研究人员发现，原始膀胱癌细胞会用“不要吃掉我”的信号做掩饰，把免疫细胞吓跑，以便它们能在稍后发育成熟，形成肿瘤。
不过研究人员已经发现一种撕下膀胱癌细胞这种伪装术的方法，他们表示，这项发现或许有助于形成能治疗几种不同癌肿的新方法。现在最要紧的是要找到一种方法，把那些患有非常危险的膀胱癌的患者，跟那些患有良性肿瘤的人分开。大部分膀胱癌生长缓慢，易于治疗，但是有15%容易扩散，具有很大的致命性。
加利福尼亚州斯坦福大学的欧文·维斯曼(Irving Weissman)博士和同事们发现，所谓的肿瘤干细胞(cancer stem cells)竟用CD-47蛋白质伪装自己。被称作巨噬细胞的免疫细胞通常会吃掉癌细胞，但是CD-47是避开它们的信号。维斯曼在一份声明中说：“这是我们第一次在肿瘤干细胞里发现‘不要吃掉我’的信号。我们正在加紧查看其他肿瘤细胞的步伐，看一看这是不是所有或者大部分肿瘤干细胞惯用的策略。”
该科研组早些时候发现，相同类型的白血病细胞也用CD-47伪装自己。膀胱肿瘤样本显示，大部分肿瘤细胞都含有丰富的CD-47蛋白。维斯曼的科研组发现，继续恶化，形成非常危险的膀胱肿瘤的患者的癌细胞里的CD-47的传递速度更快，这意味着该蛋白更加活跃。他们认为，他们可以利用这种罕见模式更好地帮助患者进行诊断，让那些拥有扩散性更强的癌细胞的患者能更及时的得到治疗。
维斯曼的科研组在美国《国家科学院院刊》（PNAS）上的报告里写道，他们还利用一种单克隆抗体(可以识别单一蛋白的一种免疫系统粒子)来防止CD-47伪装。有抗体的实验室器皿里的肿瘤细胞，不久后就被巨噬细胞消灭了。包括MabThera、赫赛汀(Herceptin)和阿瓦斯汀(Avastin)在内的几种抗癌药物都包含单克隆抗体。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS August 4, 2009, doi: 10.1073/pnas.0906549106
Identification, molecular characterization, clinical prognosis, and therapeutic targeting of human bladder tumor-initiating cells
Keith Syson Chana,b,1, Inigo Espinosac, Mark Chaoa, David Wongd, Laurie Aillesa, Max Diehna, Harcharan Gillb, Joseph Presti, Jr.b, Howard Y. Changd, Matt van de Rijnc, Linda Shortliffeb and Irving L. Weissmana,1
aInstitute for Stem Cell Biology and Regenerative Medicine, Stanford Cancer Center, Stanford University School of Medicine, Stanford, CA 94304-5542;
Departments of bUrology and
cPathology, Stanford University Medical Center, Stanford, CA 94305-5118; and
dProgram in Epithelial Biology, Stanford University, Stanford, CA 94305
Major clinical issues in bladder cancer include the identification of prediction markers and novel therapeutic targets for invasive bladder cancer. In the current study, we describe the isolation and characterization of a tumor-initiating cell (T-IC) subpopulation in primary human bladder cancer, based on the expression of markers similar to that of normal bladder basal cells (Lineage-CD44+CK5+CK20?). The bladder T-IC subpopulation was defined functionally by its enriched ability to induce xenograft tumors in vivo that recapitulated the heterogeneity of the original tumor. Further, molecular analysis of more than 300 bladder cancer specimens revealed heterogeneity among activated oncogenic pathways in T-IC (e.g., 80% Gli1, 45% Stat3, 10% Bmi-1, and 5% β-catenin). Despite this molecular heterogeneity, we identified a unique bladder T-IC gene signature by gene chip analysis. This T-IC gene signature, which effectively distinguishes muscle-invasive bladder cancer with worse clinical prognosis from non-muscle-invasive (superficial) cancer, has significant clinical value. It also can predict the progression of a subset of recurring non-muscle-invasive cancers. Finally, we found that CD47, a protein that provides an inhibitory signal for macrophage phagocytosis, is highly expressed in bladder T-ICs compared with the rest of the tumor. Blockade of CD47 by a mAb resulted in macrophage engulfment of bladder cancer cells in vitro. In summary, we have identified a T-IC subpopulation with potential prognostic and therapeutic value for invasive bladder cancer.
