Practical Classification of Triple-Negative Breast Cancer: Intratumoral Heterogeneity, Mechanisms of Drug Resistance, and Novel Therapies

Despite several efforts, transcriptomic and genomic classifications have remained merely theoretic and most of the patients are being treated with chemotherapy. Driver alterations in potentially targetable genes, including PIK3CA and AKT, have been identified across triple negative breast cancer subtypes, prompting the implementation of biomarker-driven therapeutic approaches.
[npj breast cancer]
Marra, A., Trapani, D., Viale, G., Criscitiello, C., & Curigliano, G. (2020). Practical classification of triple-negative breast cancer: intratumoral heterogeneity, mechanisms of drug resistance, and novel therapies. Npj Breast Cancer, 6(1), 1–16. https://doi.org/10.1038/s41523-020-00197-2 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Nanoparticle-Delivered Miriplatin Ultrasmall Dots Suppress Triple Negative Breast Cancer Lung Metastasis by Targeting Circulating Tumor Cells

Investigators found that active targeting nanoparticles displayed a superior DNA damage capability via enhanced-interactions with DNA and a significantly stronger effect in reducing cancer stem cell-like property of triple negative breast cancer cells, compared to conventional cisplatin and miriplatin.
[Journal of Controlled Release]
Li, Y., Qian, D., Lin, H.-P., Xie, J., Yang, P., Maddy, D., Xiao, Y., Huang, X., Wang, Z., & Yang, C. (2020). Nanoparticle-delivered miriplatin ultrasmall dots suppress triple negative breast cancer lung metastasis by targeting circulating tumor cells. Journal of Controlled Release. https://doi.org/10.1016/j.jconrel.2020.10.015 Cite
Full ArticleGraphical Abstract
Bookmark

No account yet? Register

0
Share

Bispecific Antibodies for TNBC

The authors discuss novel bispecific antibodies for TNBC and emerging TNBC targets for future bispecific antibody development.
[Trends in Cancer]
Dees, S., Ganesan, R., Singh, S., & Grewal, I. S. (2020). Bispecific Antibodies for Triple Negative Breast Cancer. Trends in Cancer, 0(0). https://doi.org/10.1016/j.trecan.2020.09.004 Cite
Abstract
Bookmark

No account yet? Register

0
Share

EZH2 Regulates Expression of FOXC1 by Mediating H3K27me3 in Breast Cancers

Scientists demonstrated that the expression of FOXC1 was associated with resistance of doxorubicin treatment of breast cancer cells.
[Acta Pharmacologica Sinica]
Zheng, X., Li, W., Yi, J., Liu, J., Ren, L., Zhu, X., Liu, S., Wang, J., & Du, G. (2020). EZH2 regulates expression of FOXC1 by mediating H3K27me3 in breast cancers. Acta Pharmacologica Sinica, 1–9. https://doi.org/10.1038/s41401-020-00543-x Cite
Abstract
Bookmark

No account yet? Register

0
Share

FBI-1 Enhanced the Resistance of Triple-Negative Breast Cancer Cells to Chemotherapeutic Agents via the miR-30c/PXR Axis

Factor that binds to the inducer of short transcripts‐1 (FBI-1) enhanced the resistance of TNBC cells to chemotherapeutic agents by repressing the expression of micoRNA-30c targeting the pregnane X receptor (PXR).
[Cell Death & Disease]
Yang, H., Ren, L., Wang, Y., Bi, X., Li, X., Wen, M., Zhang, Q., Yang, Y., Jia, Y., Li, Y., Zang, A., Wei, Y., & Dai, G. (2020). FBI-1 enhanced the resistance of triple-negative breast cancer cells to chemotherapeutic agents via the miR-30c/PXR axis. Cell Death & Disease, 11(10), 1–14. https://doi.org/10.1038/s41419-020-03053-0 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Inhibition of Chk1 by miR-320c Increases Oxaliplatin Responsiveness in Triple-Negative Breast Cancer

As checkpoint kinase 1 (Chk1) was associated with the DNA damage response (DDR), scientists investigated the effect of miR-320c on DDR in TNBC cells.
[Oncogenesis]
Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer | Oncogenesis. (n.d.). Retrieved October 13, 2020, from https://www.nature.com/articles/s41389-020-00275-x Cite
Full Article
Bookmark

No account yet? Register

0
Share

Targeting IL-3Rα on Tumor-Derived Endothelial Cells Blunts Metastatic Spread of Triple-Negative Breast Cancer via Extracellular Vesicle Reprogramming

