Retraction Watch

Tracking retractions as a window into the scientific process

Retraction appears for group whose former member was sanctioned by ORI

with 14 comments

Journal of Biological ChemistryResearchers whose former colleague was recently reprimanded by the U.S. Office of Research Integrity (ORI) have retracted a biology paper for duplication.

The retraction includes some familiar names: The last author Steven Grant, senior author of the newly retracted study, is also the last author of 11 papers flagged in a report by the ORI in December, 2015. That report focused on Girija Dasmahapatra, a co-author of the 11 studies who was also based at at Virginia Commonwealth University (VCU). Dasmahapatra left VCU in 2015, and is not listed on the latest retraction.

The retracted paper, published in The Journal of Biological Chemistry (JBC), was also co-authored by Paul Dent, a biochemist at the VCU, who we mentioned last year when he offered to retract another paper in Molecular Pharmacology after concerns arose on PubPeer. The journal has instead issued a lengthy correction (what we call a “mega-correction”).

A VCU spokesperson told us:

After VCU discovered issues with the paper, the senior author notified the journal editor and ultimately withdrew the article.

The spokesperson added:

The article’s first author, Roberto Rosato, left VCU in 2010. Jorge Almenara, Paul Fisher, Paul Dent and Steven Grant remain at VCU.

Here’s the retraction notice, issued on August 19:  

This article has been withdrawn by the authors. The image used to represent U937 cells treated without TBAP for 4 h in Fig. 4A was reused to represent U937/3.1EV cells treated with LBH for 4 h in Fig. 7B. In Fig. 4C, lanes 1 and 2 of the left pIKK-β/α panel were duplicated, lanes 1 and 3 of the right pIKK-β/α panel were duplicated, lanes 4 and5 of the left IKK-β/α panel were duplicated, and lanes 2–5 of the left actin panel were duplicated in lanes 2–5 of the right actin panel. The actin immunoblot in Fig. 6A was reused as the actin immunoblot in Fig. 7A. Part of the actin panels in Fig. 4C was reused as actin in Fig. 6B. In Fig. 6B, lanes 1 and 2 of the left actin panel were duplicated inlanes 2 and 3 of the right actin panel. In supplemental Fig. 1A, lane 3 of the actin immunoblot from Jurkat cells was reused as lane 1 of the actin immunoblot from HL-60 cells. In supplemental Fig. 3A, lanes 1 and 2 of the TRAF2 immunoblot were duplicated. The actin immunoblot from supplemental Fig. 4B was reused as the actin immunoblot in supplemental Fig. 5B.

The 2010 paper, “Histone Deacetylase Inhibitors Activate NF-κB in Human Leukemia Cells through an ATM/NEMO-related Pathway,” has so far been cited 42 times, according to Thomson Reuters Web of Science. It was recently questioned on PubPeer.

And here’s the mega-correction notice issued last month for the Molecular Pharmacology paper Dent previously offered to retract, “Human Chorionic Gonadotropin Modulates Prostate Cancer Cell Survival after Irradiation or HMG CoA Reductase Inhibitor Treatment:”

The above article [Yacoub A, Hawkins W, Hanna D, Young H, Park MA, Grant M, Roberts JD, Curiel DT, Fisher PB, Valerie K, Grant S, Hagan MP, Dent P (2007) Mol Pharm 71:259–275], contained the following errors:

It has been pointed out to us that the control 0 min time point bands in Figure 2E were duplicated. The control lanes were purposefully placed as duplicates for illustrative purposes, and the Figure Legend inadvertently neglected to mention this. To remedy this issue, these and related experiments corresponding to Figure 2D(i) and Figure 2E of the original manuscript were repeated and the new data are shown here as Panel A and Panel B, respectively.

