Publications by authors named "S Fuqua"
Evidence that CRISPR-Cas9 Y537S-mutant expressing breast cancer cells activate Yes-associated protein 1 to driving the conversion of normal fibroblasts into cancer-associated fibroblasts.
Cell Commun Signal
November 2024
Article Synopsis
- Endocrine therapy improves outcomes for ERα+ breast cancer, but resistance remains a key challenge, often linked to mutations like Y537S in the hormone-binding domain of ERα.
- Researchers conducted coculture experiments to study interactions between mutant breast cancer cells (MCF-7YS) and fibroblasts (both normal and cancer-associated) to see how these interactions influence cancer progression.
- The study found that the Y537S mutation led to changes in fibroblast behavior and protein expression, with increased YAP1 involvement, suggesting that mutant breast cancer cells can enhance their growth and invasion capabilities through interactions with the tumor microenvironment.
Endocrine therapies (ET) with cyclin-dependent kinase 4/6 (CDK4/6) inhibition are the standard treatment for estrogen receptor-α-positive (ER+) breast cancer, however drug resistance is common. In this study, proteogenomic analyses of patient-derived xenografts (PDXs) from patients with 22 ER+ breast cancer demonstrated that protein kinase, membrane-associated tyrosine/threonine one (PKMYT1), a WEE1 homolog, is estradiol (E2) regulated in E2-dependent PDXs and constitutively expressed when growth is E2-independent. In clinical samples, high PKMYT1 mRNA levels associated with resistance to both ET and CDK4/6 inhibition.
View Article and Find Full Text PDFT cell receptor engineered T cell (TCR T) therapies have shown recent efficacy against certain types of solid metastatic cancers. However, to extend TCR T therapies to treat more patients across additional cancer types, new TCRs recognizing cancer-specific antigen targets are needed. Driver mutations in AKT1, ESR1, PIK3CA, and TP53 are common in patients with metastatic breast cancer (MBC) and if immunogenic could serve as ideal tumor-specific targets for TCR T therapy to treat this disease.
View Article and Find Full Text PDFUnlabelled: Approximately one-third of endocrine-treated women with estrogen receptor alpha-positive (ER+) breast cancers are at risk of recurrence due to intrinsic or acquired resistance. Thus, it is vital to understand the mechanisms underlying endocrine therapy resistance in ER+ breast cancer to improve patient treatment. Mitochondrial fatty acid β-oxidation (FAO) has been shown to be a major metabolic pathway in triple-negative breast cancer (TNBC) that can activate Src signaling.
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