![colony survival galena colony survival galena](https://i.ytimg.com/vi/CNepzxnkWZs/maxresdefault.jpg)
Balancing immune response: crosstalk between adaptive and innate immune cells during breast cancer progression. Abstract 2859: inhibition of PD-L1 by MPD元280A leads to clinical activity in patients with metastatic triple-negative breast cancer (TNBC). Atezolizumab and nab-paclitaxel in advanced triple-negative breast cancer.
![colony survival galena colony survival galena](https://cdn.shopify.com/s/files/1/0425/8001/7316/files/Finished-Infographic.png)
Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/ 2 mutation. Olaparib for metastatic breast cancer in patients with a germline BRCA mutation. Talazoparib in patients with advanced breast cancer and a germline BRCA mutation.
#Colony survival galena series
Frequency of germline mutations in 25 cancer susceptibility genes in a sequential series of patients with breast cancer.
![colony survival galena colony survival galena](https://igg-games.com/wp-content/uploads/2018/12/Colony-Survival-PC-Crack.jpg)
BRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair. OlympiAD final overall survival and tolerability results: olaparib versus chemotherapy treatment of physician’s choice in patients with a germline BRCA mutation and HER2-negative metastatic breast cancer. Collectively, our results uncover macrophage-mediated immune suppression as a liability of PARP inhibitor treatment and demonstrate that combined PARP inhibition and macrophage-targeting therapy induces a durable reprogramming of the tumor microenvironment (TME), thus constituting a promising therapeutic strategy for TNBC. Combining PARP inhibitor therapy with colony-stimulating factor 1 receptor (CSF1R)-blocking antibodies significantly enhanced innate and adaptive antitumor immunity and extended survival in mice with BRCA-deficient tumors in vivo, and this was mediated by CD8 + T cells. Through multi-omics profiling, we show that PARP inhibitors enhance both anti- and pro-tumor features of macrophages through glucose and lipid metabolic reprogramming, driven by the sterol regulatory element-binding protein 1 (SREBF1, SREBP1) pathway. Using high-dimensional single-cell profiling of human TNBC, here we demonstrate that macrophages are the predominant infiltrating immune cell type in breast cancer susceptibility (BRCA)-associated TNBC. Nature Cancer volume 2, pages 66–82 ( 2021) Cite this articleĭespite objective responses to poly(ADP-ribose) polymerase (PARP) inhibition and improvements in progression-free survival (PFS) compared to standard chemotherapy in patients with BRCA-associated triple-negative breast cancer (TNBC), benefits are transitory. Targeting immunosuppressive macrophages overcomes PARP inhibitor resistance in BRCA1-associated triple-negative breast cancer