Publications by authors named "B L Wharram"
Unlabelled: Cancer cells reprogram energy metabolism through metabolic plasticity, adapting ATP-generating pathways in response to treatment or microenvironmental changes. Such adaptations enable cancer cells to resist standard therapy. We employed a coculture model of estrogen receptor-positive (ER+) breast cancer and mesenchymal stem cells (MSC) to model interactions of cancer cells with stromal microenvironments.
View Article and Find Full Text PDFEndocrine therapy (ET) is an effective first-line therapy for women with estrogen receptor-positive (ER + ) breast cancers. While both ionizing radiation (RT) and ET are used for the treatment of women with ER+ breast cancer, the most effective sequencing of therapy and the effect of ET on tumor radiosensitization remains unclear. Here we sought to understand the effects of inhibiting estrogen receptor (ER) signaling in combination with RT in multiple preclinical ER+ breast cancer models.
View Article and Find Full Text PDFArticle Synopsis
- CRYβB2 is found to be elevated in African American breast tumors and is linked to increased cancer stemness, growth, and metastasis.
- It upregulates genes related to stress responses and DNA repair while down-regulating apoptosis-related genes, leading to aggressive tumor traits.
- Additionally, higher levels of CRYβB2 and its interaction with nucleolin correlate with decreased survival rates in patients, highlighting its potential role in breast cancer disparities.
Lu-labeled low-molecular-weight agents for PSMA-targeted radiopharmaceutical therapy.
Eur J Nucl Med Mol Imaging
November 2019
Purpose: To develop a prostate-specific membrane antigen (PSMA)-targeted radiotherapeutic for metastatic castration-resistant prostate cancer (mCRPC) with optimized efficacy and minimized toxicity employing the β-particle radiation of Lu.
Methods: We synthesized 14 new PSMA-targeted, Lu-labeled radioligands (Lu-L1-Lu-L14) using different chelating agents and linkers. We evaluated them in vitro using human prostate cancer PSMA(+) PC3 PIP and PSMA(-) PC3 flu cells and in corresponding flank tumor models.