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triple negative breast cancer

Parallel Genomic Alterations of Antigen and Payload Targets Mediate Polyclonal Acquired Clinical Resistance to Sacituzumab Govitecan in Triple-Negative Breast Cancer

[Cancer Discovery] Scientists identified mechanisms of TNBC resistance to Sacituzumab Govitecan through RNA and whole-exome sequencing of pre-treatment and post-progression specimens.

PDSS1-Mediated Activation of CAMK2A-STAT3 Signaling Promotes Metastasis in Triple-Negative Breast Cancer

[Cancer Research] Researchers identified decaprenyl diphosphate synthase subunit 1 (PDSS1) as an essential gene for TNBC metastasis. PDSS1 expression was significantly upregulated in TNBC tissues compared to adjacent normal tissues and was positively associated with poor survival among TNBC patients.

KAT6A Acetylation of SMAD3 Regulates Myeloid-Derived Suppressor Cell Recruitment, Metastasis, and Immunotherapy in Triple-Negative Breast Cancer

[Advanced Science] Lysine acetyltransferase 6A (KAT6A)-acetylated H3K23-mediated recruitment of tripartite motif-containing 24–SMAD3 complex to chromatin increased SMAD3 activation and immune response-related cytokine expression, leading to enhanced breast cancer stem-like cell stemness, myeloid-derived suppressor cell recruitment, and TNBC metastasis.

Carrick Therapeutics Receives FDA Fast Track Designations for Two Samuraciclib Combinations for the Treatment of HR+, HER2– Advanced Breast Cancer and Locally Advanced or...

[Carrick Therapeutics] Carrick Therapeutics announced that the US FDA has granted Fast Track designations to samuraciclib in combination with fulvestrant for CDK4/6i resistant HR+, HER2- advanced breast cancer and samuraciclib in combination with chemotherapy for the treatment of locally advanced or metastatic TNBC.

CircRNA Circ-ERBB2 Elevates Warburg Effect and Facilitates Triple-Negative Breast Cancer Growth by the miR-136-5p/PDK4 Axis

[Molecular and Cellular Biology] Circular RNA circ-ERBB2 knockdown constrained TNBC growth in vivo and reduced Warburg effect, accelerated apoptosis, repressed proliferation, migration, and invasion of TNBC cells in vitro.

ICAM1 Initiates CTC Cluster Formation and Trans-Endothelial Migration in Lung Metastasis of Breast Cancer

[Nature Communications] ICAM1 expression increased by 200-fold in the lung metastases of three TNBC patient-derived xenografts, and its depletion abrogated lung colonization of TNBC cells by inhibiting homotypic tumor cell-tumor cell cluster formation.

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