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Article ; Online: Effects of Estrogens on Osteoimmunology: A Role in Bone Metastasis.

Marie, Julien C / Bonnelye, Edith

2022 Volume 13, Page(s) 899104

Abstract: Bone loss associated with estrogen deficiency indicates a fundamental role of these hormones in skeletal growth and bone remodeling. In the last decades, growing recent evidence demonstrated that estrogens can also affect the immune compartment of the ... ...

Abstract	Bone loss associated with estrogen deficiency indicates a fundamental role of these hormones in skeletal growth and bone remodeling. In the last decades, growing recent evidence demonstrated that estrogens can also affect the immune compartment of the bone. In this review, we summarize the impacts of estrogens on bone immune cells and their consequences on bone homeostasis, metastasis settlement into the bone and tumor progression. We also addressed the role of an orphan nuclear receptor ERRalpha ("Estrogen-receptor Related Receptor alpha") on macrophages and T lymphocytes, and as an immunomodulator in bone metastases. Hence, this review links estrogens to bone immune cells in osteo-oncology.
MeSH term(s)	Bone Neoplasms ; Bone Remodeling ; Bone and Bones ; Estrogens ; Humans ; Immunologic Factors
Chemical Substances	Estrogens ; Immunologic Factors
Language	English
Publishing date	2022-05-23
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.899104
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Article: Targeting Bone Metastasis in Cancers.

Bonnelye, Edith / Juárez, Patricia

Cancers

2021 Volume 13, Issue 17

Abstract: This Special Issue ... ...

Abstract	This Special Issue of
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13174490
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Article ; Online: An energetic orphan in an endocrine tissue: a revised perspective of the function of estrogen receptor-related receptor alpha in bone and cartilage.

Bonnelye, Edith / Aubin, Jane E

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2013 Volume 28, Issue 2, Page(s) 225–233

Abstract: Estrogen receptor-related receptor alpha (ERRα) is an orphan nuclear receptor with sequence homology to the estrogen receptors, ERα/β, but it does not bind estrogen. ERRα not only plays a functional role in osteoblasts but also in osteoclasts and ... ...

Abstract	Estrogen receptor-related receptor alpha (ERRα) is an orphan nuclear receptor with sequence homology to the estrogen receptors, ERα/β, but it does not bind estrogen. ERRα not only plays a functional role in osteoblasts but also in osteoclasts and chondrocytes. In addition, the ERRs, including ERRα, can be activated by coactivators such as peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC1α and β) and are implicated in adipogenesis, fatty acid oxidation, and oxidative stress defense, suggesting that ERRα-through its activity in bone resorption and adipogenesis--may regulate the insulin and leptin pathways and contribute to aging-related changes in bone and cartilage. In this review, we discuss data on ERRα and its cellular and molecular modes of action, which have broad implications for considering the potential role of this orphan receptor in cartilage and bone endocrine function, on whole-organism physiology, and in the bone aging process.
MeSH term(s)	Adipogenesis ; Animals ; Bone and Bones/metabolism ; Cartilage/metabolism ; Endocrine System/metabolism ; Glucose/metabolism ; Humans ; Receptors, Estrogen/metabolism ; ERRalpha Estrogen-Related Receptor
Chemical Substances	Receptors, Estrogen ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2013-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.1836
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Article ; Online: Bone metastasis: mechanisms, therapies, and biomarkers.

Clézardin, Philippe / Coleman, Rob / Puppo, Margherita / Ottewell, Penelope / Bonnelye, Edith / Paycha, Frédéric / Confavreux, Cyrille B / Holen, Ingunn

Physiological reviews

2020 Volume 101, Issue 3, Page(s) 797–855

Abstract: Skeletal metastases are frequent complications of many cancers, causing bone complications (fractures, bone pain, disability) that negatively affect the patient's quality of life. Here, we first discuss the burden of skeletal complications in cancer bone ...

