臨床腫瘤學雜志本周報道了一種新的治療腦癌的方法,即將免疫治療與高劑量化療相結合而不是傳統(tǒng)的全腦放療與化療結合.
這種新的療法能明顯降低因全腦放療而給腦細胞帶來的毒性,因為高劑量的全腦放療可殺死腦細胞,從而導致患者的神經系統(tǒng)功能的逐漸退化.據報道,許多腦癌患者就是死于放療輻射的毒性而不是癌癥本身.
免疫治療與放療聯合治療前(A)后(B)的腦部掃面圖
研究結果顯示,連續(xù)5年使用這種新的療法治療腦癌的患者依然還活著,這表明,這種新的治療方法似乎可以更有效的治療癌癥.
該研究的領導者,、腫瘤學家James Rubenstein教授稱:這種新的治療方法與以前全腦放療的治療方法相比,它使淋巴瘤患者的存活率增加了一倍.此外,不同于以往治療原發(fā)性中樞神經系統(tǒng)淋巴瘤的方法,新的方法對年輕患者和60歲以上的老年患者具有同樣的療效.這一發(fā)現是非常有意義的,因為這種類型的腦腫瘤在65歲及以上的老年人身上發(fā)現的概率較高.
研究人員還發(fā)現了一中可以預測治療效果的生物標志物—BCL6基因,這個基因的多少取決于淋巴腫瘤細胞的多少,這項成果可以用于指導研究專門針對淋巴癌的治療方法.
目前,針對這種新的治療方法的療效,加州大學舊金山分校和美國其他醫(yī)療中心正在對更多的人群做一項隨機臨床試驗.
原發(fā)性中樞神經系統(tǒng)淋巴瘤是一種致命的非霍奇金式淋巴瘤,美國每年約有1600人被診斷出患有原發(fā)性中樞神經系統(tǒng)淋巴瘤,這種腫瘤很難被診斷,因為這種疾病常被誤認為是其他形式的腦腫瘤或其他神經系統(tǒng)疾病,如阿爾茨海默氏癥或多發(fā)性硬化癥.
然而,不同于其他腦腫瘤的是原發(fā)性中樞神經系統(tǒng)淋巴瘤會導致嚴重的神經衰弱.而且,手術只能用于診斷原發(fā)性中樞神經系統(tǒng)淋巴瘤而不能治療,因為這種腫瘤能夠在大腦中廣泛傳播.
十幾年前,Rubenstein來到加州大學舊金山分校,他想改變這種現狀,于是與他的同事開始了化療與免疫治療相結合的方法來治療這種腦瘤的研究,這種免疫療法主要是依賴一種來自免疫系統(tǒng)組分的生物藥.
“我們希望開發(fā)一種高效低毒的新的治療原發(fā)性中樞神經系統(tǒng)淋巴瘤的方法.”魯賓斯坦說.第2期多中心臨床試驗的結果表明,這種新的療法能夠使患者長期生存下去.（生物谷Bioon.com）
doi: 10.1073/pnas.1303944110
PMC:
PMID:
Intensive Chemotherapy and Immunotherapy in Patients With Newly Diagnosed Primary CNS Lymphoma
James L. Rubenstein?,Eric D. Hsi,Jeffrey L. Johnson,Sin-Ho Jung,Megan O. Nakashima,Barbara Grant,Bruce D. Cheson andLawrence D. Kaplan
Abstract
Purpose Concerns regarding neurocognitive toxicity of whole-brain radiotherapy (WBRT) have motivated development of alternative, dose-intensive chemotherapeutic strategies as consolidation in primary CNS lymphoma (PCNSL). We performed a multicenter study of high-dose consolidation, without WBRT, in PCNSL. Objectives were to determine: one, rate of complete response (CR) after remission induction therapy with methotrexate, temozolomide, and rituximab (MT-R); two, feasibility of a two-step approach using high-dose consolidation with etoposide plus cytarabine (EA); three, progression-free survival (PFS); and four, correlation between clinical and molecular prognostic factors and outcome.
Patients and Methods Forty-four patients with newly diagnosed PCNSL were treated with induction MT-R, and patients who achieved CR received EA consolidation. We performed a prospective analysis of molecular prognostic biomarkers in PCNSL in the setting of a clinical trial.
Results The rate of CR to MT-R was 66%. The overall 2-year PFS was 0.57, with median follow-up of 4.9 years. The 2-year time to progression was 0.59, and for patients who completed consolidation, it was 0.77. Patients age > 60 years did as well as younger patients, and the most significant clinical prognostic variable was treatment delay. High BCL6 expression correlated with shorter survival.
Conclusion CALGB 50202 demonstrates for the first time to our knowledge that dose-intensive consolidation for PCNSL is feasible in the multicenter setting and yields rates of PFS and OS at least comparable to those of regimens involving WBRT. On the basis of these encouraging results, an intergroup study has been activated comparing EA consolidation with myeloablative chemotherapy in this randomized trial in PCNSL, in which neither arm involves WBRT.
