Abstract: Intrahepatic cholangiocarcinoma (iCCA) is a highly aggressive type of liver cancer that is difficult to treat due to its complicated causes. It is typically detected in advanced stages, leaving patients with few treatment options. Recent breakthroughs in genomic research have emphasized the pivotal significance of genetic changes in the initiation and advancement of intrahepatic cholangiocarcinoma (iCCA). The objective of this study was to investigate the genetic relationships that are responsible for the development and advancement of intrahepatic cholangiocarcinoma (iCCA), with a specific focus on crucial mutations, gene expressions, and molecular pathways that contribute to the formation of tumors. By performing a thorough examination of the genome, we have discovered multiple genetic abnormalities that are frequently linked to intrahepatic cholangiocarcinoma (iCCA), such as changes in the IDH1/2, FGFR2, and KRAS genes. These mutations have been discovered to promote cancer-causing processes by interfering with regular cellular functioning and increasing the likelihood of malignant transformation. Furthermore, the study has examined the influence of epigenetic alterations on gene expression, which enhances the diversity and aggressive characteristics of iCCA. The results have emphasized the significance of genetic profiling in comprehending the molecular pathways that underlie intrahepatic cholangiocarcinoma (iCCA) and highlighting prospective targets for therapy. This review has made an attempt to provide a clear understanding of the genetic characteristics of iCCA, which can lead to the development of tailored treatment strategies. This has the potential to improve outcomes for patients with this challenging condition.
Kadiri et al. (Tue,) studied this question.