 31980749
SN - 1474-175X
VL - 20
SP - 174
EP - 186
JO - Nature Reviews Cancer
JF - Nature Reviews Cancer
IS - 3
ER -