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Article ; Online: Seeking Synergy of Checkpoint Blockade through TGFβ Inhibition.

Puré, Ellen

2018 Volume 6, Issue 12, Page(s) 1444

Abstract: Immunotherapy, including checkpoint blockade, is revolutionizing the treatment of cancers, but efficacy has, however, been limited to a subset of patients and can be of limited duration due to primary and acquired resistance to treatment. An article in ... ...

Abstract	Immunotherapy, including checkpoint blockade, is revolutionizing the treatment of cancers, but efficacy has, however, been limited to a subset of patients and can be of limited duration due to primary and acquired resistance to treatment. An article in this issue shows that inhibiting TGFβ can overcome resistance to blockade of one immune checkpoint, but not another, unless one follows where the mechanism leads.
MeSH term(s)	CTLA-4 Antigen ; Fibroblasts ; Humans ; Melanoma ; Programmed Cell Death 1 Receptor ; Transforming Growth Factor beta
Chemical Substances	CTLA-4 Antigen ; Programmed Cell Death 1 Receptor ; Transforming Growth Factor beta
Language	English
Publishing date	2018-12-03
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-18-0784
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Article ; Online: Imaging of T-cell Responses in the Context of Cancer Immunotherapy.

Xiao, Zebin / Puré, Ellen

Cancer immunology research

2021 Volume 9, Issue 5, Page(s) 490–502

Abstract: Immunotherapy, which promotes the induction of cytotoxic T lymphocytes and enhances their infiltration into and function within tumors, is a rapidly expanding and evolving approach to treating cancer. However, many of the critical denominators for ... ...

Abstract	Immunotherapy, which promotes the induction of cytotoxic T lymphocytes and enhances their infiltration into and function within tumors, is a rapidly expanding and evolving approach to treating cancer. However, many of the critical denominators for inducing effective anticancer immune responses remain unknown. Efforts are underway to develop comprehensive
MeSH term(s)	Animals ; Humans ; Immunotherapy ; Magnetic Resonance Imaging ; Neoplasms/therapy ; Positron-Emission Tomography ; T-Lymphocytes ; Tomography, Emission-Computed, Single-Photon
Language	English
Publishing date	2021-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-20-0678
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Article ; Online: Cancer-associated fibroblasts: key determinants of tumor immunity and immunotherapy.

Barrett, Richard / Puré, Ellen

Current opinion in immunology

2020 Volume 64, Page(s) 80–87

Abstract: Immune-targeted approaches are rapidly changing the therapeutic landscape for cancer. In spite of that, most patients show resistance or acquire resistance to these therapies. Increasing work describing the tumor microenvironment (TME) has highlighted ... ...

Abstract	Immune-targeted approaches are rapidly changing the therapeutic landscape for cancer. In spite of that, most patients show resistance or acquire resistance to these therapies. Increasing work describing the tumor microenvironment (TME) has highlighted this space as one of the key determinants in tumor immune response and immunotherapeutic success. Frequently overlooked within this space, cancer-associated fibroblasts (CAFs) within the TME have surfaced as an important dictator of the tumor immune response. Herein, we review recent advances in defining the role of CAF-immune cell interactions in solid tumors and prospects for targeting stroma to overcome resistance to immunotherapy.
MeSH term(s)	Cancer-Associated Fibroblasts/pathology ; Cell Communication ; Humans ; Immunotherapy ; Neoplasms/pathology ; Neoplasms/therapy ; Tumor Microenvironment
Language	English
Publishing date	2020-05-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2020.03.004
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Zs.A 2773: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cancer-associated fibroblasts and their influence on tumor immunity and immunotherapy.

Barrett, Richard Lee / Puré, Ellen

eLife

2020 Volume 9

Abstract: Fibroblasts play an essential role in organogenesis and the integrity of tissue architecture and function. Growth in most solid tumors is dependent upon remodeling 'stroma', composed of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), ...

