Let’s Talk About It: Triple-Negative Breast Cancer - Cutting-Edge Research on TNBC
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Researchers from the University of Arizona have developed a drug compound that appears to stop cancer cell growth in what's known as triple-negative breast cancer. The drug, which has not yet been tested in humans, has been shown to eliminate tumors in mice, with little to no effect on normal healthy cells, making it potentially nontoxic for patients. The therapy is based on a newly discovered way that a gene known as epidermal growth factor receptor, or EGFR, leads to cancer. EGFR is a long-investigated oncogene—a gene that in certain circumstances can transform a cell into a tumor cell. Join our facilitator Nancy Touhill as she speaks with a researcher to breakdown this information for the TNBC community. For more information, visit our website at sharecancersupport.org or call our Helpline at 844.ASK.SHARE (844.275.7427).
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Let’s Talk About It: Triple-Negative Breast Cancer - Cutting-Edge Research on TNBC
- 1. A NEW WAY TO TARGET BREAST CANCER Joyce Schroeder, PhD Professor and Head Molecular and Cellular Biology University of Arizona
- 2. Breast cancer comes from specialized cells in the breast
- 3. Breast cells grow in response to hormones: Estrogen Progesterone Breast cells grow in response to growth factors: HER-family (Human Epidermal Growth Factor Receptor)
- 4. Growth Signals: the HER family
- 5. Types of Breast Cancer Luminal (hormone expressing) • Estrogen • Progesterone HER2 positive • HER2 overexpressing Triple Negative (basal) • Express HER1 and HER3
- 6. Types of Breast Cancer
- 7. HER-expressing tumors are aggressive and metastatic, with few therapeutic options
- 8. Breast cancer death is primarily due to metastasis
- 9. Finding new ways to target metastatic breast cancer Step 1: Targeting the critical drivers
- 10. In breast cancer, the HER1 protein is not only sitting on the cell surface – its inside the cell, in the nucleus
- 11. Therapeutic targeting of nHER1
- 13. nHER1 regulates a unique set of genes
- 14. Sorting Nexins regulate HER1 nuclear translocation
- 15. cSNX1.3: A nHER1 blocking peptide- based therapeutic Atwell et al., Cancer Gene Therapy, 2022 Ben Atwell, PhD
- 16. Toxicity Studies • Tissues and plasma from mice treated for a month – no toxicity • Currently working to complete other requirements by FDA for a clinical trial cPTD4 cSNX1.3 -50 0 50 100 150 cSNX1.3 Reduces Tumor Growth Treatment Change in Tumor Volume per Day (mm 3 ) ΔV = -1.848mm3 ΔV = 38.96mm3
- 17. Our novel therapeutic (cSNX1.3) induces tumor regression by activating the immune system in a non-toxic way.
- 18. Ginny Clements Breast Cancer Fund University of Arizona Dr. Ben Atwell Angelica Escoto Ryan Hecksel Barbara Sands Sara Crane Danielle DiFranco Delina Denogean Evan Waldron Aditi Ghosh Dr. Megha Padi Dr. William Montfort University of Arizona Proteomics Shared Resource University Animal Care University of Colorado - Anshutz Dr. Ben Bitler
Editor's Notes
- Luetteke Hung
- Figure 1. Retrotranslocation of the Epidermal Growth Factor Receptor. Under normal conditions, EGFR is internalized upon ligand binding and routed to the lysosome (dashed arrow). In breast cancer, EGFR is maintained in long-lived EEA1-positive endosomes and traffics to the nucleus (The left panel represents this retrograde trafficking in comparison to the canonical signal transduction pathway of EGFR shown on the right. While each can alter gene transcription, different genes can be regulated by these different functions. Based on proteomics data, p120CTN is hypothesized to be a tumor-specific transcription factor interacting with nuclear EGFR.
- Figure 2. cSNX1.3 competitively inhibits binding of EGFR to SNX1, prevents TNBC survival, blocks nuclear EGFR localization and induces tumor regression in WAP-TGF mice. A. Ribbon drawing of EGFR kinase domain and SNX1 Bar domain. The domain of SNX1 from which cSNX1.3 is derived is indicated and the PTD4 cell penetrating peptide is defined B. MST Binding curves of EGFR kinase domain (50 nM) with fluorescent dye attached through the His-tag titrated against the Bar domain, peptides cSNX1.3 (capped), cSNX1.3, and control PTD4, as well as control BSA. C. Cells were treated with cSNX1.3 compared to the EGFR tyrosine kinase inhibitor Sapitnib, and PTD4 control. D. Cells were treated similarly as in C., fractionated and evaluated for protein localization by immunoblot. E. WAP-TGF mice were allowed to develop tumors then treated for 4 weeks with cSNX1.3 or PTD4 control peptide (10ug/g body weight, 3x/week, IV).