دورية أكاديمية
Reversing an Oncogenic Epithelial-to-Mesenchymal Transition Program in Breast Cancer Reveals Actionable Immune Suppressive Pathways.
العنوان: | Reversing an Oncogenic Epithelial-to-Mesenchymal Transition Program in Breast Cancer Reveals Actionable Immune Suppressive Pathways. |
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المؤلفون: | Williams MM; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA., Hafeez SA; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA., Christenson JL; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA., O'Neill KI; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA., Hammond NG; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA., Richer JK; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. |
المصدر: | Pharmaceuticals (Basel, Switzerland) [Pharmaceuticals (Basel)] 2021 Nov 02; Vol. 14 (11). Date of Electronic Publication: 2021 Nov 02. |
نوع المنشور: | Journal Article; Review |
اللغة: | English |
بيانات الدورية: | Publisher: MDPI Country of Publication: Switzerland NLM ID: 101238453 Publication Model: Electronic Cited Medium: Print ISSN: 1424-8247 (Print) Linking ISSN: 14248247 NLM ISO Abbreviation: Pharmaceuticals (Basel) Subsets: PubMed not MEDLINE |
أسماء مطبوعة: | Original Publication: Basel, Switzerland : MDPI, c2004- |
مستخلص: | Approval of checkpoint inhibitors for treatment of metastatic triple negative breast cancer (mTNBC) has opened the door for the use of immunotherapies against this disease. However, not all patients with mTNBC respond to current immunotherapy approaches such as checkpoint inhibitors. Recent evidence demonstrates that TNBC metastases are more immune suppressed than primary tumors, suggesting that combination or additional immunotherapy strategies may be required to activate an anti-tumor immune attack at metastatic sites. To identify other immune suppressive mechanisms utilized by mTNBC, our group and others manipulated oncogenic epithelial-to-mesenchymal transition (EMT) programs in TNBC models to reveal differences between this breast cancer subtype and its more epithelial counterpart. This review will discuss how EMT modulation revealed several mechanisms, including tumor cell metabolism, cytokine milieu and secretion of additional immune modulators, by which mTNBC cells may suppress both the innate and adaptive anti-tumor immune responses. Many of these pathways/proteins are under preclinical or clinical investigation as therapeutic targets in mTNBC and other advanced cancers to enhance their response to chemotherapy and/or checkpoint inhibitors. |
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معلومات مُعتمدة: | T32 CA190216 United States CA NCI NIH HHS; F32CA239436 United States NH NIH HHS; T32CA190216 United States NH NIH HHS; W81XWH-15-1-0039 United States Department of Defense; W81XWH-19-BCRP-EA United States Department of Defense; F32 CA239436 United States CA NCI NIH HHS |
فهرسة مساهمة: | Keywords: epithelial-to-mesenchymal transition; immune suppression; immunotherapy; metastasis; triple negative breast cancer |
تواريخ الأحداث: | Date Created: 20211127 Latest Revision: 20211201 |
رمز التحديث: | 20240628 |
مُعرف محوري في PubMed: | PMC8622696 |
DOI: | 10.3390/ph14111122 |
PMID: | 34832904 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1424-8247 |
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DOI: | 10.3390/ph14111122 |