Abstract	Fibroblasts play an essential role in organogenesis and the integrity of tissue architecture and function. Growth in most solid tumors is dependent upon remodeling 'stroma', composed of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), which plays a critical role in tumor initiation, progression, metastasis, and therapeutic resistance. Recent studies have clearly established that the potent immunosuppressive activity of stroma is a major mechanism by which stroma can promote tumor progression and confer resistance to immune-based therapies. Herein, we review recent advances in identifying the stroma-dependent mechanisms that regulate cancer-associated inflammation and antitumor immunity, in particular, the interactions between fibroblasts and immune cells. We also review the potential mechanisms by which stroma can confer resistance to immune-based therapies for solid tumors and current advancements in stroma-targeted therapies.
MeSH term(s)	Animals ; Cancer-Associated Fibroblasts/immunology ; Humans ; Immunotherapy ; Tumor Escape/immunology ; Tumor Microenvironment/immunology
Language	English
Publishing date	2020-12-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.57243
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Article ; Online: Mechanisms of PDAC subtype heterogeneity and therapy response.

Espinet, Elisa / Klein, Lukas / Puré, Ellen / Singh, Shiv K

Trends in cancer

2022 Volume 8, Issue 12, Page(s) 1060–1071

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is clinically challenging due to late diagnosis and resistance to therapy. Two major PDAC subtypes have been defined based on malignant epithelial cell gene expression profiles; the basal-like/squamous subtype is ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is clinically challenging due to late diagnosis and resistance to therapy. Two major PDAC subtypes have been defined based on malignant epithelial cell gene expression profiles; the basal-like/squamous subtype is associated with a worse prognosis and therapeutic resistance as opposed to the classical subtype. Subtype specification is not binary, consistent with plasticity of malignant cell phenotype. PDAC heterogeneity and plasticity reflect partly malignant cell-intrinsic transcriptional and epigenetic regulation. However, the stromal and immune compartments of the tumor microenvironment (TME) also determine disease progression and therapy response. It is evident that integration of intrinsic and extrinsic factors can dictate subtype heterogeneity, and thus, delineating the pathways involved can help to reprogram PDAC towards a classical/druggable subtype.
MeSH term(s)	Humans ; Epigenesis, Genetic ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Tumor Microenvironment/genetics ; Pancreatic Neoplasms
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2022.08.005
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Article ; Online: Cancer-associated fibroblasts and their influence on tumor immunity and immunotherapy

Richard Lee Barrett / Ellen Puré

eLife, Vol

2020 Volume 9

Abstract: Fibroblasts play an essential role in organogenesis and the integrity of tissue architecture and function. Growth in most solid tumors is dependent upon remodeling ‘stroma’, composed of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), ...

Abstract	Fibroblasts play an essential role in organogenesis and the integrity of tissue architecture and function. Growth in most solid tumors is dependent upon remodeling ‘stroma’, composed of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), which plays a critical role in tumor initiation, progression, metastasis, and therapeutic resistance. Recent studies have clearly established that the potent immunosuppressive activity of stroma is a major mechanism by which stroma can promote tumor progression and confer resistance to immune-based therapies. Herein, we review recent advances in identifying the stroma-dependent mechanisms that regulate cancer-associated inflammation and antitumor immunity, in particular, the interactions between fibroblasts and immune cells. We also review the potential mechanisms by which stroma can confer resistance to immune-based therapies for solid tumors and current advancements in stroma-targeted therapies.
Keywords	immunotherapy ; fibroblast ; cancer ; tumor immunity ; T-cell ; macrophages ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mesenchymal Cell Plasticity and Perfidy in Epithelial Malignancy.

Puré, Ellen / Hingorani, Sunil R

Trends in cancer

2018 Volume 4, Issue 4, Page(s) 273–277

Abstract: Stromal complicity in epithelial carcinogenesis contributes to immune suppression and treatment resistance, but not all cancer-associated fibroblasts (CAFs) are bad actors. Identifying and targeting protumorigenic CAFs while preserving their ... ...

