| Vol. 13.10 – 18 March, 2021 |
| |
|
|
| Researchers suggested that breast cancer–secreted factors may promote perturbed bone growth before metastasis, which could affect the initial seeding of tumor cells. [Science Advances] |
|
|
|
| PUBLICATIONSRanked by the impact factor of the journal |
|
|
|
| Scientists performed single-cell RNA sequencing on 82,122 cells isolated from the breast cancer tissues and adjacent or prophylactic normal breast tissues from four BRCA1 mutation carriers and three non-carriers. [Cancer Research] |
|
|
|
| Using breast cancer cell lines, human primary cultures of breast tumors, and immune deficient murine models, investigators demonstrated that the POU1F1 transcription factor was functionally and clinically related to both metabolic reprogramming in breast cancer cells and fibroblasts activation. [Oncogene] |
|
|
|
| Gain- and loss-of-function experiments were conducted to investigate the biological roles of circHIF1A in TNBC. Overexpression of circHIF1A significantly promoted TNBC growth and metastasis in vitro and in vivo, while knockdown of circHIF1A exerted the opposite effects. [Oncogene] |
|
|
|
| Researchers report that the levels of p97 positively correlated with the histological grade, tumor size, and lymph node metastasis in breast cancers. [Cell Death & Disease] |
|
|
|
| Investigators found that the expression of Rab26 was suppressed in the aggressive breast cancer cells as compared to the levels in non-invasive breast cancer cells. [Cell Death & Disease] |
|
|
|
| Researchers identified the deubiquitinase USP19 and demonstrated that its silencing reduced the migratory and invasive potential of highly invasive breast cancer cell lines. [Oncogenesis] |
|
|
|
| The authors investigated the therapeutic efficacy of OMO-1, a potent and selective c-MET inhibitor, in an immunocompetent intraductal mouse model for TNBC. [npj Breast Cancer] |
|
|
|
| Resistance to eribulin was evaluated in human epidermal growth factor receptor 2-negative (HER2–) breast cancer cell lines and patient-derived tumor xenografts, and correlated with a mutation in the phosphoinositide 3-kinase (PI3K)/AKT pathway. [British Journal of Cancer] |
|
|
|
| Investigators proposed that geminin overexpression in normal mammary epithelial cells promoted the generation of TNBC metastatic precursors that homed specifically to lungs by upregulating LGR5 expression and promoting stemness, intravasation, and extravasation in these precursors. [Cancer Gene Therapy] |
|
|
|
| Scientists found specific miRs were involved in the progression of breast cancer and explored the underlying molecular mechanism. [Molecular Therapy-Oncolytics] |
|
|
|
| Employing hormone-independent mammary cancer models, Gö6976 and all-trans-retinoic acid combined treatment induced a synergistic reduction in the proliferative potential that correlated with an increased apoptosis and retinoic acid receptors modulation towards an anti-oncogenic profile. [Scientific Reports] |
|
|
|
| The authors investigated the mechanisms by which CD73 might contribute to TNBC progression. This was done by inhibiting CD73 with adenosine 5′-(α, β-methylene) diphosphate in MDA-MB-231 or 4T1 TNBC cells or through shRNA-silencing. [Scientific Reports] |
|
|
|
|
| Scientists provide a conceptual framework focused on non-genetic heterogeneity, which has been intended to offer insight into the prediction, diagnosis, and treatment of breast cancer. [Breast Cancer] |
|
|
|
|
| Celcuity, Inc. announced a clinical trial collaboration with the MD Anderson Cancer Center, Novartis AG, and Puma Biotechnology, Inc., to conduct a Phase II clinical trial. This open-label Phase II trial will evaluate the efficacy and safety of two targeted therapies, TABRECTA® and NERLYNX® in patients with previously treated metastatic HER2-negative breast cancer. [Celcuity, Inc.] |
|
|
|
| PEP-Therapy and Institut Curie announced that they have been granted approval from the French National Agency for Medicines and Health Products (ANSM) to proceed with the first-in-human clinical trial of PEP-Therapy’s lead drug candidate, PEP-010. [PEP-Therapy] |
|
|
|
|
|
|
|
| Thomas Jefferson University – Philadelphia, Pennsylvania, United States |
|
|
|
| University of Arizona Cancer Center – Tucson, Arizona, United States |
|
|
|
| Baylor College of Medicine – Houston, Texas, United States |
|
|
|
| Tulane School of Medicine – New Orleans, Louisiana, United States |
|
|
|
| University of Illinois at Urbana-Champaign – Urbana, Illinois, United States |
|
|
|
|