Korc M
Department of Medicine, University of California at Irvine, Irvine, California 92697, USA.
Surg Oncol Clin N Am. 1998 Jan;7(1):25-41.
Human pancreatic cancers overexpress a number of important tyrosine growth factor receptors and their ligands. These include the epidermal growth factor (EGF) receptor (EGFR) and related receptors, multiple ligands that bind to EGFR, certain fibroblast growth factors (FGF) receptors (FGFR) and ligands, and insulin-like growth factor I (IGF-I) and its receptor. The excessive activation of mitogenic signaling cascades that are modulated by these overexpressed ligands and receptors is compounded by the presence of mutations in the K-ras oncogene. Pancreatic cancers also overexpress transforming growth factor betas (TGF-betas) that usually inhibit the growth of epithelial cells. Pancreatic cancers, however, underexpress the type I TGF-beta receptor and harbor mutations in the smad4 gene, alterations that prevent TGF-betas from inhibiting cancer cell growth but that do not confer onto pancreatic actions that promote cancer growth in vivo. Together, these perturbations confer onto pancreatic cancer cells a tremendous growth advantage.
人类胰腺癌过度表达多种重要的酪氨酸生长因子受体及其配体。这些包括表皮生长因子（EGF）受体（EGFR）及相关受体、多种与EGFR结合的配体、某些成纤维细胞生长因子（FGF）受体（FGFR）及其配体，以及胰岛素样生长因子I（IGF-I）及其受体。由这些过度表达的配体和受体调节的促有丝分裂信号级联的过度激活，因K-ras癌基因中的突变而加剧。胰腺癌还过度表达通常抑制上皮细胞生长的转化生长因子β（TGF-β）。然而，胰腺癌中I型TGF-β受体表达不足，且smad4基因存在突变，这些改变阻止了TGF-β抑制癌细胞生长，但并未赋予胰腺在体内促进癌症生长的作用。这些扰动共同赋予胰腺癌细胞巨大的生长优势。
