Homologous Recombination Repair Deficiency and the Immune Response in Breast Cancer: A Literature Review

Other authors

Institut Català de la Salut

[Pellegrino B, Musolino A] Medical Oncology and Breast Unit, University Hospital of Parma, Parma, Italy. [Llop-Guevara A, Serra V] Experimental Therapeutics Group, Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain. [De Silva P] Molecular Immunology Unit, Institut Jules Bordet and Universite Libre de Bruxelles, Bruxelles, Belgium. [Hlavata Z] Medical Oncology Department, CHR Mons-Hainaut, Mons, Belgium

Vall d'Hebron Barcelona Hospital Campus

Publication date

2021-10-27T12:55:34Z

2021-10-27T12:55:34Z

2019

2020-02-01



Abstract

Càncer de mama; Immunoteràpia; Danys en l’ADN


Cáncer de mama; Inmunoterapia; Daño en el ADN


Breast Cancer; Immunotherapy; DNA damage


The success of cancer immunotherapy with immune checkpoint blockade (ICB) has demonstrated the importance of targeting a preexisting immune response in a broad spectrum of tumors. This is particularly novel and relevant for less immunogenic tumors, such as breast cancer (BC), where the efficacy of ICB was more evident in the triple-negative (TNBC) subtype, in earlier stages, and in association with chemotherapy. Tumors harboring homologous recombination DNA repair (HRR) deficiency (HRD) are supposed to have a higher number of mutations, hence a higher tumor mutational burden, which could potentially make them more sensitive to immunotherapy. However, the mechanisms involved in ICB sensitivity and patient selection are still yet to be defined in BC: whether the innate system could play a role and how the adaptive immunity could be linked with HRR pathways are the two key points of debate that we will discuss in this article. The aim of this review was to close the loop between what was found in clinical trial results so far, go back to laboratory theory and preclinical results and point out what needs to be clarified from now on.


B.P. was supported by European Society of Medical Oncology ( ESMO) with the aid of a grant from Roche.

Document Type

Article


Published version

Language

English

Publisher

Elsevier

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Attribution-NonCommercial-NoDerivatives 4.0 International

http://creativecommons.org/licenses/by-nc-nd/4.0/

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