Abstract	Skeletal metastases are frequent complications of many cancers, causing bone complications (fractures, bone pain, disability) that negatively affect the patient's quality of life. Here, we first discuss the burden of skeletal complications in cancer bone metastasis. We then describe the pathophysiology of bone metastasis. Bone metastasis is a multistage process: long before the development of clinically detectable metastases, circulating tumor cells settle and enter a dormant state in normal vascular and endosteal niches present in the bone marrow, which provide immediate attachment and shelter, and only become active years later as they proliferate and alter the functions of bone-resorbing (osteoclasts) and bone-forming (osteoblasts) cells, promoting skeletal destruction. The molecular mechanisms involved in mediating each of these steps are described, and we also explain how tumor cells interact with a myriad of interconnected cell populations in the bone marrow, including a rich vascular network, immune cells, adipocytes, and nerves. We discuss metabolic programs that tumor cells could engage with to specifically grow in bone. We also describe the progress and future directions of existing bone-targeted agents and report emerging therapies that have arisen from recent advances in our understanding of the pathophysiology of bone metastases. Finally, we discuss the value of bone turnover biomarkers in detection and monitoring of progression and therapeutic effects in patients with bone metastasis.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Bone Density Conservation Agents/therapeutic use ; Bone Neoplasms/drug therapy ; Bone Neoplasms/metabolism ; Bone Neoplasms/secondary ; Bone and Bones/metabolism ; Bone and Bones/pathology ; Denosumab/therapeutic use ; Humans
Chemical Substances	Biomarkers ; Bone Density Conservation Agents ; Denosumab (4EQZ6YO2HI)
Language	English
Publishing date	2020-12-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00012.2019
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Article ; Online: The Chemokine Receptor CCR3 Is Potentially Involved in the Homing of Prostate Cancer Cells to Bone: Implication of Bone-Marrow Adipocytes.

Guérard, Adrien / Laurent, Victor / Fromont, Gaëlle / Estève, David / Gilhodes, Julia / Bonnelye, Edith / Le Gonidec, Sophie / Valet, Philippe / Malavaud, Bernard / Reina, Nicolas / Attané, Camille / Muller, Catherine

International journal of molecular sciences

2021 Volume 22, Issue 4

Abstract: Bone metastasis remains the most frequent and the deadliest complication of prostate cancer (PCa). Mechanisms leading to the homing of tumor cells to bone remain poorly characterized. Role of chemokines in providing navigational cues to migrating cancer ... ...

Abstract	Bone metastasis remains the most frequent and the deadliest complication of prostate cancer (PCa). Mechanisms leading to the homing of tumor cells to bone remain poorly characterized. Role of chemokines in providing navigational cues to migrating cancer cells bearing specific receptors is well established. Bone is an adipocyte-rich organ since 50 to 70% of the adult bone marrow (BM) volume comprise bone marrow adipocytes (BM-Ads), which are likely to produce chemokines within the bone microenvironment. Using in vitro migration assays, we demonstrated that soluble factors released by
MeSH term(s)	Adipocytes/metabolism ; Adipocytes/pathology ; Aging/pathology ; Bone Marrow/drug effects ; Bone Marrow/pathology ; Bone and Bones/drug effects ; Bone and Bones/pathology ; Cell Line, Tumor ; Chemokine CCL7/metabolism ; Chemotaxis/drug effects ; Culture Media, Conditioned/pharmacology ; Humans ; Male ; Neoplasm Metastasis ; Obesity/complications ; Prostatic Neoplasms/complications ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Receptors, CCR3/metabolism
Chemical Substances	Chemokine CCL7 ; Culture Media, Conditioned ; Receptors, CCR3
Language	English
Publishing date	2021-02-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22041994
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Article ; Online: Single-Cell RNA-Sequencing Reveals the Breadth of Osteoblast Heterogeneity.

Yoshioka, Hirotaka / Okita, Saki / Nakano, Masashi / Minamizaki, Tomoko / Nubukiyo, Asako / Sotomaru, Yusuke / Bonnelye, Edith / Kozai, Katsuyuki / Tanimoto, Kotaro / Aubin, Jane E / Yoshiko, Yuji

JBMR plus

2021 Volume 5, Issue 6, Page(s) e10496

Abstract: The current paradigm of osteoblast fate is that the majority undergo apoptosis, while some further differentiate into osteocytes and others flatten and cover bone surfaces as bone lining cells. Osteoblasts have been described to exhibit heterogeneous ... ...

