新一期英国《自然》杂志刊登报告说，患有前列腺癌的实验鼠在接受激素治疗后常出现一系列反应，最终导致癌症更严重地复发，而在这个过程中一种免疫细胞的“叛变”扮演了重要角色。
美国加利福尼亚大学等机构的研究人员报告说，由于前列腺癌细胞的生长需要睾丸激素，因此目前常用其他激素抑制睾丸激素的作用，以控制前列腺癌发展。这一方法可延长患者数月或数年的生命，但随后常出现更严重的复发。
研究人员经对患病实验鼠分析发现，导致上述现象的原因是激素疗法可引起前列腺发炎，而炎症又引来免疫细胞B细胞，原本帮助身体和疾病斗争的B细胞这时释放大量淋巴毒素，使前列腺癌细胞的生长不再需要睾丸激素，于是癌症复发并更难治疗。
如果设法去除实验鼠体内的B细胞以及相应的淋巴毒素，可将实验鼠癌症复发的间隔延长3至4周，这大约相当于人类的2至3年。
研究人员说，免疫细胞“叛变”导致前列腺癌复发是一个全新发现。
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《自然》发表论文摘要（英文）
Nature 464, 302-305 (11 March 2010) | doi:10.1038/nature08782; Received 1 May 2009; Accepted 29 December 2009
B-cell-derived lymphotoxin promotes castration-resistant prostate cancer
Massimo Ammirante1,4, Jun-Li Luo2,4, Sergei Grivennikov1, Sergei Nedospasov3 " Michael Karin1
Top of pageAbstractProstate cancer (CaP) progresses from prostatic intraepithelial neoplasia through locally invasive adenocarcinoma to castration-resistant metastatic carcinoma1. Although radical prostatectomy, radiation and androgen ablation are effective therapies for androgen-dependent CaP, metastatic castration-resistant CaP is a major complication with high mortality2. Androgens stimulate growth and survival of prostate epithelium and early CaP. Although most patients initially respond to androgen ablation, many develop castration-resistant CaP within 12–18 months2. Despite extensive studies, the mechanisms underlying the emergence of castration-resistant CaP remain poorly understood and their elucidation is critical for developing improved therapies. Curiously, castration-resistant CaP remains androgen-receptor dependent, and potent androgen-receptor antagonists induce tumour regression in castrated mice3. The role of inflammation in castration-resistant CaP has not been addressed, although it was reported that intrinsic NF-κB activation supports its growth4. Inflammation is a localized protective reaction to injury or infection, but it also has a pathogenic role in many diseases, including cancer5. Whereas acute inflammation is critical for host defence, chronic inflammation contributes to tumorigenesis and metastatic progression. The inflammation-responsive IκB kinase (IKK)-β and its target NF-κB have important tumour-promoting functions within malignant cells and inflammatory cells6. The latter, including macrophages and lymphocytes, are important elements of the tumour microenvironment7, 8, 9, but the mechanisms underlying their recruitment remain obscure, although they are thought to depend on chemokine and cytokine production10. We found that CaP progression is associated with inflammatory infiltration and activation of IKK-α, which stimulates metastasis by an NF-κB-independent, cell autonomous mechanism11. Here we show that androgen ablation causes infiltration of regressing androgen-dependent tumours with leukocytes, including B cells, in which IKK-β activation results in production of cytokines that activate IKK-α and STAT3 in CaP cells to enhance hormone-free survival.
