Swain Sashikanta, Narayan Ravi Kant, Mishra Pravash Ranjan
Department of Anatomy, All India Institute of Medical Sciences, Bhubaneswar, India.
Front Cell Dev Biol. 2024 Aug 22;12:1461278. doi: 10.3389/fcell.2024.1461278. eCollection 2024.
Pancreatic cancer continues to be a deadly disease because of its delayed diagnosis and aggressive tumor biology. Oncogenes and risk factors are being reported to influence the signaling pathways involved in pancreatic embryogenesis leading to pancreatic cancer genesis. Although studies using rodent models have yielded insightful information, the scarcity of human pancreatic tissue has made it difficult to comprehend how the human pancreas develops. Transcription factors like IPF1/, HLXB9, , Islet-1, and signaling pathways, including Hedgehog, TGF-β, and Notch, are directing pancreatic organogenesis. Any derangements in the above pathways may lead to pancreatic cancer. : and are tumor suppressor genes, and the mutations in and somatic loss of are the drivers of pancreatic cancer. This review clarifies the complex signaling mechanism involved in pancreatic cancer, the same signaling pathways in pancreas development, the current therapeutic approach targeting signaling molecules, and the mechanism of action of risk factors in promoting pancreatic cancer.
由于胰腺癌诊断延迟且肿瘤生物学行为侵袭性强，它仍然是一种致命疾病。据报道，癌基因和风险因素会影响参与胰腺胚胎发生的信号通路，从而导致胰腺癌的发生。尽管使用啮齿动物模型的研究已经产生了有见地的信息，但人类胰腺组织的稀缺使得难以理解人类胰腺是如何发育的。像IPF1/、HLXB9、胰岛-1这样的转录因子，以及包括Hedgehog、TGF-β和Notch在内的信号通路，都在指导胰腺器官发生。上述任何通路的紊乱都可能导致胰腺癌。：和是肿瘤抑制基因，和的突变以及的体细胞缺失是胰腺癌的驱动因素。本综述阐明了胰腺癌所涉及的复杂信号机制、胰腺发育中的相同信号通路、目前针对信号分子的治疗方法以及风险因素促进胰腺癌的作用机制。
