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2013-3-22 乳癌的標靶治療
- 2. 主治療 輔助治療 手術 1. 化療 2. 放射治療 3. 荷爾蒙治療 4. 標 治療靶
- 3. 標靶陽性病人使用 Herceptin( 賀癌平 ) 比標靶陰性預後好
- 4. 三陰性乳癌 荷爾蒙受體 動情激素接受體陰性 ER (-) 黃體激素接受體陰性 PR (-) 標靶陰性 Her-2 (-)
- 7. 什麼是標靶治療 ?
- 8. 正常的 HER2 表現
- 9. HER2 過度表現
- 10. Herceptin( 賀癌平 ) 結合至 HER2
- 11. Herceptin ( 賀癌平 ) 結合殺手細胞 或吞噬細胞 殺死癌細胞
- 14. 目前已有哪些標靶治療藥 ? Herceptin 賀癌平 Lapatinib 泰嘉錠 Pertuzumab (Perjata) T-DM1 (Kadcyla)
- 15. Pertuzumab (Perjata) • FDA( 美國食品藥物管理局 ) 2012-6 月核准 • 歐洲 2013-3 月核准
- 16. T-DM1 (Kadcyla) • FDA( 美國食品藥物管理局 ) 2013-3-23 核准
- 17. 其他標靶藥 • Avastin( 癌思停 ) • Everolimus(Afinitor) • Neratinib • Gefitinib
- 18. 其他標靶藥
- 19. Avastin ( 癌思停 ) 抗血管新生 Somatic mutation Small avascular tumor Tumor secretion of proangiogenic factors stimulates angiogenesis Rapid tumor growth and metastasis Angiogenic inhibitors may reverse this process Folkman J. N Engl J Med. 1971;285:1182-1186.
- 20. 賀癌平 (Herceptin) 優於 泰嘉錠 Lapatinib
- 21. 賀癌平 (Herceptin) 優於 泰嘉錠 Lapatinib 0 5 10 15 20 25 30 35 40 45 NEO-ALT GEPAR Lapatinib Trastuzumab Neo-ALTTO GEPARQUINTO Inability to give planned doses of lapatinib ~35% in both studies
- 22. 雙標靶藥物治療
- 23. 雙標靶藥物治療
- 24. 只用標靶不打化療 ?
- 25. Herceptin ( 賀癌平 )
- 26. Herceptin ( 賀癌平 ) • 靜脈點滴注射 • 三週一次 • 施打一年 • 健保給付 (1 手術後輔助 限淋巴轉移者 ) • (2 轉移乳癌 ) • 副作用 : 心臟搏出力下降 ( 發生率 4% 可 恢復 )
- 27. Herceptin ( 賀癌平 ) • Herceptin ( 賀癌平 ) 打二年沒比打一年好 • Herceptin ( 賀癌平 ) 打半年沒有打一年好
- 28. Lapatinib 泰嘉錠 • 口服標靶藥 • 轉移乳癌第二線標靶藥 ( 賀癌平失效 後 ) • 健保不給付 • 常見副作用 : 腹瀉
- 29. • Trastuzumab continually suppresses HER2 activity • Flags cells for destruction by the immune system • Pertuzumab inhibits HER2 forming dimer pairs • Suppresses multiple HER signaling pathways • Flags cells for destruction by the immune system HER2 receptor Trastuzumab Pertuzumab Subdomain IV of HER2 Dimerization domain of HER2 Trastuzumab and pertuzumab bind to different regions on HER2 and have synergistic activity
- 30. • Trastuzumab continually suppresses HER2 activity • Flags cells for destruction by the immune system • Pertuzumab inhibits HER2 forming dimer pairs • Suppresses multiple HER signaling pathways • Flags cells for destruction by the immune system HER2 receptor Trastuzumab Pertuzumab Subdomain IV of HER2 Dimerization domain of HER2 Trastuzumab and pertuzumab bind to different regions on HER2 and have synergistic activity
- 32. This presentation contains non-licensed product information. T-DM1 MoA: Endocytosis • HER2 receptor–T-DM1 complex is internalized into the tumor cell via endocytosis Erickson et al. Cancer Res 2006
- 33. This presentation contains non-licensed product information. T-DM1 MoA: Lysosomal degradation • Once endocytosis is complete, trastuzumab and the HER2 receptor are degraded and a cytotoxic metabolite* is released Erickson et al. Cancer Res 2006 Lewis Phillips et al. Cancer Res 2008 *Lysine-bound emtansine plus linker
- 34. Thanks !!
Hinweis der Redaktion
- 13-05-01 CCO Pfizer CME Virtual Presentation May 2010 To better understand these developments, it is useful to go to the original hypothesis regarding the concept of using antiangiogenic drugs for cancer treatment that Judah Folkman, MD, published in 1971, and to note how much has changed since then. The basic elements of the hypothesis, as shown here, are well known. Small incipient tumor masses will not grow beyond the size of approximately 1-2 millimeters unless they can develop a blood vessel supply to provide the necessary oxygen and nutrients to allow progressive expansion of tumor mass. Dr. Folkman envisaged that during the course of tumor development, cells within some of the small microscopic occult tumors—for reasons that were unknown back then—would start to secrete a single tumor angiogenesis factor (TAF); we now call TAF a signaling molecule. TAF would diffuse out from the tumor cell population, bind to adjacent endothelial cells of mature blood vessels, and trigger a form of angiogenesis called sprouting angiogenesis, leading to the development of new blood vessel capillaries. Those capillaries would then infiltrate the microscopic tumor mass and set in motion the possibility of progressive expansion of tumor mass and hematogenous metastatic spread. Dr. Folkman hypothesized that it might be possible to block this process, for example, by developing a monoclonal antibody to the hypothetical TAF molecule made by the tumor cell population. Blocking the activity of TAF would reverse or retard the process of tumor angiogenesis and reintroduce a state of tumor dormancy, thereby prolonging survival. One of the ways that the angiogenesis model changed is that there is no longer any evidence of a single TAF. Instead, a large family of different proangiogenic growth factors contributes to the development of new blood vessels. In addition, the model now includes evidence that starving a tumor of oxygen and inducing an elevated state of tumor hypoxia can have both positive and negative effects, at least in theory, and probably in practice.