Publications by authors named "P Kabos"
Purpose: The development of endocrine resistance remains a significant challenge in the clinical management of estrogen receptor-positive () breast cancer. Metabolic reprogramming is a prominent component of endocrine resistance and a potential therapeutic intervention point. However, a limited understanding of which metabolic changes are conserved across the heterogeneous landscape of ER+ breast cancer or how metabolic changes factor into ER DNA binding patterns hinder our ability to target metabolic adaptation as a treatment strategy.
View Article and Find Full Text PDFProgesterone receptors (PR) can regulate transcription by RNA Polymerase III (Pol III), which transcribes small non-coding RNAs, including all transfer RNAs (tRNAs). We have previously demonstrated that PR is associated with the Pol III complex at tRNA genes and that progestins downregulate tRNA transcripts in breast tumor models. To further elucidate the mechanism of PR-mediated regulation of Pol III, we studied the interplay between PR, the Pol III repressor Maf1, and TFIIIB, a core transcription component.
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- * A study analyzed breast tissue from individuals with different BMI categories, revealing notable ECM changes in obese subjects, including higher levels of certain proteins associated with blood vessel formation.
- * Key proteins identified, like peroxidasin (PXDN) and galectins (LGALS1 and LGALS3), are correlated with poor survival outcomes in breast cancer, suggesting obesity may promote cancer progression through modifications in the ECM.
Article Synopsis
- A phase II trial investigated the effectiveness of combining enzalutamide with fulvestrant in treating ER+/HER2- breast cancer to see if it reduces residual tumors at surgery compared to fulvestrant alone.
- * The combination treatment showed a significantly higher rate of achieving complete tumor response (PEPI=0) and improved immune activation in tumors compared to fulvestrant only.
- * Results indicated that the combination therapy not only lowered Ki67 levels (a marker for cancer proliferation) but also altered the tumor immune environment, suggesting increased anti-tumor activity.
Background: Lipid metabolic reprogramming is increasingly recognized as a hallmark of endocrine resistance in estrogen receptor-positive (ER+) breast cancer. In this study, we investigated alterations in lipid metabolism in ER+ breast cancer cell lines with acquired resistance to common endocrine therapies and evaluated the efficacy of a clinically relevant fatty acid synthase (FASN) inhibitor.
Methods: ER+ breast cancer cell lines resistant to Tamoxifen (TamR), Fulvestrant (FulvR), and long-term estrogen withdrawal (EWD) were derived.