In Panel A (corresponding to Figure 2D(i)), we observe that hCG increased ERBB1 Y1173 phosphorylation over a 2h time course that was very similar to the originally published data. The ERBB1 Y845 phosphorylation also exhibited a similar pattern of phosphorylation, though the level of increased phosphorylation did not exhibit as high a peak at 60 min and at 90 min as was presented in the originally published data. The hCG –stimulated phosphorylation of ERBB1 Y1068 and ERBB1 Y1173 in the present studies and those in our previously published data were very similar. However, repeat data for P-ERB1(Y992) was omitted due to a poor antibody that failed to recognize the substrate. It should be noted that the data in this revised Figure 2D(i) does not impact the major findings of the paper.

Panel B presents new data corresponding to original Figure 2E with independent vehicle controls at each time point. LNCaP cells, 24 hours after plating, were treated with 2 mU/ml hCG or its vehicle (phosphate-buffered saline). After hCG treatment (0-180 min, as indicated), cells were isolated, lysed in SDS-PAGE sample buffer, and equal protein concentrations were subjected to SDS-PAGE followed by immunoblotting to determine the phosphorylation status of ERBB1 Tyr1068/Tyr1173/ Tyr845 and of ERK1/2 and the expression level of ERK2 and ERBB1 protein. Repeat data for P-ERB1(Y992) was omitted due to a poor antibody that failed to recognize the substrate. The data presented herein are representative of multiple experiments, n = 3.

In Panel B we previously observed that both hCG and ionizing radiation individually increased ERBB1 Y1173 and ERBB1 Y1068 phosphorylation after 30 min and 180 min, and similar data were obtained in the present studies. In the prior studies combined treatment with hCG and radiation caused a modest further increase that was not observed in our present assays. Similar to the original studies, we observed that hCG and radiation promoted an increase in ERBB1 Y845 phosphorylation after 30 min, but not at 180 min.

For treatments with radiation that were also associated with AKT T308 phosphorylation, present studies observed greater levels of AKT S473 phosphorylation compared to the modest increase observed in the original studies. The changes in ERK1/2 and in JNK1/2 phosphorylation in the present studies and those previously published were very similar though in the present studies the synergy of interaction for ERK1/2 activation was less apparent. It should be noted that the data in this revised Figure 2E does not impact on the major findings of the paper.

The authors regret these errors and any inconvenience it may have caused.

The 2007 paper has been cited eight times, and its correction has yet to be cited.

Dent has previously logged four other errata (1, 2, 3, 4) for issues related to images; Grant is a co-author of one of these papers.

According to the ORI, all 11 papers mentioned in the 2015 report will either be retracted or corrected; so far, one study in Leukemia has been pulled. Dent is a co-author of nine of these papers.

Several other papers authored by Dent, Grant, Paul Fisher (eighth author of the newly retracted paper) and others are being questioned on PubPeer.

In 2014, Fisher received the “Virginia’s Outstanding Scientist of 2014” award at the Science Museum of Virginia’s General Assembly Reception.

The VCU spokesperson added that the lab where the research was done has since taken “corrective steps” to ensure such errors don’t take place in the future.

We reached out to Grant, who referred us to the VCU spokesperson’s comments.

We also contacted Dent, and will update the post with anything else we learn.

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Comments
  • fernando pessoa September 5, 2016 at 1:34 pm

    Mol Pharmacol. 2006 Jan;69(1):216-25. Epub 2005 Sep 27.
    The histone deacetylase inhibitor LAQ824 induces human leukemia cell death through a process involving XIAP down-regulation, oxidative injury, and the acid sphingomyelinase-dependent generation of ceramide.
    Rosato RR1, Maggio SC, Almenara JA, Payne SG, Atadja P, Spiegel S, Dent P, Grant S.
    Author information
    1Department of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA.

