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Article ; Online: Inflammatory fibroblasts make rectal cancer resistant to radiation therapy.

Mhaidly, Rana / Mechta-Grigoriou, Fatima

2022 Volume 40, Issue 2, Page(s) 122–124

Abstract: Colorectal cancer (CRC) is one of the most prevalent cancers worldwide. Still, the molecular mechanisms that drive CRC therapy resistance are incompletely understood. In this issue of Cancer Cell, Nicolas et al. combine several approaches to unravel a ... ...

Abstract	Colorectal cancer (CRC) is one of the most prevalent cancers worldwide. Still, the molecular mechanisms that drive CRC therapy resistance are incompletely understood. In this issue of Cancer Cell, Nicolas et al. combine several approaches to unravel a critical role for inflammatory cancer-associated fibroblasts (iCAFs) and interleukin 1α (IL1α) signaling in radiotherapy resistance.
MeSH term(s)	Cancer-Associated Fibroblasts ; Fibroblasts ; Humans ; Rectal Neoplasms/radiotherapy
Language	English
Publishing date	2022-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2022.01.005
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Zs.A 5650: 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: Tumor Cells and Cancer-Associated Fibroblasts: An Updated Metabolic Perspective.

Gentric, Géraldine / Mechta-Grigoriou, Fatima

Cancers

2021 Volume 13, Issue 3

Abstract: During the past decades, metabolism and redox imbalance have gained considerable attention in the cancer field. In addition to the well-known Warburg effect occurring in tumor cells, numerous other metabolic deregulations have now been reported. Indeed, ... ...

Abstract	During the past decades, metabolism and redox imbalance have gained considerable attention in the cancer field. In addition to the well-known Warburg effect occurring in tumor cells, numerous other metabolic deregulations have now been reported. Indeed, metabolic reprograming in cancer is much more heterogeneous than initially thought. In particular, a high diversity of carbon sources used by tumor cells has now been shown to contribute to this metabolic heterogeneity in cancer. Moreover, the molecular mechanisms newly highlighted are multiple and shed light on novel actors. Furthermore, the impact of this metabolic heterogeneity on tumor microenvironment has also been an intense subject of research recently. Here, we will describe the new metabolic pathways newly uncovered in tumor cells. We will also have a particular focus on Cancer-Associated Fibroblasts (CAF), whose identity, function and metabolism have been recently under profound investigation. In that sense, we will discuss about the metabolic crosstalk between tumor cells and CAF.
Language	English
Publishing date	2021-01-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13030399
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Article ; Online: Role of cancer-associated fibroblast subpopulations in immune infiltration, as a new means of treatment in cancer.

Mhaidly, Rana / Mechta-Grigoriou, Fatima

Immunological reviews

2021 Volume 302, Issue 1, Page(s) 259–272

Abstract: The tumor microenvironment (TME) has been identified as one of the driving factors of tumor progression and invasion. Within this microenvironment, cancer-associated fibroblasts (CAF) have multiple tumor-promoting functions and play key roles in drug ... ...

Abstract	The tumor microenvironment (TME) has been identified as one of the driving factors of tumor progression and invasion. Within this microenvironment, cancer-associated fibroblasts (CAF) have multiple tumor-promoting functions and play key roles in drug resistance, through multiple mechanisms, including extracellular matrix (ECM) remodeling, production of growth factors, cytokines, and chemokines, and modulation of metabolism and angiogenesis. More recently, a growing body of evidence has shown that CAF also modulate immune cell activity and suppress anti-tumor immune response. In this review, we describe the current knowledge on CAF heterogeneity in terms of identity and functions. Moreover, we analyze how distinct CAF subpopulations differentially interact with immune cells, with a particular focus on T lymphocytes. We address how specific CAF subsets contribute to cancer progression through induction of an immunosuppressive microenvironment. Finally, we highlight potential therapeutic strategies for targeting CAF subpopulations in cancer.
MeSH term(s)	Cancer-Associated Fibroblasts ; Humans ; Neoplasms/therapy ; T-Lymphocytes ; Tumor Microenvironment
Language	English
Publishing date	2021-05-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.12978
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Article ; Online: Fibroblast heterogeneity in tumor micro-environment: Role in immunosuppression and new therapies.

