A former cancer biologist at the Moffitt Cancer Center in Tampa, Florida has retracted 19 papers from a single journal.
Jin Cheng, who studies how ovarian cancer develops, withdrew 19 papers from the Journal of Biological Chemistry originally published over the last 15 years, and corrected another. All of the retractions are for image manipulation.
For example, here’s the notice for “Activation of phosphatidylinositol 3-kinase/Akt pathway by androgen through interaction of p85α, androgen receptor, and Src,” a paper originally published in 2003:
This article has been withdrawn by the authors. The same data were used to represent different experimental conditions. Specifically, lanes 1–3 of the H2B panel of Fig. 4Bwere reused in lanes 1–3 of the H2B panel from Fig. 6B. Lanes 1 and 6 of the phospho-Akt panel from Fig. 4C were duplicated. Lanes 3 and 4 of the lower FLAG panel in Fig. 4Cwere reused in lanes 7 and 8 of the lower FLAG panel in Fig. 5A. The PI(3,4)P2 spots from lanes 1 and 2 from Fig. 7 were reused in lanes 7 and 8 of the same panel. Additionally, some PI(4)P1 spots were pasted in. The authors state that the overall conclusions of this work are not affected.
Cheng has been awarded multiple NIH R01 grants, totaling millions of dollars, according to NIH RePORTER. A person answering the phone number listed for Cheng’s lab said he had retired. The email address listed on many of his papers bounced.
Here are the 19 retractions:
- Activation of phosphatidylinositol 3-kinase/Akt pathway by androgen through interaction of p85α, androgen receptor, and Src, cited 125 times, according to Clarivate Analytics’ Web of Science, formerly part of Thomson Reuters.
- Identification of Aurora-A as a direct target of E2F3 during G2/M cell cycle progression, cited 23 times
- Akt attenuation of the serine protease activity of HtrA2/Omi through phosphorylation of serine 212, cited 30 times
- Molecular cloning and characterization of the human AKT1 promoter uncovers its up-regulation by the Src/Stat3 pathway, cited 36 times
- ArgBP2γ interacts with Akt and p21-activated kinase-1 and promotes cell survival, cited 24 times
- Akt phosphorylation and stabilization of X-linked inhibitor of apoptosis protein (XIAP), cited 298 times
- AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1. IMPLICATION OF AKT2 IN CHEMORESISTANCE, cited 158 times
- Phosphatidylinositol 3-kinase/Akt pathway regulates tuberous sclerosis tumor suppressor complex by phosphorylation of tuberin, cited 289 times
- Inhibition of JNK by cellular stress- and tumor necrosis factor α-induced AKT2 through activation of the NFκB pathway in human epithelial cells, cited 37 times
- Positive feedback regulation between Akt2 and MyoD during muscle differentiation. CLONING OF Akt2 PROMOTER, cited 42 times
- MicroRNA MiR-214 regulates ovarian cancer cell stemness by targeting p53/Nanog, cited 57 times
- Identification of Akt interaction protein PHF20/TZP that transcriptionally regulates p53, cited 11 times
- IKBKE protein activates Akt independent of phosphatidylinositol 3-kinase/PDK1/mTORC2 and the pleckstrin homology domain to sustain malignant transformation, cited 52 times
- Phosphorylation and activation of androgen receptor by Aurora-A, cited 18 times
- MicroRNA-155 regulates cell survival, growth, and chemosensitivity by targeting FOXO3a in breast cancer, cited 181 times
- A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation, cited 33 times
- IKKϵ phosphorylation of estrogen receptor α Ser-167 and contribution to tamoxifen resistance in breast cancer, cited 35 times
- Phosphoinositide 3-kinase/Akt inhibits MST1-mediated pro-apoptotic signaling through phosphorylation of threonine 120, cited 49 times
- MicroRNA-221/222 negatively regulates estrogen receptor α and is associated with tamoxifen resistance in breast cancer, cited 302 times
The current issue of the JBC also includes a correction of one of Cheng’s papers, “Long non-coding RNAs (LncRNA) regulated by transforming growth factor (TGF) β. LncRNA-HIT-MEDIATED TGF-INDUCED EPITHELIAL TO MESENCHYMAL TRANSITION IN MAMMARY EPITHELIA,” a study that has been cited 17 times.
Update, 11 p.m. Eastern, 10/21/16: Moffitt gave us the following statement:
Moffitt Cancer Center adheres to the highest ethical standards in both research and clinical care. Moffitt has collaborated with the Journal of Biological Chemistry to resolve this issue, and review of this matter is ongoing. Patient care, safety or protocols were not affected in any way.
And University of South Florida Health, with whom the Moffitt is affiliated, said:
Jin Q. Cheng is not a paid USF Health faculty member. We are unaware of any investigations at USF regarding his work.
As of today he still holds a courtesy appointment with USF Health. However, USF reserves the right to address any concerns regarding courtesy appointments at its discretion.
We will look into this matter to determine if any action if necessary.
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