    Pubpeer: https://pubpeer.com/publications/16189296

    Figures 3C and 4C.

    http://i.imgur.com/yxKUWA7.jpg
    http://i.imgur.com/OYqrZeB.jpg

    Figure 1C.
    http://i.imgur.com/vPlkxxu.jpg

  • fernando pessoa September 5, 2016 at 1:36 pm

    Mol Cancer Ther. 2008 Oct;7(10):3285-97. doi: 10.1158/1535-7163.MCT-08-0385.
    Role of histone deacetylase inhibitor-induced reactive oxygen species and DNA damage in LAQ-824/fludarabine antileukemic interactions.
    Rosato RR1, Almenara JA, Maggio SC, Coe S, Atadja P, Dent P, Grant S.
    Author information
    1Department of Medicine, Massey Cancer Center, Virginia Commonwealth University, Richmond, Virginia 23298, USA.

    Pubpeer: https://pubpeer.com/publications/18852132

    Figure 3B. http://i.imgur.com/SdZPylG.jpg

    Figure 5A. http://i.imgur.com/GiOtDsO.jpg

    Figure 6C. http://i.imgur.com/MjKi7ZH.jpg

  • fernando pessoa September 5, 2016 at 1:39 pm

    Mol Cancer Ther. 2007 Feb;6(2):692-702.
    Mechanism and functional role of XIAP and Mcl-1 down-regulation in flavopiridol/vorinostat antileukemic interactions.
    Rosato RR1, Almenara JA, Kolla SS, Maggio SC, Coe S, Giménez MS, Dent P, Grant S.
    Author information
    1Massey Cancer Center, Virginia Commonwealth University, Medical College of Virginia Campus, MCV Station Box 980035, Richmond, VA 23298.

    Pubpeer: https://pubpeer.com/publications/17308065

    Figure 3C.
    http://i.imgur.com/wKjXMH0.jpg

    Figure 4.
    http://i.imgur.com/0mYckx5.jpg

  • fernando pessoa September 5, 2016 at 1:41 pm

    Mol Cancer Ther. 2005 Nov;4(11):1772-85.
    Potentiation of the lethality of the histone deacetylase inhibitor LAQ824 by the cyclin-dependent kinase inhibitor roscovitine in human leukemia cells.
    Rosato RR1, Almenara JA, Maggio SC, Atadja P, Craig R, Vrana J, Dent P, Grant S.
    Author information
    1Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, MCV Station Box 230, Richmond, VA 23298, USA.

    Pubpeer: https://pubpeer.com/publications/16275999

    Figure 2. http://i.imgur.com/SA409Fv.jpg

    Figure 3B. http://i.imgur.com/hVbBgB1.jpg

    Figures 2,3 and 6. http://i.imgur.com/Tgq5fcP.jpg

  • fernando pessoa September 5, 2016 at 1:44 pm

    Cancer Res. 2007 Oct 1;67(19):9490-500.
    The multikinase inhibitor sorafenib potentiates TRAIL lethality in human leukemia cells in association with Mcl-1 and cFLIPL down-regulation.
    Rosato RR1, Almenara JA, Coe S, Grant S.
    Author information
    1Department of Medicine, Massey Cancer Center, Virginia Commonwealth University, Richmond, Virginia 23298, USA.

    Pubpeer: https://pubpeer.com/publications/17909059

    Figure 3C. http://i.imgur.com/P2tgOfW.jpg

    Figure 4C. http://i.imgur.com/iO8ZB07.jpg

  • fernando pessoa September 5, 2016 at 1:47 pm

    Mol Pharmacol. 2004 Mar;65(3):571-81.
    Evidence of a functional role for p21WAF1/CIP1 down-regulation in synergistic antileukemic interactions between the histone deacetylase inhibitor sodium butyrate and flavopiridol.
    Rosato RR1, Almenara JA, Yu C, Grant S.
    Author information
    1Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA.

