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腾讯登录Cancer Cell：抑制GM-CSF或成胰腺癌治疗新方法
| 导读 | 近日，一项发表在<em>Cancer Cell</em>杂志上的研究论文证实：胰腺癌细胞产生一种蛋白质，吸引人体免疫细胞，帮助癌细胞生长。研究还表明阻断该蛋白可能是一种有效的治疗胰腺癌手段。
胰腺癌（pancreatic carcinoma），是胰脏出现的癌症，其恶性肿瘤会在患者的胰脏生长。通常认为胰腺癌是常见肿瘤中恶性程度最高，也是死亡率最高的。40～70岁多见，男... |
近日，一项发表在<em>Cancer Cell</em>杂志上的研究论文证实：胰腺癌细胞产生一种蛋白质，吸引人体免疫细胞，帮助癌细胞生长。研究还表明阻断该蛋白可能是一种有效的治疗胰腺癌手段。
胰腺癌（pancreatic carcinoma），是胰脏出现的癌症，其恶性肿瘤会在患者的胰脏生长。通常认为胰腺癌是常见肿瘤中恶性程度最高，也是死亡率最高的。40～70岁多见，男性多于女性。近年来发病率有增高趋势。
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研究人员使用胰腺癌小鼠模型发现KRAS突变触发胰腺肿瘤表达一种叫做GM-CSF的蛋白质。他们还发现肿瘤源性GM-CSF聚集在肿瘤组织的不成熟的免疫细胞周围，然后诱导这些细胞变成所谓的髓源性抑制细胞，从而抑制其他免疫细胞，这样胰腺细胞就能逃脱人体的免疫系统，进而生长和分裂。而阻断GM-CSF的产生可以抑制髓源性抑制细胞，恢复免疫系统进而阻止肿瘤的发展。
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<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061221135653.gif" alt="" width="115" height="150" border="0" />
<a title="" href="http://dx.doi.org/10.1016/j.ccr.2012.04.025" target="_blank">doi:10.1016/j.ccr.2012.04.025</a>
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<br/><strong>Tumor-Derived Granulocyte-Macrophage Colony-Stimulating Factor Regulates Myeloid Inflammation and T Cell Immunity in Pancreatic Cancer</strong><br/>
Lauren J. Bayne, Gregory L. Beatty, Nirag Jhala, Carolyn E. Clark, Andrew D. Rhim, Ben Z. Stanger, Robert H. Vonderheide, et al.
Cancer-associated inflammation is thought to be a barrier to immune surveillance, particularly in pancreatic ductal adenocarcinoma (PDA). Gr-1<sup><span style="font-size: x-small;">+</span></sup> CD11b<sup><span style="font-size: x-small;">+</span></sup> cells are a key feature of cancer inflammation in PDA, but remain poorly understood. Using a genetically engineered mouse model of PDA, we show that tumor-derived granulocyte-macrophage colony-stimulating factor (GM-CSF) is necessary and sufficient to drive the development of Gr-1<sup><span style="font-size: x-small;">+</span></sup> CD11b<sup><span style="font-size: x-small;">+</span></sup> cells that suppressed antigen-specific T cells. In vivo, abrogation of tumor-derived GM-CSF inhibited the recruitment of Gr-1<sup><span style="font-size: x-small;">+</span></sup> CD11b<sup><span style="font-size: x-small;">+</span></sup> cells to the tumor microenvironment and blocked tumor development<img src="http://www.bioon.com/biology/UploadFiles/201206/20120612211528746.gif" alt="" border="0" />a finding that was dependent on CD8<sup><span style="font-size: x-small;">+</span></sup> T cells. In humans, PDA tumor cells prominently expressed GM-CSF in vivo. Thus, tumor-derived GM-CSF is an important regulator of inflammation and immune suppression within the tumor microenvironment.
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胰腺癌（pancreatic carcinoma），是胰脏出现的癌症，其恶性肿瘤会在患者的胰脏生长。通常认为胰腺癌是常见肿瘤中恶性程度最高，也是死亡率最高的。40～70岁多见，男性多于女性。近年来发病率有增高趋势。
<!--more-->
研究人员使用胰腺癌小鼠模型发现KRAS突变触发胰腺肿瘤表达一种叫做GM-CSF的蛋白质。他们还发现肿瘤源性GM-CSF聚集在肿瘤组织的不成熟的免疫细胞周围，然后诱导这些细胞变成所谓的髓源性抑制细胞，从而抑制其他免疫细胞，这样胰腺细胞就能逃脱人体的免疫系统，进而生长和分裂。而阻断GM-CSF的产生可以抑制髓源性抑制细胞，恢复免疫系统进而阻止肿瘤的发展。
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061221135653.gif" alt="" width="115" height="150" border="0" />
<a title="" href="http://dx.doi.org/10.1016/j.ccr.2012.04.025" target="_blank">doi:10.1016/j.ccr.2012.04.025</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Tumor-Derived Granulocyte-Macrophage Colony-Stimulating Factor Regulates Myeloid Inflammation and T Cell Immunity in Pancreatic Cancer</strong><br/>
Lauren J. Bayne, Gregory L. Beatty, Nirag Jhala, Carolyn E. Clark, Andrew D. Rhim, Ben Z. Stanger, Robert H. Vonderheide, et al.
Cancer-associated inflammation is thought to be a barrier to immune surveillance, particularly in pancreatic ductal adenocarcinoma (PDA). Gr-1<sup><span style="font-size: x-small;">+</span></sup> CD11b<sup><span style="font-size: x-small;">+</span></sup> cells are a key feature of cancer inflammation in PDA, but remain poorly understood. Using a genetically engineered mouse model of PDA, we show that tumor-derived granulocyte-macrophage colony-stimulating factor (GM-CSF) is necessary and sufficient to drive the development of Gr-1<sup><span style="font-size: x-small;">+</span></sup> CD11b<sup><span style="font-size: x-small;">+</span></sup> cells that suppressed antigen-specific T cells. In vivo, abrogation of tumor-derived GM-CSF inhibited the recruitment of Gr-1<sup><span style="font-size: x-small;">+</span></sup> CD11b<sup><span style="font-size: x-small;">+</span></sup> cells to the tumor microenvironment and blocked tumor development<img src="http://www.bioon.com/biology/UploadFiles/201206/20120612211528746.gif" alt="" border="0" />a finding that was dependent on CD8<sup><span style="font-size: x-small;">+</span></sup> T cells. In humans, PDA tumor cells prominently expressed GM-CSF in vivo. Thus, tumor-derived GM-CSF is an important regulator of inflammation and immune suppression within the tumor microenvironment.
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