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Dr. Moore's Presentation

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  • ORR and CBR are highly significant: <0001; the final OS analysis will be conducted after 392 deaths
  • 48% had received tmx, 16% fulvestrant and 26% had one chemo regimen

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  • 1. SHARE and WEILL CORNELL BREAST CENTER Metastatic breast cancer: Update 2012 Anne Moore, MD Linda Vahdat, MD Christine
  • 2. Metastatic breast cancer• Spread of breast cancer outside of the breast and axillary lymph nodes – About 20-30 % of women treated for stage 1, 2 or 3 breast cancer will later develop metastatic cancer – Breast cancer can start as metastatic cancer
  • 3. Metastatic breast cancer• Now considered “a chronic disease”• Have a strategic plan
  • 4. The woman with metastatic disease• Tools: – Surgery – Radiation therapy – Zometa for bone strengthening
  • 5. The woman with metastatic disease• Tools: – Chemotherapy – Hormonal therapy for ER/PR positive – Her-2 directed therapy for HER 2 positive – Anti-angiogenesis approach – Clinical trials • New drugs, new approaches • Vaccines• What about diet, supplements, vitamins, immune boosters?
  • 6. [TITLE]
  • 7. [TITLE]
  • 8. Does the ER/PR/HER 2 change between the primary cancer and the metastasis?• Estrogen receptor- 126 patients – Was positive and now negative-14% – Was negative and now positive-8%• HER 2- 121 patients – Was positive and now negative-17% – Was negative and now positive- 0% Luis, DFCI. ASCO education session 2012
  • 9. [TITLE]Luis, ASCO education session, 2012
  • 10. How do we stop cancer cells from dividing? DNA
  • 11. How do we stop cancer cells from dividing?Chemotherapy directly attacks the DNA: Cells cant divide.
  • 12. BUT DNA can repair itself so we need to outsmart cell division in other ways DNA
  • 13. TARGETED TREATMENT:INACTIVATE THE ESTROGEN RECEPTOR Estrogen Estrogen receptor
  • 14. TARGETED TREATMENT: INACTIVATE THE ESTROGEN RECEPTORTake away estrogenUse a “fake” estrogen:TamoxifenDestroy the estrogenreceptor:Faslodex
  • 15. BUT the cells can bypass the estrogen receptor blockade and startto divide again so we need to outsmart estrogen dependent celldivision in other ways
  • 16. Estrogen activates the estrogen receptor and cellsproliferate through activation of the mTOR pathway
  • 17. mTOR blockade blocks estrogen receptor activationBlock mTOR EVEROLIMUS IS AN MTOR INHIBITOR
  • 18. BOLERO 2: ASCO UPDATE
  • 19. RESULTS• CLINICAL BENEFIT RATE-Those women who had a complete response, a partial response or stable disease for more than 6 months – 26.4% for exemestane – 51.3% for exemestane and everolimus
  • 20. Characteristics of these women with metastatic ER+ breast cancer• Average age: 61• Disease free interval before first recurrence: 5 year• All had received anastrazole or letrozole- 84% had shown a response.• 53% had received >3 treatments for metastatic disease including chemotherapy• The women were in good shape
  • 21. Women receiving both pills, Exemestane (Aromasin) and Everolimus (Afinitor) had more side effects• mouth sores• Infections• Rash• Pneumonitis• high blood sugar
  • 22. Will we use everolimus with hormone therapy? Pt. recurs on or after adjuvant letrozole: Tamoxifen Fulvestrant Then: ?exemestane alone or with everolimusas an alternative to chemotherapyThis trial is exciting because it opens a new pathwayfor drug development in breast cancer
  • 23. HER-2 POSITIVE METASTATIC BREAST CANCER
  • 24. Lapatinib (Tykerb) (a pill) targets the Her2receptor X X X
  • 25. PERTUZUMAB HAS JUST BEEN APPROVED FOR HER 2 + METASTATIC BREAST CANCER
  • 26. Pertuzumab• Approved for first line metastatic breast cancer treatment with herceptin and docetaxel (taxotere)• Very weak by itself but boosts herceptin effect even for women who have had herceptin already
  • 27. Herceptin linked to a strong chemotherapy drug [TITLE]
  • 28. [TITLE]
  • 29. [TITLE]
  • 30. [TITLE]
  • 31. The Future is Promising for Metastatic Breast Cancer