Epithelial Mesenchymal Transition and Immune Response in Metaplastic Breast Carcinoma

Altres autors/es

Institut Català de la Salut

[González-Martínez S] Clinical Researcher, Hospital Ramón y Cajal, 28034 Madrid, Spain. [Pérez-Mies B, Palacios J] Department of Pathology, Hospital Ramón y Cajal, 28034 Madrid, Spain. Institute Ramón y Cajal for Health Research (IRYCIS), 28034 Madrid, Spain. CIBER-ONC, Instituto de Salud Carlos III, 28029 Madrid, Spain. Faculty of Medicine, University of Alcalá de Henares, Alcalá de Henares, 28801 Madrid, Spain. [Pizarro D, Caniego-Casas T] Institute Ramón y Cajal for Health Research (IRYCIS), 28034 Madrid, Spain. [Cortés J] CIBER-ONC, Instituto de Salud Carlos III, 28029 Madrid, Spain. Faculty of Biomedical and Health Sciences, Department of Medicine, Universidad Europea de Madrid, 28670 Madrid, Spain. International Breast Cancer Center (IBCC), Quironsalud Group, 08017 Barcelona, Spain. Medica Scientia Innovation Research, 08007 Barcelona, Spain. Medica Scientia Innovation Research, Ridgewood, NJ 07450, USA. Vall d’Hebron Institute of Oncology (VHIO), Barcelona, Spain

Vall d'Hebron Barcelona Hospital Campus

Data de publicació

2022-01-31T11:03:01Z

2022-01-31T11:03:01Z

2021-07



Resum

Transició epitelial-mesenquimal; Carcinoma de mama metaplàstic


Transición epitelio-mesenquimatosa; Carcinoma de mama metaplasico


Epithelial-mesenchymal transition; Metaplastic breast carcinoma


Metaplastic breast carcinoma (MBC) is a heterogeneous group of infrequent triple negative (TN) invasive carcinomas with poor prognosis. MBCs have a different clinical behavior from other types of triple negative breast cancer (TNBC), being more resistant to standard chemotherapy. MBCs are an example of tumors with activation of epithelial–mesenchymal transition (EMT). The mechanisms involved in EMT could be responsible for the increase in the infiltrative and metastatic capacity of MBCs and resistance to treatments. In addition, a relationship between EMT and the immune response has been seen in these tumors. In this sense, MBC differ from other TN tumors showing a lower number of tumor-infiltrating lymphocytes (TILS) and a higher percentage of tumor cells expressing programmed death-ligand 1 (PD-L1). A better understanding of the relationship between the immune system and EMT could provide new therapeutic approaches in MBC.


This review was funded by grants from the Instituto de Salud Carlos III (ISCIII) (PI19/01331) and CIBERONC (CB16/12/00316 and CB16/12/00449), co-financed by the European Development Regional Fund. ‘A way to achieve Europe’ (FEDER), and by the Spanish Association Against Cancer Scientific Foundation (Grupos Coordinados Traslacionales aecc 2018).

Tipus de document

Article


Versió publicada

Llengua

Anglès

Publicat per

MDPI

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