Triple negative breast cancer (TNBC) that fails to respond to neoadjuvant chemotherapy (NACT) can be

IR adipocyte exosomes modify TME, increase EMT and promote metastasis to distant organs, likely through miRNA pathways. We suggest metabolic diseases such as T2D reshape the TME, promoting metastasis ...

Diet influences macronutrient availability to cells, and although mechanisms of sensing dietary glucose and amino acids are well characterized, less is known about sensing lipids. We defined a nutrien...

Triple-negative breast cancer (TNBC) is characterized by high risks of relapse or metastatic disease. Mattavelli et al. identify a chemokine axis that recruits immunosuppressive monocytes to tumor-dra...

How tumor cells overcome anti-tumor immune responses and drive cancer recurrence is not well understood. Yu et al. demonstrate how therapy-resistant breast cancer cells synthesize and secrete arachido...

Wang et al. establish an in vivo proteomic labeling (IVPL) system combining the Btn-Ph-3F substrate with APEX2-EGFPf/f Cre crosses to map cell-type-specific proteomes in intact organs and trace patient-derived exosomal proteins. IVPL identifies LDHAL6A as a pro-metastatic driver and highlights its potential as a therapeutic target in TNBC.

Abstract. The inter- and intra-tumor heterogeneity of triple negative breast cancers (TNBC), which is reflected in diverse drug responses, interplays with tumor evolution. Here, we developed a preclin...

Oncogene - Breast cancer stem cell-derived exosomal lnc-PDGFD induces fibroblast-niche formation and promotes lung metastasis

Cell Death & Differentiation - Macrophage-secreted brain-derived neurotrophic factor promotes tumor growth in triple-negative breast cancer by inducing axonogenesis

Abstract. Patients with triple negative breast cancer (TNBC) and comorbid Type 2 Diabetes (T2D), characterized by insulin resistance of adipose tissue, have higher risk of metastasis and shorter survi...

Background Triple-negative breast cancer (TNBC) is an aggressive subclass of breast cancer with limited treatment options and a strong tendency to metastasize to the lung. Tumor-derived extracellular vesicles (EVs) are key mediators of stromal reprogramming in the pre-metastatic niche. Annexin A2 (AnxA2) is overexpressed in TNBC and linked to signal transduction, cytoskeletal remodeling, and poor prognosis, but its role in shaping EV cargo composition and consequent stromal behavior remains unclear. Methods EVs were isolated from the conditioned media of MDA-MB-4175 (LM2) TNBC cells with stable AnxA2 knockdown and control cells using differential ultracentrifugation. EVs were characterized and validated using nanoparticle tracking analysis, Western blotting, and cryo-electron microscopy. EV proteomes were profiled using quantitative proteomics, followed by bioinformatic analyses. Functional and pathway enrichment was performed to identify proteome signatures altered by AnxA2 depletion.

Wang et al. establish an in vivo proteomic labeling (IVPL) system combining the Btn-Ph-3F substrate with APEX2-EGFPf/f Cre crosses to map cell-type-specific proteomes in intact organs and trace patient-derived exosomal proteins. IVPL identifies LDHAL6A as a pro-metastatic driver and highlights its potential as a therapeutic target in TNBC.

Patients with triple negative breast cancer (TNBC) and comorbid Type 2 Diabetes (T2D), characterized by insulin resistance of adipose tissue, have higher risk of metastasis and shorter survival.…

Here, we present a protocol for establishing patient-derived xenograft (PDX) mouse models of chemoresistant triple-negative breast cancer (TNBC). We describe steps for tumor collection, surgical implantation, and serial expansion. We then detail procedures for histopathological validation and in vivo therapeutic assessment to confirm the maintenance of chemoresistance across passages. These models provide a clinically relevant platform to investigate mechanisms of treatment resistance, evaluate ...

Cancer cell lines, derived from tumors, have become essential tools in life science research and are

Breaking Update: Here’s a clear explanation of the latest developments related to Breaking News:Scientists Discover Molecule that Blocks Breast Cancer– What Just Happened and why it matters right now. SCIENTISTS have discovered a molecule that impedes the growth of triple-negative breast cancer (TNBC). SU212 is a small molecule derived from aza-podophyllotoxin that inhibits enolase 1 (ENO1), a glycolytic enzyme that is overexpressed by cancer cells and plays a key role in cancer metabolism.

How tumor cells overcome anti-tumor immune responses and drive cancer recurrence is not well understood. Yu et al. demonstrate how therapy-resistant breast cancer cells synthesize and secrete arachido...

In a promising advancement for breast cancer therapeutics, researchers have uncovered a potent synergy between Tanshinone IIA, a bioactive compound derived from traditional Chinese medicine, and olaparib, a well-known PARP inhibitor, in inducing apoptosis in triple-negative breast cancer (TNBC) cells. The study, recently published in Medical Oncology, explores this combination’s efficacy across both BRCA-proficient and BRCA-deficient TNBC cell lines, offering new hope for tackling one of the most aggressive and treatment-resistant subtypes of breast cancer.