Mhaidly, Rana / Mechta-Grigoriou, Fatima

Seminars in immunology

2020 Volume 48, Page(s) 101417

Abstract: In tumors, Cancer-Associated Fibroblasts (CAFs) constitute the most prominent component of the tumor microenvironment (TME). CAFs are heterogeneous and composed of different CAF subsets exerting distinct functions in tumors. Specific CAF subpopulations ... ...

Abstract	In tumors, Cancer-Associated Fibroblasts (CAFs) constitute the most prominent component of the tumor microenvironment (TME). CAFs are heterogeneous and composed of different CAF subsets exerting distinct functions in tumors. Specific CAF subpopulations actively influence various aspects of tumor growth, including cancer cell survival and proliferation, angiogenesis, extracellular matrix (ECM) remodeling, metastatic spread and chemoresistance. During the past decade, some CAF subsets have also been shown to modulate anti-tumor immune response. Indeed, they can increase the content in regulatory T lymphocytes and inhibit the activity of effector and cytotoxic immune cells. These functions are mainly controlled by their constitutive secretion of cytokines, chemokines, growth factors and ECM proteins, either directly in the surrounding extracellular space or through micro-vesicles. Some CAFs also express key regulators of immune checkpoints. The different roles played by CAFs, both as immunosuppressor or as physical support for tumor cell progression, set them as promising targets for anti-tumor therapies. In this review, we describe the main current knowledge on CAFs heterogeneity and immunosuppressive microenvironment, as well as their potential therapeutic implications.
MeSH term(s)	Animals ; Cancer-Associated Fibroblasts/physiology ; Cell- and Tissue-Based Therapy ; Fibroblasts/physiology ; Humans ; Immune Tolerance ; Macrophages/immunology ; Neoplasms/immunology ; Neoplasms/therapy ; T-Lymphocytes, Regulatory/immunology ; Tumor Microenvironment
Language	English
Publishing date	2020-10-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1018141-6
ISSN	1096-3618 ; 1044-5323
ISSN (online)	1096-3618
ISSN	1044-5323
DOI	10.1016/j.smim.2020.101417
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Article ; Online: Fibroblast heterogeneity in solid tumors: From single cell analysis to whole-body imaging.

Peltier, Agathe / Seban, Romain-David / Buvat, Irène / Bidard, François-Clément / Mechta-Grigoriou, Fatima

Seminars in cancer biology

2022 Volume 86, Issue Pt 3, Page(s) 262–272

Abstract: Cancer-Associated Fibroblasts (CAFs) represent the most prominent component of the tumor microenvironment (TME). Recent studies demonstrated that CAF are heterogeneous and composed of different subpopulations exerting distinct functions in cancer. CAF ... ...

Abstract	Cancer-Associated Fibroblasts (CAFs) represent the most prominent component of the tumor microenvironment (TME). Recent studies demonstrated that CAF are heterogeneous and composed of different subpopulations exerting distinct functions in cancer. CAF populations differentially modulate various aspects of tumor growth, including cancer cell proliferation, extra-cellular matrix remodeling, metastatic dissemination, immunosuppression and resistance to treatment. Among other markers, the Fibroblast Activation Protein (FAP) led to the identification of a specific CAF subpopulation involved in metastatic spread and immunosuppression. Expression of FAP at the surface of CAF is detected in many different cancer types of poor prognosis. Thus, FAP recently appears as an appealing target for therapeutic and molecular imaging applications. In that context,
MeSH term(s)	Humans ; Gelatinases/metabolism ; Positron Emission Tomography Computed Tomography/methods ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism ; Single-Cell Analysis ; Whole Body Imaging ; Membrane Proteins/metabolism ; Neoplasms/diagnostic imaging ; Neoplasms/metabolism ; Fibroblasts/metabolism ; Tumor Microenvironment
Chemical Substances	Gelatinases (EC 3.4.24.-) ; Serine Endopeptidases (EC 3.4.21.-) ; Membrane Proteins
Language	English
Publishing date	2022-04-27
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2022.04.008
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Zs.A 2922: Show issues

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Article ; Online: YAP/TEAD involvement in resistance to paclitaxel chemotherapy in lung cancer.

