操纵、伪造实验数据长达12年之久（从2002年到2014年），俄亥俄州立大学教授Samson Jacob仍然熬到了名誉教授的荣休身份。而学校的一项学术不端调查，却让他名誉扫地。2021年5月，Samson Jacob被取消退休职位。俄亥俄州立大学表示Samson Jacob在研究中存在不当行为，并且他的实验室存在“放任数据操纵”的风气。校方表示“他已与大学没有任何关系”。
俄亥俄州立大学调查发现有20篇研究论文存在学术不端。截至到2023年12月17日，Samson Jacob被撤回17篇文章（在2023年12月15日被撤回4篇Cancer Research 文章）。
2021年2月，经过俄亥俄州立大学(Ohio State University)调查委员会长达5年、对67项指控的调查，公布了一份长达209页的调查报告。报告显示，在2002-2014年，Samson Jacob团队发表的论文中明显存在大量被操纵的图像，委员会确信“Samson Jacob实验室中存在一种允许的操纵数据文化，尤其是对照组数据，这不是由于疏忽造成的错误。” 调查发现有20篇研究论文存在学术不端。此前的2018年，雅各布等已被撤稿9篇，更正1篇。委员会要求，立即撤回其余的10篇，并建议对其进行制裁。
目前，委员会的建议正在实施中。2021年5月，Samson Jacob被取消退休职位。俄亥俄州立大学表示Samson Jacob在研究中存在不当行为，并且他的实验室存在“放任数据操纵”的风气。校方表示“他已与大学没有任何关系”。 委员会提出了3点建议：一是禁止雅各布进行所有研究、带研究生等其他研究者，并禁止在3年内提交联邦资助申请；二是撤销他的退休职位和杰出教师身份；三是要求自报告之日起的3年内，取消他的PI身份。[1]PTPROt inactivates the oncogenic fusion protein BCR/ABL and suppresses transformation of K562 cells，Journal of Biological Chemistry ；
[2]Identification of T-cadherin as a novel target of DNA methyltransferase 3B and its role in the suppression of nerve growth factor-mediated neurite outgrowth in PC12 cells，Journal of Biological Chemistry；[3]Role of DNA methyltransferases in regulation of human ribosomal RNA gene transcription，Journal of Biological Chemistry；[4]Treatment of PC12 cells with nerve growth factor induces proteasomal degradation of T-cadherin that requires tyrosine phosphorylation of its cadherin domain，Journal of Biological Chemistry；[5]Role of de novo DNA methyltransferases and methyl CpG-binding proteins in gene silencing in a rat hepatoma，Journal of Biological Chemistry；[6]Identification of a novel cyclic AMP-response element (CRE-II) and the role of CREB-1 in the cAMP-induced expression of the survival motor neuron (SMN) gene，Journal of Biological Chemistry；[7]Mitochondrial transcription factor A and its downstream targets are up-regulated in a rat hepatoma，Journal of Biological Chemistry；[8]Down-regulation of micro-RNA-1 (miR-1) in lung cancer. Suppression of tumorigenic property of lung cancer cells and their sensitization to doxorubicin-induced apoptosis by miR-1，Journal of Biological Chemistry；[9]Anti-microRNA-222 (anti-miR-222) and -181B suppress growth of tamoxifen-resistant xenografts in mouse by targeting TIMP3 protein and modulating mitogenic signal，Journal of Biological Chemistry；[10]HOXB13, a target of DNMT3B, is methylated at an upstream CpG island, and functions as a tumor suppressor in primary colorectal tumors,PLOS ONE ;
[11]Protein tyrosine phosphatase receptor-type O (PTPRO) exhibits characteristics of a candidate tumor suppressor in human lung cancer,PNAS ;[12]DNA methyltransferase 3b regulates nerve growth factor-induced differentiation of PC12 cells by recruiting histone deacetylase 2,Molecular and Cellular Biology ;[13]5-Aza-Deoxycytidine Induces Selective Degradation of DNA Methyltransferase 1 by a Proteasomal Pathway That Requires the KEN Box, Bromo-Adjacent Homology Domain, and Nuclear Localization Signal,Molecular and Cellular Biology ;[14]Methylation Mediated Silencing of MicroRNA-1 Gene and Its Role in Hepatocellular Carcinogenesis,Cancer Res ;[15]A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking DNA Methyltransferase 1 Activity and Inducing Its Degradation,Cancer Res ;[16]Loss of Metallothionein Predisposes Mice to Diethylnitrosamine-Induced Hepatocarcinogenesis by Activating NF-κB Target Genes,Cancer Res ;
[17]Physical and Functional Interaction of DNA Methyltransferase 3A with Mbd3 and Brg1 in Mouse Lymphosarcoma Cells,Cancer Res ;
https://retractionwatch.com/2022/07/25/exclusive-osu-investigation-finds-dishonesty-and-permissive-culture-of-data-manipulation-in-cancer-research-lab/
