Pathways for aberrant angiogenesis in pancreatic cancer.
Pathways for aberrant angiogenesis in pancreatic cancer.
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DOI：
10.1186/1476-4598-2-8
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发表时间：
2003-01-07
期刊：
影响因子：
37.3
通讯作者：
Korc, M
中科院分区：
文献类型：
--
作者：
Korc, M
胰腺导管腺癌（PDAC）是一种毁灭性疾病。尽管决定其生物侵袭性的具体机制尚不清楚，但其特征是各种分子改变以及有丝分裂和血管生成生长因子及其受体的过度表达。pdac还表达高水平的血管内皮生长因子（VEGF）。最近的研究表明，在裸鼠模型中，抑制VEGF表达可以降低胰腺癌细胞的致瘤性，并且VEGF可以对某些胰腺癌细胞直接发挥有丝分裂作用。这些发现表明，癌细胞来源的VEGF通过旁分泌血管生成途径和自分泌有丝分裂途径促进胰腺癌在体内的生长，并为这种致命疾病的治疗干预提供了新的机会。
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease. Although the specific mechanisms that dictate its biological aggressiveness are not clearly established, it is characterized by a variety of molecular alterations as well as by the overexpression of mitogenic and angiogenic growth factors and their receptors. PDACs also express high levels of vascular endothelial growth factor (VEGF). Recent studies indicate that suppression of VEGF expression attenuates pancreatic cancer cell tumorigenicity in a nude mouse model, and that VEGF can exert direct mitogenic effects on some pancreatic cancer cells. These findings suggest that cancer cell derived VEGF promotes pancreatic cancer growth in vivo via a paracrine angiogenic pathway and an autocrine mitogenic pathway, and provide novel opportunities for therapeutic intervention in this deadly disease.