Abstract	Stromal complicity in epithelial carcinogenesis contributes to immune suppression and treatment resistance, but not all cancer-associated fibroblasts (CAFs) are bad actors. Identifying and targeting protumorigenic CAFs while preserving their antitumorigenic counterparts is the challenge. The risk is the possibility of making things worse; the reward is the potential to transform the care of and prognosis for patients with solid tumors.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cancer-Associated Fibroblasts/drug effects ; Cancer-Associated Fibroblasts/physiology ; Carcinogenesis/drug effects ; Carcinogenesis/immunology ; Carcinogenesis/pathology ; Cell Plasticity/drug effects ; Cell Plasticity/physiology ; Cell Transformation, Neoplastic/drug effects ; Drug Resistance, Neoplasm ; Extracellular Matrix/drug effects ; Extracellular Matrix/immunology ; Extracellular Matrix/pathology ; Humans ; Immune Tolerance/drug effects ; Mesenchymal Stem Cells/drug effects ; Mesenchymal Stem Cells/physiology ; Neoplasms, Glandular and Epithelial/drug therapy ; Neoplasms, Glandular and Epithelial/immunology ; Neoplasms, Glandular and Epithelial/pathology ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/immunology
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2018-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2018.02.007
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Article ; Online: Pro-tumorigenic roles of fibroblast activation protein in cancer: back to the basics.

Puré, Ellen / Blomberg, Rachel

Oncogene

2018 Volume 37, Issue 32, Page(s) 4343–4357

Abstract: Fibroblast activation protein (FAP) is a cell-surface serine protease that acts on various hormones and extracellular matrix components. FAP is highly upregulated in a wide variety of cancers, and is often used as a marker for pro-tumorigenic stroma. It ... ...

Abstract	Fibroblast activation protein (FAP) is a cell-surface serine protease that acts on various hormones and extracellular matrix components. FAP is highly upregulated in a wide variety of cancers, and is often used as a marker for pro-tumorigenic stroma. It has also been proposed as a molecular target of cancer therapies, and, especially in recent years, a great deal of research has gone into design and testing of diverse FAP-targeted treatments. Yet despite this growing field of research, our knowledge of FAP's basic biology and functional roles in various cancers has lagged behind its use as a tumor-stromal marker. In this review, we summarize and analyze recent advances in understanding the functions of FAP in cancer, most notably its prognostic value in various tumor types, cellular effects on various cell types, and potential as a therapeutic target. We highlight outstanding questions in the field, the answers to which could shape preclinical and clinical studies of FAP.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Endopeptidases ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gelatinases/metabolism ; Humans ; Membrane Proteins/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Serine Endopeptidases/metabolism ; Tumor Microenvironment/physiology
Chemical Substances	Membrane Proteins ; Endopeptidases (EC 3.4.-) ; Serine Endopeptidases (EC 3.4.21.-) ; fibroblast activation protein alpha (EC 3.4.21.-) ; Gelatinases (EC 3.4.24.-)
Language	English
Publishing date	2018-05-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-018-0275-3
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Zs.A 2218: Show issues

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Article ; Online: The road to integrative cancer therapies: emergence of a tumor-associated fibroblast protease as a potential therapeutic target in cancer.

Puré, Ellen

Expert opinion on therapeutic targets

2009 Volume 13, Issue 8, Page(s) 967–973

Abstract: Great inroads have been made in defining the oncogenic pathways intrinsic to neoplastic cells and the mechanisms by which they are activated in tumors. Knowledge of these pathways provides numerous opportunities that are actively being pursued to develop ...