Abstract	The current paradigm of osteoblast fate is that the majority undergo apoptosis, while some further differentiate into osteocytes and others flatten and cover bone surfaces as bone lining cells. Osteoblasts have been described to exhibit heterogeneous expression of a variety of osteoblast markers at both transcriptional and protein levels. To explore further this heterogeneity and its biological significance, Venus-positive (Venus
Language	English
Publishing date	2021-05-17
Publishing country	England
Document type	Journal Article
ISSN	2473-4039
ISSN (online)	2473-4039
DOI	10.1002/jbm4.10496
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Article ; Online: Integrin alpha5 in human breast cancer is a mediator of bone metastasis and a therapeutic target for the treatment of osteolytic lesions.

Pantano, Francesco / Croset, Martine / Driouch, Keltouma / Bednarz-Knoll, Natalia / Iuliani, Michele / Ribelli, Giulia / Bonnelye, Edith / Wikman, Harriet / Geraci, Sandra / Bonin, Florian / Simonetti, Sonia / Vincenzi, Bruno / Hong, Saw See / Sousa, Sofia / Pantel, Klaus / Tonini, Giuseppe / Santini, Daniele / Clézardin, Philippe

Oncogene

2021 Volume 40, Issue 7, Page(s) 1284–1299

Abstract: Bone metastasis remains a major cause of mortality and morbidity in breast cancer. Therefore, there is an urgent need to better select high-risk patients in order to adapt patient's treatment and prevent bone recurrence. Here, we found that integrin ... ...

Abstract	Bone metastasis remains a major cause of mortality and morbidity in breast cancer. Therefore, there is an urgent need to better select high-risk patients in order to adapt patient's treatment and prevent bone recurrence. Here, we found that integrin alpha5 (ITGA5) was highly expressed in bone metastases, compared to lung, liver, or brain metastases. High ITGA5 expression in primary tumors correlated with the presence of disseminated tumor cells in bone marrow aspirates from early stage breast cancer patients (n = 268; p = 0.039). ITGA5 was also predictive of poor bone metastasis-free survival in two separate clinical data sets (n = 855, HR = 1.36, p = 0.018 and n = 427, HR = 1.62, p = 0.024). This prognostic value remained significant in multivariate analysis (p = 0.028). Experimentally, ITGA5 silencing impaired tumor cell adhesion to fibronectin, migration, and survival. ITGA5 silencing also reduced tumor cell colonization of the bone marrow and formation of osteolytic lesions in vivo. Conversely, ITGA5 overexpression promoted bone metastasis. Pharmacological inhibition of ITGA5 with humanized monoclonal antibody M200 (volociximab) recapitulated inhibitory effects of ITGA5 silencing on tumor cell functions in vitro and tumor cell colonization of the bone marrow in vivo. M200 also markedly reduced tumor outgrowth in experimental models of bone metastasis or tumorigenesis, and blunted cancer-associated bone destruction. ITGA5 was not only expressed by tumor cells but also osteoclasts. In this respect, M200 decreased human osteoclast-mediated bone resorption in vitro. Overall, this study identifies ITGA5 as a mediator of breast-to-bone metastasis and raises the possibility that volociximab/M200 could be repurposed for the treatment of ITGA5-positive breast cancer patients with bone metastases.
MeSH term(s)	Aged ; Antibodies, Monoclonal/administration & dosage ; Bone Neoplasms/drug therapy ; Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Bone Neoplasms/secondary ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Adhesion/drug effects ; Cell Adhesion/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Integrins/genetics ; Kaplan-Meier Estimate ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology ; Osteolysis/genetics ; Progression-Free Survival
Chemical Substances	Antibodies, Monoclonal ; ITGA5 protein, human ; Integrins ; volociximab (496K5Z02NW)
Language	English
Publishing date	2021-01-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01603-6
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Article: In vivo phosphoantigen levels in bisphosphonate-treated human breast tumors trigger Vγ9Vδ2 T-cell antitumor cytotoxicity through ICAM-1 engagement.

Benzaïd, Ismahène / Mönkkönen, Hannu / Bonnelye, Edith / Mönkkönen, Jukka / Clézardin, Philippe

Clinical cancer research : an official journal of the American Association for Cancer Research

2012 Volume 18, Issue 22, Page(s) 6249–6259

Abstract: Purpose: Nitrogen-containing bisphosphonates (N-BP) such as zoledronate and risedronate exhibit antitumor effects. They block the activity of farnesyl pyrophosphate synthase (FPPS) in the mevalonate pathway, leading to intracellular accumulation of ... ...

