United States

ENDO 2021

Meet the Scientist: Drugs, Steroids, and Cancer: Bridging the Worlds of Endocrinology, Metabolism, and Oncology

ENDO is the leading meeting for endocrinology research and clinical care worldwide. 

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ENDO 2020

ENDO is the place where leading experts, researchers, and the most respected clinicians in the field come together to share the latest findings in hormone science and discuss breakthroughs in clinical care.

technical paper

Clark T. Sawin Memorial History of Endocrinology Lecture: The Lessons Learned from the History of Identifying and Addressing Health Disparities in Endocrinology and Diabetes

Genes and Surveillance for Patients and Family With Familial Pheochromocytoma and Paraganglioma Syndromes

Does the Treatment of Hyperthyroidism Lead to Cancer?

RAI Treatment of Adults with Hyperthyroidism is Safe with Regards to Cancer Risk

Meet the Scientist: Examining the Chromatin Landscape - Epigenetic Enzymes and Transcriptional Heterogeneity

This House Believes that Following MEN1 Surveillance Guidelines Can Do More Harm than Good

Lipid Management in Patients with Endocrine Disorders: An Endocrine Society Clinical Practice Guideline

Endocrine Society Business Meeting

Steroid Receptor Co-Activators Regulate Metabolic Kinases to Drive Therapy Resistant ER+ Breast Cancer

Hormonal regulation of Semaphorin 7a promotes therapeutic resistance in breast cancer
Background: The majority of all breast cancers (BC) are estrogen receptor positive (ER+). While ER-targeting endocrine therapies have improved patient survival, many of these tumors develop drug resistance and recur within 20 years. Therefore, novel targets are needed to predict for recurrence and to treat recurrent ER+BC. Previous reports describe a tumor-promotional role for Semaphorin 7A (SEMA7A) in ER- disease; yet, the role of SEMA7A in ER+ disease is poorly characterized. Hypothesis: SEMA7A promotes cell survival and drug resistance in ER+ BC. Methods: We overexpressed SEMA7A in ER+ BC cells, then used the ER-targeting agents tamoxifen and fulvestrant to test how SEMA7A-expressing cells respond to endocrine therapy. In vitro, we used proliferation and cell survival assays. In vivo, we implanted ER+ BC cells, then treated the animals with fulvestrant to measure how SEMA7A affects tumor growth and metastasis. We also utilized drug resistant cells, which have high endogenous SEMA7A levels, to measure markers of stemness and multi-drug resistance via flow cytometry. Results: We first found that SEMA7A expression correlates with decreased relapse free survival in patients with ER+BC who received endocrine therapy (Kmplotter; p=0.042). We also observe that SEMA7A is hormonally regulated in ER+BC, but its expression does not uniformly decrease with endocrine therapy agents. Instead, long term estrogen deprivation and ER-targeting drug treatments increase SEMA7A expression, likely through the action of other hormone receptors such as the androgen receptor, which also increases with long term estrogen deprivation. Further, in ER+ cell lines, overexpression of SEMA7A promotes in vitro growth in the face of estrogen-deprivation, tamoxifen, or fulvestrant treatments. In vivo, SEMA7A promotes fulvestrant resistance in the primary tumor and induces lung metastases. Finally, we report that pro-survival signaling is a therapeutic vulnerability of ER+SEMA7A+ tumors. Conclusion: These studies describe that SEMA7A promotes drug resistance in ER+ BC. We propose that targeting pro-survival signaling may prove efficacious for treating SEMA7A+ tumors, which are less likely to respond to endocrine therapies.

Hormonal Regulation of Semaphorin 7a Promotes Therapeutic Resistance in ER+ Breast Cancer

https://d3smihljt9218e.cloudfront.net/transcript/25883/subtitle/27332a130dc949fc44bf9679e322bd9f.vtt

English (automatic)

Meet the Scientist: Drugs, Steroids, and Cancer: Bridging the Worlds of Endocrinology, Metabolism, and Oncology

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