在p53和Cdh1缺失的胃腺癌小鼠模型中，添加致癌Kras（又名Tcon小鼠）加速了肿瘤的发生和转移。
2019年6月19日，纪念斯隆凯特琳癌症中心Sam S Yoon（音译，尹善善）团队在MOLECULAR CANCER RESEARCH 在线发表题为“KRAS Activation in Gastric Adenocarcinoma Stimulates Epithelial-to-Mesenchymal Transition to Cancer Stem-Like Cells and Promotes Metastasis”的研究论文，该研究表明KRAS在胃腺癌细胞中的激活可刺激EMT向CSCs过渡，从而促进转移。本研究为研究KRAS抑制剂在胃腺癌患者中阻断转移和逆转化疗耐药提供了理论依据。
但是，在2024年11月1日，该文章被撤回，主要原因是图片重复使用。
截至到2024年11月3日，由Sam S Yoon作为负责人的已经被撤回包括在MOLECULAR CANCER RESEARCH，Cancer Research，CLINICAL CANCER RESEARCH 及Cell Death & Disease 发表的14篇高水平文章（2024年11月1日被撤回3篇文章），后续会有更多的文章被撤回，iNature持续关注。
应编辑们的要求，这篇文章已被撤回。内部审查检测到本文中以及本文与其他文章之间的图像重复。具体来说，本文图4B中第0天的单细胞图像看起来是相同的。此外，本文的补充图5B与先前发表的一篇已撤稿的Molecular Cancer Research文章的补充图1C之间(2)，以及本文补充图5B中经pd0325901处理的CD44+ AGS与CD44−KATOIII球体之间存在可疑的球体免疫荧光图像重复。这份撤稿通知的副本已发送到所有8位作者最后已知的电子邮件地址。3名作者（Soo-Jeong Cho、Kevin K. Chang、Sam S. Yoon）同意撤回论文；5位作者（Changhwan Yoon, Jacob Till, Jian-xian Lin, Chang-ming Huang, Sandra Ryeom）没有回应。本文(1)中的数据似乎在以后的文章中发表。具体来说，本文的补充图5C与随后一篇被撤稿的文章的图4E之间存在明显的western blot重复(3)。本文图3C中的显微图像似乎与另一篇同样被撤稿的文章的图2F中存在重复(4)。此外，本文图5C与该文章图3E之间似乎存在大量的图像重复(4)。[1]Yoon C , Till J , Cho S-J , Chang KK , Lin J-X , Huang C-M , et al . KRAS activation in gastric adenocarcinoma stimulates epithelial-to-mesenchymal transition to cancer stem–like cells and promotes metastasis. Mol Cancer Res 2019;17:1945–57.
[2]Yoon C , Cho S-J , Chang KK , Park DJ , Ryeom S , Yoon SS . RETRACTED: Role of Rac1 pathway in epithelial-to-mesenchymal transition and cancer stem-like cell phenotypes in gastric adenocarcinoma. Mol Cancer Res 2017;15:1106–16.[3] Choi SI , Yoon C , Park MR , Lee DH , Kook M-C , Lin J-X , et al . RETRACTED: CDX1 expression induced by CagA-expressing Helicobacter pylori Promotes gastric tumorigenesis. Mol Cancer Res 2019;17:2169–83.
[4]Lu J , Bang H , Kim SM , Cho S-J , Ashktorab H , Smoot DT , et al . RETRACTED ARTICLE: Lymphatic metastasis-related TBL1XR1 enhances stemness and metastasis in gastric cancer stem-like cells by activating ERK1/2-SOX2 signaling. Oncogene 2021;40:922–36.Sam S Yoon作为主要负责人被撤回的文章列表：[1]Differential effects of VEGFR-1 and VEGFR-2 inhibition on tumor metastases based on host organ environment，Cancer Research；
[2]Variable Inhibition of Thrombospondin 1 against Liver and Lung Metastases through Differential Activation of Metalloproteinase ADAMTS1，Cancer Research；[3]CD44 Expression Denotes a Subpopulation of Gastric Cancer Cells in Which Hedgehog Signaling Promotes Chemotherapy Resistance，CLINICAL CANCER RESEARCH；[4]KMT2C Mutations in Diffuse-Type Gastric Adenocarcinoma Promote Epithelial-to-Mesenchymal Transition，CLINICAL CANCER RESEARCH；[5]Chemotherapy Resistance in Diffuse-Type Gastric Adenocarcinoma Is Mediated by RhoA Activation in Cancer Stem-Like Cells，CLINICAL CANCER RESEARCH；[6]PI3K/Akt pathway and Nanog maintain cancer stem cells in sarcomas，Oncogenesis；[7]Platelet-derived growth factor receptor-α and -β promote cancer stem cell phenotypes in sarcomas，Oncogenesis；[8]KRAS activation in gastric cancer stem-like cells promotes tumor angiogenesis and metastasis，BMC Cancer ；[9]PIK3R3, part of the regulatory domain of PI3K, is upregulated in sarcoma stem-like cells and promotes invasion, migration, and chemotherapy resistance，Cell Death & Disease；[10]Lymphatic metastasis-related TBL1XR1 enhances stemness and metastasis in gastric cancer stem-like cells by activating ERK1/2-SOX2 signaling，Oncogene；[11]Multimodal targeting of tumor vasculature and cancer stem-like cells in sarcomas with VEGF-A inhibition, HIF-1α inhibition, and hypoxia-activated chemotherapy，Oncotarget；[12]KRAS Activation in Gastric Adenocarcinoma Stimulates Epithelial-to-Mesenchymal Transition to Cancer Stem-Like Cells and Promotes Metastasis，MOLECULAR CANCER RESEARCH；[13]Role of Rac1 Pathway in Epithelial-to-Mesenchymal Transition and Cancer Stem-like Cell Phenotypes in Gastric Adenocarcinoma，MOLECULAR CANCER RESEARCH；
[14]CDX1 Expression Induced by CagA-Expressing Helicobacter pylori Promotes Gastric Tumorigenesis，MOLECULAR CANCER RESEARCH；https://aacrjournals.org/cancerres/article/84/20/3490/749076/Retraction-Differential-Effects-of-VEGFR-1-and
