| Vol. 13.35 – 16 September, 2021 |
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| Scientists developed a prolactin-humanized Nod-SCID-IL2Rγ (NSG) mouse (NSG-Pro) with physiological human prolactin levels and showed that NSG-Pro mice facilitated establishment of therapy-naïve, estrogen-dependent PDX tumors that progressed to lethal metastatic disease. [Science Advances] |
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| PUBLICATIONSRanked by the impact factor of the journal |
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| Investigators reported that the cytoplasmic unconventional Myosin X (MYO10) regulated genome stability, through which it mediated inflammation in cancer. Inhibiting inflammation or disrupting Myo10 significantly suppressed the growth of both human and mouse breast tumors in mice. [Science Advances] |
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| The authors reported that inhibition of CDK4/6 promoted βTrCP1-mediated ubiquitination and proteasomal degradation of RB1, and facilitated SP1-mediated CDK6 transcriptional activation. [Nature Communications] |
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| Comparison of Tripartite motif containing protein 24 (TRIM24) in mouse mammary epithelia (Trim24COE) metaplastic carcinosarcoma morphology, TRIM24 protein levels and a derived Trim24COE gene signature revealed strong correlation with human metaplastic breast cancers (MpBC) tumors and MpBC patient-derived xenograft models. [Nature Communications] |
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| Using a murine TNBC model, scientists showed that USP9x knockdown abrogated Notch activation, reducing the production of the proinflammatory cytokines, C-C motif chemokine ligand 2 and interleukin-1 beta. [Proceedings of the National Academy of Sciences of the United States of America] |
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| Using longitudinal intravital imaging of a Rac1-Förster resonance energy transfer (FRET) biosensor mouse coupled with in vivo photoswitching to track intratumoral movement, researchers helped guide treatment scheduling in a live breast cancer setting to impair metastatic progression. [Cell Reports] |
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| The PIM family of kinases has emerged as a factor that is both overexpressed in TNBC and associated with poor outcomes. The authors’ screening effort identified PIM and the 20S proteasome inhibition as the most synergistic combination. [Cell Chemical Biology] |
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| In silico analysis showed that epithelial membrane protein 3 (EMP3) was associated with favorable survival, and negatively regulated cell cycle S-phase. Loss and gain of function studies demonstrated that EMP3 inhibited breast cancer cell S-phage entry, DNA replication, DNA damage repair, and stem-like properties. [Cell Death & Disease] |
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| Researchers observed that TRIM3 was dramatically overexpressed in breast cancer, which correlated with tamoxifen resistance. Furthermore, TRIM3 overexpression significantly correlated with poor survival of patients with ER+ breast cancer treated with tamoxifen. [Oncogenesis] |
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| Investigators enriched ubiquitinated proteins (UPs) from epirubicin (EPB)-induced multi-drug-resistant cancer stem-like breast cancer cell line and tested the efficacy of α-Al2O3-UPs-4T1/EPB as therapeutic vaccine alone and in combination with the stimulator of interferon genes (STING) agonist in mice with drug-resistant and metastatic breast cancer. [Frontiers in Immunology] |
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| The authors demonstrated that TC10, a member of a Cdc42 subfamily of p21 small GTPases, regulated the membrane type 1 matrix metalloproteinase-driven extracellular matrix degradation at invadopodia. [Communications Biology] |
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| Scientists identified the transcriptional landscape associated with TNBC resistance to neoadjuvant chemotherapy at the single cell level by analyzing publicly-available transcriptome data from more than 5,000 single cells derived from four extinction and four persistence patients, revealing remarkable tumor heterogeneity. [Molecular Therapy-Oncolytics] |
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| TNBC cells treated with doxorubicin exhibited reduced branched-chain ketoacid dehydrogenase kinase (BCKDK) expression and intracellular branched-chain ketoacids (BCKAs). Genetic and pharmacological inhibition of BCKDK in TNBC cell lines also showed a similar reduction in intracellular and secreted BCKAs. [Cell Death Discovery] |
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| The authors discuss the prevalence of the genomic alterations targeted by agents for tumor-agnostic treatment in breast cancer, their detection methods, the clinical characteristics of patients whose tumors have these alterations, and available data regarding the efficacy of these agents in breast cancer. [npj Breast Cancer] |
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| Ubiquitin carboxyl terminal hydrolase L1 (UCHL1), a ubiquitin C-terminal hydrolase belonging to the deubiquitinase family of enzymes, is highly expressed in metastatic estrogen receptor negative breast cancer and TNBC, and several key reports have revealed emerging and important roles for UCHL1 in breast cancer. [British Journal of Cancer] |
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| T–Cure Bioscience, Inc. announced that the US FDA has approved the Investigational New Drug application to initiate a Phase I clinical study evaluating a T cell receptor (TCR)–based product candidate for the treatment of tumors expressing Kita–Kyushu lung cancer antigen 1 (KK-LC-1), such as gastric, cervical, lung, breast cancers and other KK–LC–1 positive epithelial cancers. [T–Cure Bioscience, Inc.] |
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| Dalhousie University – Halifax, Nova Scotia, Canada |
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| University of South Carolina – Columbia – Columbia, South Carolina, United States |
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| University of Glasgow – Glasgow, Scotland, United Kingdom |
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| St. Jude Children’s Research Hospital – Memphis, Tennessee, United States |
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| University of Pennsylvania – Philadelphia, Pennsylvania, United States |
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