CCL8 Mediates Crosstalk between Endothelial Colony Forming Cells and Triple-Negative Breast Cancer Cells through IL-8, Aggravating Invasion and Tumorigenicity

Using an indirect co-culture system, scientists showed that co-culture increased the invasive and migratory phenotypes of both MDA-MB-231 TNBC cells and endothelial colony-forming cells.
[Oncogene]
CCL8 mediates crosstalk between endothelial colony forming cells and triple-negative breast cancer cells through IL-8, aggravating invasion and tumorigenicity | Oncogene. (n.d.). Retrieved April 8, 2021, from https://www.nature.com/articles/s41388-021-01758-w Cite
Abstract
Bookmark

No account yet? Register

0
Share

FDA Approves Trodelvy® the First Treatment for Metastatic Triple-Negative Breast Cancer Shown to Improve Progression-Free Survival and Overall Survival

Gilead Sciences, Inc. announced that the FDA has granted full approval to Trodelvy® for adult patients with unresectable locally advanced or metastatic TNBC who have received two or more prior systemic therapies, at least one of them for metastatic disease.
[Gilead Sciences, Inc.]
Press Release
Bookmark

No account yet? Register

0
Share

MCPIP1-Mediated NFIC Alternative Splicing Inhibits Proliferation of Triple-Negative Breast Cancer via Cyclin D1-RB-E2F1 Axis

Investigators showed that monocyte chemotactic protein induced protein 1 (MCPIP1) was downregulated in 80 TNBC tissues and five TNBC cell lines compared to adjacent paracancerous tissues and one human immortalized breast epithelial cell line, while its high expression levels were associated with increased overall survival in TNBC patients.
[Cell Death & Disease]
Chen, F., Wang, Q., Yu, X., Yang, N., Wang, Y., Zeng, Y., Zheng, Z., Zhou, F., & Zhou, Y. (2021). MCPIP1-mediated NFIC alternative splicing inhibits proliferation of triple-negative breast cancer via cyclin D1-Rb-E2F1 axis. Cell Death & Disease, 12(4), 1–16. https://doi.org/10.1038/s41419-021-03661-4 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Targeting Nucleotide Metabolism Enhances the Efficacy of Anthracyclines and Anti-Metabolites in Triple-Negative Breast Cancer

Deoxyuridine 5′-triphosphate nucleotidohydrolase inhibition significantly sensitized TNBC cell lines to fluoropyrimidines and anthracyclines through imbalanced nucleotide pools and increased DNA damage leading to decreased proliferation and increased cell death.
[npj Breast Cancer]
Davison, C., Morelli, R., Knowlson, C., McKechnie, M., Carson, R., Stachtea, X., McLaughlin, K. A., Prise, V. E., Savage, K., Wilson, R. H., Mulligan, K. A., Wilson, P. M., Ladner, R. D., & LaBonte, M. J. (2021). Targeting nucleotide metabolism enhances the efficacy of anthracyclines and anti-metabolites in triple-negative breast cancer. Npj Breast Cancer, 7(1), 1–13. https://doi.org/10.1038/s41523-021-00245-5 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Merck Receives Complete Response Letter From US FDA for Supplemental Biologics License Application (sBLA) for KEYTRUDA® (pembrolizumab) in High-Risk Early-Stage Triple-Negative Breast Cancer (TNBC)

Merck announced that the FDA has issued a Complete Response Letter regarding Merck’s supplemental Biologics License Application seeking approval for KEYTRUDA, the company’s anti-PD-1 therapy, for the treatment of patients with high-risk early-stage triple-negative breast cancer, in combination with chemotherapy as neoadjuvant treatment, then continuing as a single agent as adjuvant treatment after surgery.
[Merck (BusinessWire, Inc.)]
Press Release
Bookmark

No account yet? Register

0
Share

Targeted Therapy to β3 Integrin Reduces Chemoresistance in Breast Cancer Bone Metastases

