EP11-癌症為何不斷復發？從臨床病理視角解密巨噬細胞的抗癌奇招 The Science of Relapse

【與漢康讀懂腫瘤免疫新藥的抗癌革命】由漢康生技企劃製作
當現有治療工具越來越多，甚至進入精準醫療時代，為什麼癌症還是會反覆復發？
為什麼殺死了大部分的腫瘤，卻殺不死最狡猾的「腫瘤幹細胞」？
當全球大廠在 CD47 靶點上因「溶血毒性」紛紛折戟，漢康生技如何透過巧妙的分子設計逆轉局勢？
本集我們邀請到漢康生技科學委員、德州大學西南醫學中心病理專家——陳明義教授，帶我們從第一線臨床視角，看懂下一代腫瘤免疫新藥的致勝關鍵。

精彩內容：

• 癌症復發的真相： 為什麼化療與放療在殺死腫瘤的同時，卻也讓「腫瘤幹細胞（Cancer Stem Cells）」成功逃逸並導致無止盡的復發？

• 靶向治療的終極條件： 為什麼完美的靶點必須符合「腫瘤高表達、正常細胞零表達」的嚴苛標準？

• 破解 CD47 的溶血魔咒： 漢康的 HCB101 如何透過 AI 結構生物學設計 SIRPα「誘餌（Decoy）」，精準毒殺腫瘤卻能完美避開紅血球？

• 1+1>2 的協同療法（Synergistic Therapy）： 為什麼「低劑量化放療」搭配「巨噬細胞免疫藥物」，能大幅降低全身毒性並提高長期存活率？

• FBDB 平臺的延伸潛力： 如何透過降低藥物的「抗原性（Antigenicity）」來延長有效循環時間？具備三個標靶手臂（Arm）的三特異性融合蛋白 HCB301，又將如何讓腫瘤無處可逃？

【About This Episode】
When there are more treatment tools than ever in the era of precision medicine, why do cancers still frequently relapse? Why do conventional treatments kill the bulk of the tumor but fail to eliminate the cunning "cancer stem cells"? As global pharma giants stumble over severe hemolytic toxicity in CD47-targeted therapies, how does HanchorBio reverse the tide with clever molecular design? In this episode, we invite Dr. Ming-Yi Chen, a pathology expert at UT Southwestern Medical Center and Scientific Committee member of HanchorBio, to reveal the winning strategies of next-generation immuno-oncology drugs from a frontline clinical perspective.

【Key Takeaways】
The Truth About Cancer Relapse: Why do chemotherapy and radiation kill mature tumors but inadvertently allow "cancer stem cells" to escape and cause endless recurrence?
The Ultimate Criterion for Targeted Therapy: Why must a perfect target adhere to the strict standard of being highly expressed on tumors but completely absent on normal cells?
Breaking the CD47 Hemolytic Curse: How does HanchorBio's HCB101 use an AI-designed SIRPα "decoy" to precisely target tumors while perfectly avoiding red blood cells?
Synergistic Therapy (1+1>2): Why does combining "low-dose chemo/radiation" with "macrophage-directed immunotherapy" drastically reduce systemic toxicity and improve long-term survival?
The Extended Potential of the FBDB Platform: How does reducing a drug's "antigenicity" prolong its effective circulation time? And how will HCB301, a tri-specific antibody with three targeting arms, leave tumors with nowhere to hide?