Using human TNBC cell lines for in vitro studies, researchers found that, unlike native tumor–endothelial cells extracellular vesicles (EVs), anti-IL-3R-EVs increased apoptosis and reduced cell viability and migration.
[Oncogenesis]
Targeting IL-3Rα on tumor-derived endothelial cells blunts metastatic spread of triple-negative breast cancer via extracellular vesicle reprogramming | Oncogenesis. (n.d.). Retrieved October 13, 2020, from https://www.nature.com/articles/s41389-020-00274-y Cite
Full Article
Bookmark

No account yet? Register

0
Share

Transcriptome-Wide Analysis and Modelling of Prognostic Alternative Splicing Signatures in Invasive Breast Cancer: A Prospective Clinical Study

RNA sequencing of IBC samples from The Cancer Genome Atlas was acquired. Alternative splicingevents were screened by conducting univariate and multivariate Cox analysis and least absolute shrinkage and selection operator regression.
[Scientific Reports]
Wang, L., Wang, Y., Su, B., Yu, P., He, J., Meng, L., Xiao, Q., Sun, J., Zhou, K., Xue, Y., & Tan, J. (2020). Transcriptome-wide analysis and modelling of prognostic alternative splicing signatures in invasive breast cancer: a prospective clinical study. Scientific Reports, 10(1), 16504. https://doi.org/10.1038/s41598-020-73700-1 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Exploiting Chromosomal Instability of PTEN-Deficient Triple-Negative Breast Cancer Cell Lines for the Sensitization against PARP1 Inhibition in a Replication-Dependent Manner

Scientists recognized the tumor suppressor gene Phosphatase and Tensin homolog (PTEN) as a potential gene causing CIN in TNBC and showed that TNBC with low expression levels of PTEN can be sensitized for the treatment with poly-(ADP-ribose)-polymerase 1 (PARP1) inhibitors, independent of Breast Cancer (BRCA) mutations or a BRCA-like phenotype.
[Cancers]
Rieckhoff, J., Meyer, F., Classen, S., Zielinski, A., Riepen, B., Wikman, H., Petersen, C., Rothkamm, K., Borgmann, K., & Parplys, A. C. (2020). Exploiting Chromosomal Instability of PTEN-Deficient Triple-Negative Breast Cancer Cell Lines for the Sensitization against PARP1 Inhibition in a Replication-Dependent Manner. Cancers, 12(10), 2809. https://doi.org/10.3390/cancers12102809 Cite
Abstract
Bookmark

No account yet? Register

0
Share

Hybrid Cellular Membrane Nanovesicles Amplify Macrophage Immune Responses against Cancer Recurrence and Metastasis

The hybrid cell membrane nanovesicles blocked CD47-signal regulatory protein alpha signaling axis while promoting M2-to-M1 repolarization within the tumor microenvironment, significantly preventing both local recurrence and distant metastasis in malignant melanoma models.
[Nature Communications]
Rao, L., Wu, L., Liu, Z., Tian, R., Yu, G., Zhou, Z., Yang, K., Xiong, H.-G., Zhang, A., Yu, G.-T., Sun, W., Xu, H., Guo, J., Li, A., Chen, H., Sun, Z.-J., Fu, Y.-X., & Chen, X. (2020). Hybrid cellular membrane nanovesicles amplify macrophage immune responses against cancer recurrence and metastasis. Nature Communications, 11(1), 4909. https://doi.org/10.1038/s41467-020-18626-y Cite
Full Article
Bookmark

No account yet? Register

0
Share

Annurca Apple Polyphenol Extract Promotes Mesenchymal-to-Epithelial Transition and Inhibits Migration in Triple-Negative Breast Cancer Cells through ROS/JNK Signaling

By qualitatively and quantitatively monitoring the real-time movements of live cells researchers provided the first evidence that pple polyphenol extract inhibited the migration of MDA-MB-231 and MDA-MB-468 TNBC cells and downregulated metalloproteinase-2 and metalloproteinase-9.
[Scientific Reports]
Vuoso, D. C., D’Angelo, S., Ferraro, R., Caserta, S., Guido, S., Cammarota, M., Porcelli, M., & Cacciapuoti, G. (2020). Annurca apple polyphenol extract promotes mesenchymal-to-epithelial transition and inhibits migration in triple-negative breast cancer cells through ROS/JNK signaling. Scientific Reports, 10(1), 15921. https://doi.org/10.1038/s41598-020-73092-2 Cite
Full Article
Bookmark

No account yet? Register

0
Share
Share