Mouse models of Kras activation in gastric cancer.
Mouse models of Kras activation in gastric cancer.
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DOI：
10.1038/s12276-022-00882-1
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发表时间：
2022-11
影响因子：
12.8
通讯作者：
Choi, Eunyoung
中科院分区：
文献类型：
--
作者：
Won, Yoonkyung;Choi, Eunyoung
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. Improvements to genetically engineered mouse models for studying a specific oncogene, a gene with the potential to cause cancer, in gastrointestinal (GI) cancers could help identify the precise cellular origins of these diseases. Mutations affecting the Kirsten rat sarcoma viral oncogene (Kras) are among the most common drivers of cancer. Kras activation varies in terms of incidence rates and roles across GI cancers. Eunyoung Choi and Yoonkyung Won at Vanderbilt University Medical Center in Nashville, USA, reviewed the current scope of genetically engineered mouse models for studying Kras in gastric, pancreatic, and colorectal cancers. Such models have contributed extensively to knowledge of alternate functions of Kras activation during carcinogenic process in different types of cell lineages or organs, and identification of molecular signatures underlying Kras activation.
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影响因子：
24.5
作者：
Deng N;Goh LK;Wang H;Das K;Tao J;Tan IB;Zhang S;Lee M;Wu J;Lim KH;Lei Z;Goh G;Lim QY;Tan AL;Sin Poh DY;Riahi S;Bell S;Shi MM;Linnartz R;Zhu F;Yeoh KG;Toh HC;Yong WP;Cheong HC;Rha SY;Boussioutas A;Grabsch H;Rozen S;Tan P
通讯作者：
Tan P
影响因子：
64.5
作者：
Chen B;Scurrah CR;McKinley ET;Simmons AJ;Ramirez-Solano MA;Zhu X;Markham NO;Heiser CN;Vega PN;Rolong A;Kim H;Sheng Q;Drewes JL;Zhou Y;Southard-Smith AN;Xu Y;Ro J;Jones AL;Revetta F;Berry LD;Niitsu H;Islam M;Pelka K;Hofree M;Chen JH;Sarkizova S;Ng K;Giannakis M;Boland GM;Aguirre AJ;Anderson AC;Rozenblatt-Rosen O;Regev A;Hacohen N;Kawasaki K;Sato T;Goettel JA;Grady WM;Zheng W;Washington MK;Cai Q;Sears CL;Goldenring JR;Franklin JL;Su T;Huh WJ;Vandekar S;Roland JT;Liu Q;Coffey RJ;Shrubsole MJ;Lau KS
通讯作者：
Lau KS
影响因子：
8.8
作者：
Eser, S.;Schnieke, A.;Schneider, G.;Saur, D.
通讯作者：
Saur, D.
影响因子：
24.5
作者：
Caldwell B;Meyer AR;Weis JA;Engevik AC;Choi E
通讯作者：
Choi E
影响因子：
7.3
作者：
Davies, Emma J.;Durban, Victoria Marsh;Clarke, Alan R.
通讯作者：
Clarke, Alan R.