Abstract	Purpose: Nitrogen-containing bisphosphonates (N-BP) such as zoledronate and risedronate exhibit antitumor effects. They block the activity of farnesyl pyrophosphate synthase (FPPS) in the mevalonate pathway, leading to intracellular accumulation of mevalonate metabolites (IPP/ApppI), which are recognized as tumor phosphoantigens by Vγ9Vδ2 T cells. However, mechanisms responsible for Vγ9Vδ2 T-cell recognition of N-BP-treated tumors producing IPP/ApppI remain unclear. Experimental design: The effects of N-BPs on Vγ9Vδ2 T-cell expansion and anticancer activity were evaluated in vitro and in animal models of human breast cancers. The modalities of recognition of breast tumors by Vγ9Vδ2 T cells in N-BP-treated animals were also examined. Results: We found a strong correlation between Vγ9Vδ2 T-cell anticancer activity and intracellular accumulation of IPP/ApppI in risedronate-treated breast cancer cells in vitro. In addition, following risedronate treatment of immunodeficient mice bearing human breast tumors, human Vγ9Vδ2 T cells infiltrated and inhibited growth of tumors that produced high IPP/ApppI levels but not those expressing low IPP/ApppI levels. The combination of doxorubicin with a N-BP improved, however, Vγ9Vδ2 T-cell cytotoxicity against breast tumors expressing low IPP/ApppI levels. Moreover, Vγ9Vδ2 T-cell cytotoxicity in mice treated with risedronate or zoledronate did not only depend on IPP/ApppI accumulation in tumors but also on expression of tumor cell surface receptor intercellular adhesion molecule-1 (ICAM-1), which triggered the recognition of N-BP-treated breast cancer cells by Vγ9Vδ2 T cells in vivo. Conclusion: These findings suggest that N-BPs can have an adjuvant role in cancer therapy by activating Vγ9Vδ2 T-cell cytotoxicity in patients with breast cancer that produces high IPP/ApppI levels after N-BP treatment.
MeSH term(s)	Animals ; Antigens, Neoplasm/immunology ; Antigens, Neoplasm/metabolism ; Antineoplastic Agents/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/immunology ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cytotoxicity, Immunologic/drug effects ; Etidronic Acid/analogs & derivatives ; Etidronic Acid/pharmacology ; Female ; Geranyltranstransferase/metabolism ; Hemiterpenes/immunology ; Hemiterpenes/metabolism ; Humans ; Immunologic Factors/pharmacology ; Intercellular Adhesion Molecule-1/metabolism ; Leukocytes, Mononuclear/drug effects ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Organophosphorus Compounds/immunology ; Organophosphorus Compounds/metabolism ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Risedronate Sodium ; T-Lymphocytes, Cytotoxic/drug effects ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Antigens, Neoplasm ; Antineoplastic Agents ; Hemiterpenes ; Immunologic Factors ; Organophosphorus Compounds ; Receptors, Antigen, T-Cell, gamma-delta ; Intercellular Adhesion Molecule-1 (126547-89-5) ; isopentenyl pyrophosphate (358-71-4) ; Geranyltranstransferase (EC 2.5.1.10) ; Etidronic Acid (M2F465ROXU) ; Risedronate Sodium (OFG5EXG60L)
Language	English
Publishing date	2012-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-12-0918
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Article ; Online: TWIST1 expression in breast cancer cells facilitates bone metastasis formation.

Croset, Martine / Goehrig, Delphine / Frackowiak, Agnieszka / Bonnelye, Edith / Ansieau, Stéphane / Puisieux, Alain / Clézardin, Philippe

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2014 Volume 29, Issue 8, Page(s) 1886–1899

Abstract: The transcription factor TWIST1 induces epithelial-mesenchymal transition and/or escape to the oncogenic-induced failsafe program, facilitating the intravasation of breast cancer cells in the systemic circulation and their dissemination to the lungs. Its ...

