한빛사논문
- 조회548
Yoonkyung Won1,2 and Eunyoung Choi 1,2,3
1Department of Surgery, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
2Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
3Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA
Corresponding author: Correspondence to Eunyoung Choi.
Abstract
Gastric cancer has one of the highest incidence rates and is one of the leading causes of cancer-related mortality worldwide. Sequential steps within the carcinogenic process are observed in gastric cancer as well as in pancreatic cancer and colorectal cancer. Kirsten rat sarcoma viral oncogene homolog (KRAS) is the most well-known oncogene and can be constitutively activated by somatic mutations in the gene locus. For over 2 decades, the functions of Kras activation in gastrointestinal (GI) cancers have been studied to elucidate its oncogenic roles during the carcinogenic process. Different approaches have been utilized to generate distinct in vivo models of GI cancer, and a number of mouse models have been established using Kras-inducible systems. In this review, we summarize the genetically engineered mouse models in which Kras is activated with cell-type and/or tissue-type specificity that are utilized for studying carcinogenic processes in gastric cancer as well as pancreatic cancer and colorectal cancer. We also provide a brief description of histological phenotypes and characteristics of those mouse models and the current limitations in the gastric cancer field to be investigated further.
논문정보
- Review Paper
- 2022년 11월 (BRIC 등록일 2022-12-14)
- 국외 연구진
- 의약학 > 종양의학
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