近日，一項發(fā)表在Cancer Cell雜志上的研究論文證實：胰腺癌細胞產(chǎn)生一種蛋白質(zhì),，吸引人體免疫細胞,，幫助癌細胞生長。研究還表明阻斷該蛋白可能是一種有效的治療胰腺癌手段,。
胰腺癌（pancreatic carcinoma）,，是胰臟出現(xiàn)的癌癥，其惡性腫瘤會在患者的胰臟生長,。通常認為胰腺癌是常見腫瘤中惡性程度最高,，也是死亡率最高的。40～70歲多見,，男性多于女性,。近年來發(fā)病率有增高趨勢。
研究人員使用胰腺癌小鼠模型發(fā)現(xiàn)KRAS突變觸發(fā)胰腺腫瘤表達一種叫做GM-CSF的蛋白質(zhì),。他們還發(fā)現(xiàn)腫瘤源性GM-CSF聚集在腫瘤組織的不成熟的免疫細胞周圍,，然后誘導這些細胞變成所謂的髓源性抑制細胞，從而抑制其他免疫細胞,，這樣胰腺細胞就能逃脫人體的免疫系統(tǒng),，進而生長和分裂。而阻斷GM-CSF的產(chǎn)生可以抑制髓源性抑制細胞,，恢復免疫系統(tǒng)進而阻止腫瘤的發(fā)展,。（生物谷：Bioon.com）
doi:10.1016/j.ccr.2012.04.025
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Tumor-Derived Granulocyte-Macrophage Colony-Stimulating Factor Regulates Myeloid Inflammation and T Cell Immunity in Pancreatic Cancer
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+ CD11b+ 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+ CD11b+ cells that suppressed antigen-specific T cells. In vivo, abrogation of tumor-derived GM-CSF inhibited the recruitment of Gr-1+ CD11b+ cells to the tumor microenvironment and blocked tumor developmenta finding that was dependent on CD8+ 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.
