Oncogenic mutations in KRAS drive common metabolic programmes that facilitate tumour survival, growth and immune evasion in colorectal carcinoma, non-small-cell lung cancer and pancreatic ductal adenocarcinoma. However, the impacts of mutant KRAS signalling on malignant cell programmes and tumour properties are also dictated by tumour suppressor losses and physiological features specific to the cell and tissue of origin. Here we review convergent and disparate metabolic networks regulated by oncogenic mutant KRAS in colon, lung and pancreas tumours, with an emphasis on co-occurring mutations and the role of the tumour microenvironment. Furthermore, we explore how these networks can be exploited for therapeutic gain.

KRAS 中的致癌突变驱动共同的代谢程序，促进结直肠癌、非小细胞肺癌和胰腺导管腺癌中的肿瘤存活、生长和免疫逃避。然而，突变体 KRAS 信号传导对恶性细胞程序和肿瘤特性的影响也取决于肿瘤抑制基因的缺失以及细胞和组织来源特有的生理特征。在这里，我们回顾了在结肠、肺和胰腺肿瘤中由致癌突变体 KRAS 调节的趋同和不同的代谢网络，重点是共同发生的突变和肿瘤微环境的作用。此外，我们探索了如何利用这些网络来获得治疗收益。