Abstract:
:The loss-of-function mutation of formyl peptide receptor 1 (FPR1) has a negative impact on the progression-free and overall survival of breast cancer patients treated with anthracycline-based adjuvant chemotherapy. This effect may be attributed to the fact that chemotherapy-induced antitumor immunity requires FPR1 and that such anticancer immune responses are responsible for the long-term effects of chemotherapy. Here, we investigated the possible contribution of FPR1 to the efficacy of a combination of mitoxantrone (MTX) and cyclophosphamide (CTX) for the treatment of hormone-induced breast cancer. Breast cancer induced by a combination of medroxyprogesterone acetate (MPA) and 7,12-Dimethylbenz[a]anthracene (DMBA) could be successfully treated with MTX plus CTX in thus far that tumor growth was retarded and overall survival was extended (as compared to vehicle-only treated controls). However, the therapeutic efficacy of the combination therapy was completely abolished when FPR1 receptors were blocked by means of cyclosporin H (CsH). Future genetic studies on neoadjuvant chemotherapy-treated breast cancers are warranted to validate these findings at the clinical level.
journal_name
Oncoimmunologyjournal_title
Oncoimmunologyauthors
Baracco EE,Pietrocola F,Buqué A,Bloy N,Senovilla L,Zitvogel L,Vacchelli E,Kroemer Gdoi
10.1080/2162402X.2016.1139275subject
Has Abstractpub_date
2016-02-18 00:00:00pages
e1139275issue
6eissn
2162-4011issn
2162-402Xpii
1139275journal_volume
5pub_type
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