Abstract	Great inroads have been made in defining the oncogenic pathways intrinsic to neoplastic cells and the mechanisms by which they are activated in tumors. Knowledge of these pathways provides numerous opportunities that are actively being pursued to develop targeted therapies for cancer. Complementary studies, focused on the non-transformed components of the tumor microenvironment (TME), have revealed that the extrinsic cues provided by the TME are also essential for tumor cells to manifest a fully transformed phenotype, angiogenesis and metastasis. Delineation of these cues and their underlying cellular and molecular pathways will thus lead to a new era of integrative cancer therapy based on combinatorial drug regimens that act synergistically to destroy the neoplastic cells by targeting both the intrinsic and extrinsic pro-oncogenic pathways. Tumor-associated fibroblasts (TAFs) and proteases are two of the key regulators of epithelial-derived tumors that represent potential targets of such integrative therapies. Herein, we consider the potential therapeutic benefit of inhibiting the function of fibroblast activation protein (FAP), a cell surface serine protease with dipeptidyl peptidase and endopeptidase activity that is expressed on TAFs and pericytes, in an integrative approach to treating cancer.
MeSH term(s)	Animals ; Antigens, Neoplasm/metabolism ; Biomarkers, Tumor/antagonists & inhibitors ; Combined Modality Therapy/methods ; Combined Modality Therapy/trends ; Drug Delivery Systems/methods ; Drug Delivery Systems/trends ; Fibroblasts/drug effects ; Fibroblasts/enzymology ; Fibroblasts/pathology ; Gelatinases/antagonists & inhibitors ; Gelatinases/metabolism ; Humans ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/metabolism ; Neoplasms/enzymology ; Neoplasms/pathology ; Neoplasms/therapy ; Serine Endopeptidases/metabolism ; Serine Proteinase Inhibitors/therapeutic use
Chemical Substances	Antigens, Neoplasm ; Biomarkers, Tumor ; Membrane Proteins ; Serine Proteinase Inhibitors ; Serine Endopeptidases (EC 3.4.21.-) ; fibroblast activation protein alpha (EC 3.4.21.-) ; Gelatinases (EC 3.4.24.-)
Language	English
Publishing date	2009-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1517/14728220903103841
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Zs.A 5244: Show issues

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Article ; Online: Can Targeting Stroma Pave the Way to Enhanced Antitumor Immunity and Immunotherapy of Solid Tumors?

Puré, Ellen / Lo, Albert

Cancer immunology research

2016 Volume 4, Issue 4, Page(s) 269–278

Abstract: Solid tumors are complex organ-like structures. The potential of normal neighboring cells to contribute to the initiation, progression, and metastasis of epithelial-derived carcinomas has long been appreciated. However, the role of host cells has proven ... ...

Abstract	Solid tumors are complex organ-like structures. The potential of normal neighboring cells to contribute to the initiation, progression, and metastasis of epithelial-derived carcinomas has long been appreciated. However, the role of host cells has proven complex. Through multiple local and systemic mechanisms, nontransformed host cells can promote transition from a tumor-resistant to tumor-permissive environment, drive neoplastic transformation of epithelial cells, promote tumor growth, progression, and metastasis, but also constrain tumorigenesis. This complexity reflects the spatially and temporally dynamic involvement of multiple cell types and processes, including the development and recruitment of inflammatory, immune, endothelial, and mesenchymal stromal cells, and the remodeling of extracellular matrix. Our mechanistic understanding, as well as our ability to translate advances in our understanding of these mechanisms for therapeutic benefit, is rapidly advancing. Further insights will depend on delineating pathways that mediate the communication networks between inflammatory and immune cells with tumor and mesenchymal stromal cells and extracellular matrix. Here, we discuss the diversity of mesenchymal stromal cell populations and how context can dictate either their promotion or constraint of tumorigenesis. We review evidence for plasticity that allows for reprogramming of stromal cells and how tumor immunogenicity and desmoplasia influence the balance of immune-independent and immune-dependent regulation of tumor growth. The pivotal roles of matrix and mesenchymal stromal cells in modulating inflammation, antitumor immunity, and the efficacy of immune-based therapies are discussed. These concepts have emerged from data obtained from tumors of multiple organs, but we focus mostly on studies of pancreatic ductal adenocarcinomas.
MeSH term(s)	Animals ; Cell Communication ; Cell Transformation, Neoplastic ; Humans ; Immunity ; Immunomodulation ; Immunotherapy ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Signal Transduction ; Stromal Cells/immunology ; Stromal Cells/metabolism ; Stromal Cells/pathology ; Tumor Microenvironment
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-16-0011
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