Abstract	The transcription factor TWIST1 induces epithelial-mesenchymal transition and/or escape to the oncogenic-induced failsafe program, facilitating the intravasation of breast cancer cells in the systemic circulation and their dissemination to the lungs. Its involvement in breast cancer bone metastasis is unknown. To address this question, human osteotropic MDA-MB-231/B02 breast cancer cells were stably transfected with a Tet-inducible vector encoding for TWIST1, whose expression was specifically repressed in the presence of doxycycline (dox). The intra-arterial inoculation of transfectants expressing TWIST1 in immunodeficient mice substantially increased the extent of osteolytic lesions in these animals, being 50% larger than that of animals bearing mock-transfected tumors, as determined by radiography. This difference was accompanied by a sharp reduction of the bone volume (indicating a higher bone destruction) and a twofold increase in the tumor volume compared with mice bearing mock-transfected tumors, as determined by histomorphometry. Importantly, the suppression of TWIST1 expression in MDA-MB-231/B02 cells in the presence of dox abolished the stimulatory effect of TWIST1 on bone metastasis formation in vivo. Additionally, examination of the bone marrow from untreated and dox-treated animals on day 7 after tumor cell inoculation, at which time there was no evidence of radiographic osteolytic lesions, revealed that the number of tumor cell colonies that were recovered from the bone marrow of untreated mice was dramatically increased compared with that of dox-fed animals. In vitro, TWIST1 expression promoted tumor cell invasion and enhanced microRNA 10b (miR-10b) expression, a proinvasive factor, but was dispensable for growth of tumor cells. In vivo, the repression of miR-10b substantially decreased the presence of TWIST1-expressing breast cancer cells in the bone marrow. Overall, these results establish that TWIST1 facilitates breast cancer bone metastasis formation through a mechanism dependent of miR-10b, which leads to increase tumor burden and bone destruction.
MeSH term(s)	Animals ; Blotting, Western ; Bone Neoplasms/secondary ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Differentiation ; Cell Line, Tumor ; Doxycycline/pharmacology ; Female ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Mice, Inbred BALB C ; MicroRNAs/genetics ; Neoplasm Metastasis ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Osteoclasts/cytology ; Twist-Related Protein 1/genetics ; Twist-Related Protein 1/metabolism
Chemical Substances	MIRN10 microRNA, mouse ; MicroRNAs ; Nuclear Proteins ; TWIST1 protein, human ; Twist-Related Protein 1 ; Doxycycline (N12000U13O)
Language	English
Publishing date	2014-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.2215
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Article ; Online: ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response.

Bouchet, Mathilde / Lainé, Alexandra / Boyault, Cyril / Proponnet-Guerault, Mathilde / Meugnier, Emmanuelle / Bouazza, Lamia / Kan, Casina W S / Geraci, Sandra / El-Moghrabi, Soumaya / Hernandez-Vargas, Hector / Benetollo, Claire / Yoshiko, Yuji / Duterque-Coquillaud, Martine / Clézardin, Philippe / Marie, Julien C / Bonnelye, Edith

Cancer research

2020 Volume 80, Issue 13, Page(s) 2914–2926

Abstract: Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone ... ...

Abstract	Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal that ERRα inhibits the progression of bone metastases of breast cancer cells by increasing the immune activity of the bone microenvironment. Overexpression of ERRα in breast cancer bone metastases induced expression of chemokines CCL17 and CCL20 and repressed production of TGFβ3. Subsequently, CD8
MeSH term(s)	Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Bone Neoplasms/immunology ; Bone Neoplasms/metabolism ; Bone Neoplasms/prevention & control ; Bone Neoplasms/secondary ; Breast Neoplasms/immunology ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Breast Neoplasms/prevention & control ; Cell Proliferation ; Chemokine CCL17/genetics ; Chemokine CCL17/metabolism ; Chemokine CCL20/genetics ; Chemokine CCL20/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Prognosis ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Transforming Growth Factor beta3/genetics ; Transforming Growth Factor beta3/metabolism ; Tumor Cells, Cultured ; Tumor Microenvironment/immunology ; Xenograft Model Antitumor Assays ; ERRalpha Estrogen-Related Receptor
Chemical Substances	Biomarkers, Tumor ; CCL17 protein, human ; CCL20 protein, human ; Chemokine CCL17 ; Chemokine CCL20 ; Receptors, Estrogen ; TGFB3 protein, human ; Transforming Growth Factor beta3
Language	English
Publishing date	2020-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-19-3584
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