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| 1 | Oct 4+/Tenascin C+ neuroblastoma cells serve as progenitors of tumor-derived endothelial cells显示文摘Neuroblastoma (NB ) 联系了 endothelial microvessels (他们) 可以被导出肿瘤的 endothelial 房间(侦探) 衬里,那是遗传上不稳定的并且 chemoresistant。这里,我们由集中于 Octamer 有约束力的抄写因素 4 在 NB 探讨了侦探祖先的鉴定(Oct-4 ) 作为一个通常认为的标记。Oct-4 + 房间在主要 NB 样品被检测(n = 23 ) ,变形骨头髓把发成送气音(n = 10 ) , NB 房间线(n = 4 ) ,并且 orthotopic 肿瘤(n = 10 ) 在 immunodeficient 老鼠由 HTLA-230 NB 房间线形成了。大多数 Oct-4 + 房间显示出 perivascular 分布,与他们中的 5% 个一起在 perinecrotic 区域的 homing。自从他们与恶意的房间分享了 MYCN oncogene 的扩大,所有 Oct-4 + 房间是导出肿瘤的。表示的 Perivascular Oct-4 + 细胞起源房间相关的、神经祖先相关、 NB 相关的标记包括表面 Tenascin C (TNC ) ,那不在 perinecrotic Oct-4 + 细胞和体积肿瘤细胞。在 vitro 区分进在包含脉管的 endothelial 生长因素(VEGF ) 的媒介在文化之上表示 vascular-endothelial-cadherin,前列腺特定的膜抗原和 CD31 的象 endothelial 一样房间的 TNC + 然而并非 TNC − HTLA-230 房间。TNC + 然而并非 TNC − HTLA-230 房间形成了 neurospheres 什么时候在没有浆液的媒介有教养。房间部分是 tumorigenic,但是仅仅肿瘤由包含的他们由侦探衬里的 TNC + 房间形成了。在结论,我们在 NB 肿瘤识别了包含 Oct-4 + 肿瘤房间的二个通常认为的壁龛。Oct-4 +/TNC+ perivascular NB 房间显示了粘性的高度并且用作侦探的祖先。Oct4 +/TNC+ 祖先的治疗学的指向可以抵抗导出 NB 的 EC 的贡献到肿瘤恶化和 chemoresistance。 | Annalisa Pezzolo Federica Parodi Danilo MarimPietri Lizzia Raffaghello Claudia Cocco Angela Pistorio Manuela Mosconi Claudio Gambini Michele Cilli Silvia Deaglio Fabio Malavasi Vito Pistoia | 2011 | Cell Research2011，21，10： | 2 |
| 2 | Expression of P2X7 Receptor Increases In Vivo Tumor Growth显示文摘 | Elena Adinolfi Lizzia Raffaghello Anna Lisa Giuliani Luigi Cavazzini Marina Capece Paola Chiozzi Giovanna Bianchi Guido Kroemer Vito Pistoia Francesco Di Virgilio | 2012 | Cancer Research2012，，： | 1 |
| 3 | Expression of P2X7 receptor increases in vivo tumor growth显示文摘 | Elena Adinolfi Lizzia Raffaghelto Anna L Giutiaa | 2012 | Cancer Res2012，72，12： | 1 |
| 4 | Pancreatic metastasis from mycosis fungoides mimicking primary pancreatic tumor显示文摘Mycosis fungoides(MF) is a cutaneous T-cell lymphoma that can undergo local progression with possible systemic dissemination. We report a case of a patient affected by MF with a pancreatic mass that was a diagnostic challenge between primitive tumor and pancreatic metastasis from MF. Clinical setting findings and imaging studies raised the suspicion of a pancreatic primary neoplasm. A diagnostic clue was provided by the combined histomorphologic/immunohistochemical study of pancreatic and cutaneous biopsies, which revealed a pancreatic localization of MF. Considering the rarity of metastatic localization of MF to the pancreas, we next investigated whether chemokinechemokine receptor interactions could be involved in the phenomenon to provide new insight into the possible mechanisms underlying metastatic localization of MF to the pancreas. Histological analyses of archival pancreatic tissue demonstrated that glucagon-secreting cells of the pancreatic islets expressed the CCL27 chemokine, which may have attracted in our case metastatic MF cells expressing the complementary receptor CCR10. | Paola Ceriolo Valentina Fausti Elisa Cinotti Silvia Bonadio Lizzia Raffaghello Giovanna Bianchi Giulio Fraternali Orcioni Roberto Fiocca Franco Rongioletti Vito Pistoia Giacomo Borgonovo | 2016 | World Journal of Gastroenterology2016，22，12： | 0 |
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