Brosseau, S / Abreu, P / Bouchez, C / Charon, L / Kieffer, Y / Gentric, G / Picant, V / Veith, I / Camonis, J / Descroix, S / Mechta-Grigoriou, F / Parrini, M C / Zalcman, G

Molecular and cellular biochemistry

2024

Abstract: The Yes-associated protein (YAP) oncoprotein has been linked to both metastases and resistance to targeted therapy of lung cancer cells. We aimed to investigate the effect of YAP pharmacological inhibition, using YAP/TEA domain (TEAD) transcription ... ...

Abstract	The Yes-associated protein (YAP) oncoprotein has been linked to both metastases and resistance to targeted therapy of lung cancer cells. We aimed to investigate the effect of YAP pharmacological inhibition, using YAP/TEA domain (TEAD) transcription factor interaction inhibitors in chemo-resistant lung cancer cells. YAP subcellular localization, as a readout for YAP activation, cell migration, and TEAD transcription factor functional transcriptional activity were investigated in cancer cell lines with up-regulated YAP, with and without YAP/TEAD interaction inhibitors. Parental (A549) and paclitaxel-resistant (A549R) cell transcriptomes were analyzed. The half-maximal inhibitory concentration (IC
Language	English
Publishing date	2024-03-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-024-04949-7
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Article ; Online: Le traitement antioxydant protège contre l’emphysème mais favorise la survenue et la progression du cancer du poumon.

Breau, Marielle / Bernard, David / Mechta-Grigoriou, Fatima / Adnot, Serge

Medecine sciences : M/S

2020 Volume 36, Issue 3, Page(s) 200–203

Title translation	Antioxidant treatment promotes lung cancer while protecting against lung emphysema.
MeSH term(s)	Acetylcysteine/adverse effects ; Acetylcysteine/therapeutic use ; Animals ; Antioxidants/adverse effects ; Antioxidants/therapeutic use ; Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Cellular Senescence/drug effects ; Cellular Senescence/genetics ; Cytoprotection/drug effects ; Cytoprotection/genetics ; Humans ; Lung/cytology ; Lung/drug effects ; Lung/metabolism ; Lung Neoplasms/chemically induced ; Lung Neoplasms/genetics ; Mice ; Mice, Knockout ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/physiology ; Pulmonary Emphysema/prevention & control
Chemical Substances	Antioxidants ; JunD protein, human ; Proto-Oncogene Proteins c-jun ; junD protein, mouse ; Acetylcysteine (WYQ7N0BPYC)
Language	French
Publishing date	2020-03-31
Publishing country	France
Document type	News
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2020030
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Zs.B 2872: Show issues

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Article ; Online: Ants detect cancer cells through volatile organic compounds.

Piqueret, Baptiste / Bourachot, Brigitte / Leroy, Chloé / Devienne, Paul / Mechta-Grigoriou, Fatima / d'Ettorre, Patrizia / Sandoz, Jean-Christophe

iScience

2022 Volume 25, Issue 3, Page(s) 103959

Abstract: Cancer is among the world's leading causes of death. A critical challenge for public health is to develop a noninvasive, inexpensive, and efficient tool for early cancer detection. Cancer cells are characterized by an altered metabolism, producing unique ...

Abstract	Cancer is among the world's leading causes of death. A critical challenge for public health is to develop a noninvasive, inexpensive, and efficient tool for early cancer detection. Cancer cells are characterized by an altered metabolism, producing unique patterns of volatile organic compounds (VOCs) that can be used as cancer biomarkers. Dogs can detect VOCs via olfactory associative learning, but training dogs is costly and time-consuming. Insects, such as ants, have a refined sense of smell and can be rapidly trained. We show that individual ants need only a few training trials to learn, memorize, and reliably detect the odor of human cancer cells. These performances rely on specific VOC patterns, as shown by gas chromatography/mass spectrometry. Our findings suggest that using ants as living tools to detect biomarkers of human cancer is feasible, fast, and less laborious than using other animals.
Language	English
Publishing date	2022-02-22
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.103959
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Article ; Online: Des pistes de réflexion pour la recherche sur l’endométriose en France.