Researchers showed that β3 integrin induction by the bone microenvironment promotes resistance to chemotherapy through an altered metabolic response that can be defused by combination with αvβ3-targeted mTORC1 inhibitor nanotherapy.
[Molecular Cancer Therapeutics]
Fox, G. C., Su, X., Davis, J. L., Xu, Y., Kwakwa, K. A., Ross, M. H., Fontana, F., Xiang, J., Esser, A. K., Cordell, E., Pagliai, K., Dang, H. X., Sivapackiam, J., Stewart, S. A., Maher, C. A., Bakewell, S. J., Sharma, V., Achilefu, S., Veis, D. J., … Weilbaecher, K. N. (2021). Targeted therapy to β3 integrin reduces chemoresistance in breast cancer bone metastases. Molecular Cancer Therapeutics. https://doi.org/10.1158/1535-7163.MCT-20-0931 Cite
Abstract
Bookmark

No account yet? Register

0
Share

Co-Dependency for MET and FGFR1 in Basal Triple-Negative Breast Cancers

Investigators utilized an established Met-dependent transgenic mouse model of TNBC, human cell lines and patient-derived xenografts to investigate the role of MET in TNBC tumorigenesis.
[npj Breast Cancer]
Sung, V. Y. C., Knight, J. F., Johnson, R. M., Stern, Y. E., Saleh, S. M., Savage, P., Monast, A., Zuo, D., Duhamel, S., & Park, M. (2021). Co-dependency for MET and FGFR1 in basal triple-negative breast cancers. Npj Breast Cancer, 7(1), 1–15. https://doi.org/10.1038/s41523-021-00238-4 Cite
Full Article
Bookmark

No account yet? Register

0
Share

The Human Intermediate Prolactin Receptor Is a Mammary Proto-Oncogene

An analogous truncated mouse prolactin receptor (mPRLr) was found to be oncogenic when co-expressed with wild-type mPRLr. The authors determined if a similar transforming event occurs with the hPRLr in human breast epithelial cells.
[npj Breast Cancer]
Grible, J. M., Zot, P., Olex, A. L., Hedrick, S. E., Harrell, J. C., Woock, A. E., Idowu, M. O., & Clevenger, C. V. (2021). The human intermediate prolactin receptor is a mammary proto-oncogene. Npj Breast Cancer, 7(1), 1–11. https://doi.org/10.1038/s41523-021-00243-7 Cite
Full Article
Bookmark

No account yet? Register

0
Share

LncRNA MIR503HG Inhibits Cell Proliferation and Promotes Apoptosis in TNBC Cells via the miR-224-5p/HOXA9 Axis

The authors investigated the molecular mechanism and influences of MIR503HG, miR-224-5p and HOXA9 on TNBC cell growth and migration.
[Molecular Therapy-Oncolytics]
Wang, S.-M., Pang, J., Zhang, K.-J., Zhou, Z.-Y., & Chen, F.-Y. (2021). LncRNA MIR503HG inhibits cell proliferation and promotes apoptosis in TNBC cells via the miR-224-5p/HOXA9 axis. Molecular Therapy - Oncolytics, 0(0). https://doi.org/10.1016/j.omto.2021.03.009 Cite
AbstractFull ArticleGraphical Abstract
Bookmark

No account yet? Register

0
Share

BCL9/BCL9L Promotes Tumorigenicity through Immune-Dependent and Independent Mechanisms in Triple Negative Breast Cancer

Investigators demonstrated that the expression of BCL9 and BCL9L was directly correlated with malignancy in TNBC patient tumors and that BCL9 and BCL9L promoted tumor cell growth, cell migration and metastasis in TNBC models.
[Oncogene]
Wang, X., Feng, M., Xiao, T., Guo, B., Liu, D., Liu, C., Pei, J., Liu, Q., Xiao, Y., Rosin-Arbesfeld, R., Shi, Y., Zhou, Y., Yang, M., Feng, Y.-X., Jiang, Y., Shao, Z., Yu, K., & Zhu, D. (2021). BCL9/BCL9L promotes tumorigenicity through immune-dependent and independent mechanisms in triple negative breast cancer. Oncogene, 1–16. https://doi.org/10.1038/s41388-021-01756-y Cite
Abstract
Bookmark

No account yet? Register

0
Share

Breakthrough Immunotherapy Earns First Regulatory Approval for Triple Negative Breast Cancer (TNBC)

Immunicom, Inc. announced that the ImmunopheresisTM LW-02 blood-filtering column, its leading immuno-oncology product with FDA Breakthrough Device status, has received regulatory clearance in Europe for use in adults with advanced, refractory TNBC.
[Immunicom, Inc.]
Press Release
Bookmark

No account yet? Register

0
Share
Share