    Pubpeer: https://pubpeer.com/publications/14978235

    Figure 2B. http://i.imgur.com/zlrSYMD.jpg

    Figures 2B and 6A. http://i.imgur.com/9Gjsahj.jpg

  • fernando pessoa September 5, 2016 at 1:49 pm

    Mol Cancer Ther. 2002 Feb;1(4):253-66.
    The cyclin-dependent kinase inhibitor flavopiridol disrupts sodium butyrate-induced p21WAF1/CIP1 expression and maturation while reciprocally potentiating apoptosis in human leukemia cells.
    Rosato RR1, Almenara JA, Cartee L, Betts V, Chellappan SP, Grant S.
    Author information
    1Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, MCV Station, Box 230, Richmond, VA 23298, USA.

    Pubpeer: https://pubpeer.com/publications/12467221

    Figure 1C. http://i.imgur.com/49sZapN.jpg

    Figure 5B. http://i.imgur.com/SKDkBXG.jpg

  • fernando pessoa September 5, 2016 at 1:51 pm

    LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanism.
    Rosato R1, Hock S, Dent P, Dai Y, Grant S.
    Author information
    1Division of Hematology/Oncology, Department of Medicine, Virginia Commonwealth University and the Massey Cancer Center, Richmond, VA 23298, USA.

    Pubpeer: https://pubpeer.com/publications/22074700

    Figure 1E. http://i.imgur.com/rBb5caw.jpg

  • fernando pessoa September 5, 2016 at 1:52 pm

    Mol Cancer Ther. 2003 Dec;2(12):1273-84.
    Simultaneous activation of the intrinsic and extrinsic pathways by histone deacetylase (HDAC) inhibitors and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) synergistically induces mitochondrial damage and apoptosis in human leukemia cells.
    Rosato RR1, Almenara JA, Dai Y, Grant S.
    Author information
    1Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA.

    Pubpeer: https://pubpeer.com/publications/14707268

    Figure 5B. http://i.imgur.com/3lt2wp1.jpg

  • fernando pessoa September 5, 2016 at 2:11 pm

    Surely VCU is going to try to stop the bleeding at one point?

  • Morty September 6, 2016 at 8:40 am

    “The VCU spokesperson added that the lab where the research was done has since taken “corrective steps” to ensure such errors don’t take place in the future. ”

    How about the previous sins? When will the literature be corrected? There seems to be quite many articles which are not trustworthy.

    I am surprised that there are no consequences for the PIs, irrespective if all the issues are related to sloppiness or misconduct.

  • fernando pessoa September 6, 2016 at 11:19 am

    As long as the lucre keeps rolling in.

  • fernandopessoa September 6, 2016 at 11:33 am

    Another Roberto R Rosato, Steven Grant paper.
    FEBS Lett 581:5075. Citation, including affiliations here: http://imgur.com/G6mAY04

    Figures 4 and 5.
    http://i.imgur.com/ozgx3BS.png

    https://pubpeer.com/publications/B13C22042299E84105E35CA523B30D#fb78792

  • fernandopessoa September 26, 2016 at 9:26 am

    2016 correction 2008 Paul B Fisher, Steven Grant, Paul Dent paper.

    J Biol Chem. 2016 Sep 23;291(39):20823. doi: 10.1074/jbc.A116.803444.
    Multiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signaling.
    Zhang G, Park MA, Mitchell C, Walker T, Hamed H, Studer E, Graf M, Rahmani M, Gupta S, Hylemon PB, Fisher PB, Grant S, Dent P.
    PMID: 27664064

    https://pubpeer.com/publications/748BD6E9A0BE78A2E284CF855CF8E8

    2016 correction figure 3A.
    http://www.jbc.org/content/291/39/20823.long

    VOLUME 283 (2008) PAGES 24343–24358

    PAGE 24348:

    In Fig. 3A, the image of mouse hepatocytes overexpressing p21 and treated with PD184352 (PD) and deoxycholic acid (DCA) was duplicated from the image of mouse hepatocytes infected with control virus and treated with PD184352 and deoxycholic acid. This error has now been corrected. This error does not affect the results or conclusions of this work.

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