Rosenbaum, Jean / Bourdel, Nicolas / Khochbin, Saadi / Kvaskoff, Marina / Matsuzaki, Sachiko / Mechta-Grigoriou, Fatima / Pluchino, Nicola / Sandra, Olivier / Vaiman, Daniel

Medecine sciences : M/S

2022 Volume 38, Issue 3, Page(s) 274–279

Abstract: Endometriosis is a chronic disease in which lesions resembling endometrial tissue are found outside the uterus, mainly in the pelvis or abdomen. It may affect 10% of women of childbearing age. It is the cause of a significant alteration in quality of ... ...

Title translation	Avenues of reflection for endometriosis research in France.
Abstract	Endometriosis is a chronic disease in which lesions resembling endometrial tissue are found outside the uterus, mainly in the pelvis or abdomen. It may affect 10% of women of childbearing age. It is the cause of a significant alteration in quality of life and a major cost to the health system. Few research teams are working on this subject, and its pathophysiology is still poorly understood. This article proposes avenues of reflection for research on endometriosis in France, notably based on the mobilization of related scientific communities (involved in cancer, development, epigenetics, and neurosciences research studies).
MeSH term(s)	Endometriosis/genetics ; Endometriosis/pathology ; Endometrium/pathology ; Endometrium/physiology ; Epigenesis, Genetic ; Female ; Humans ; Quality of Life ; Uterus
Language	French
Publishing date	2022-03-25
Publishing country	France
Document type	Journal Article
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2022027
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Article ; Online: Deciphering the spatial landscape and plasticity of immunosuppressive fibroblasts in breast cancer.

Croizer, Hugo / Mhaidly, Rana / Kieffer, Yann / Gentric, Geraldine / Djerroudi, Lounes / Leclere, Renaud / Pelon, Floriane / Robley, Catherine / Bohec, Mylene / Meng, Arnaud / Meseure, Didier / Romano, Emanuela / Baulande, Sylvain / Peltier, Agathe / Vincent-Salomon, Anne / Mechta-Grigoriou, Fatima

Nature communications

2024 Volume 15, Issue 1, Page(s) 2806

Abstract: Although heterogeneity of FAP+ Cancer-Associated Fibroblasts (CAF) has been described in breast cancer, their plasticity and spatial distribution remain poorly understood. Here, we analyze trajectory inference, deconvolute spatial transcriptomics at ... ...

Abstract	Although heterogeneity of FAP+ Cancer-Associated Fibroblasts (CAF) has been described in breast cancer, their plasticity and spatial distribution remain poorly understood. Here, we analyze trajectory inference, deconvolute spatial transcriptomics at single-cell level and perform functional assays to generate a high-resolution integrated map of breast cancer (BC), with a focus on inflammatory and myofibroblastic (iCAF/myCAF) FAP+ CAF clusters. We identify 10 spatially-organized FAP+ CAF-related cellular niches, called EcoCellTypes, which are differentially localized within tumors. Consistent with their spatial organization, cancer cells drive the transition of detoxification-associated iCAF (Detox-iCAF) towards immunosuppressive extracellular matrix (ECM)-producing myCAF (ECM-myCAF) via a DPP4- and YAP-dependent mechanism. In turn, ECM-myCAF polarize TREM2+ macrophages, regulatory NK and T cells to induce immunosuppressive EcoCellTypes, while Detox-iCAF are associated with FOLR2+ macrophages in an immuno-protective EcoCellType. FAP+ CAF subpopulations accumulate differently according to the invasive BC status and predict invasive recurrence of ductal carcinoma in situ (DCIS), which could help in identifying low-risk DCIS patients eligible for therapeutic de-escalation.
MeSH term(s)	Humans ; Female ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Carcinoma, Intraductal, Noninfiltrating/pathology ; Fibroblasts/pathology ; Cancer-Associated Fibroblasts/pathology ; Extracellular Matrix/pathology ; Tumor Microenvironment ; Folate Receptor 2
Chemical Substances	FOLR2 protein, human ; Folate Receptor 2
Language	English
Publishing date	2024-04-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-47068-z
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