Prominent cancer researcher loses nine papers, making 10

Andrew Dannenberg (credit Patricia Kuharic)

The Journal of Biological Chemistry (JBC) has retracted nine papers in bulk by a group of cancer researchers in New York led by the prominent scientist Andrew Dannenberg

The work of Dannenberg’s group at Weill Cornell — and the figures in particular — has been the subject of scrutiny on PubPeer for more than two years. 

The group also lost an article more than a decade ago in The Lancet, bringing their total so far to 10. Cancer Discovery subjected a paper to an expression of concern in August. Much of the tainted work was funded by grants from the U.S. government, as well as from funding authorities in other countries.  

According to the notice for 2014’s “p53 protein regulates Hsp90 ATPase activity and thereby Wnt signaling by modulating Aha1 expression“:

This article has been withdrawn by the authors. In Fig. 1D, the first lane of the p53 immunoblot was reused as actin in the same figure panel. In Fig. 2B, lanes 1 and 2 of the actin immunoblot were reused in lanes 5 and 6. Lane 2 of the actin immunoblot in Fig. 4K was reused in lanes 3 and 4. The HOP immunoblot in Fig. 4J was reused in Fig. 4 (K and L) as actin. The actin immunoblot in Fig. 4H was reused in Fig. 4 (L and I) as actin. The actin immunoblot in Fig. 5A was reused in Fig. 5B. In Fig. 5H, the c-Myc and Naked-1 immunoblots are the same. There are undeclared gel splices in Figs. 5F, 7C, 7F, and 8I. A portion of the actin immunoblot in Fig. 10A was reused in Fig. 10B as Aha1.

That’s fundamentally the same as the retraction statements for the eight other papers, which date as far back as the early 2000s. Several authors overlap, but only two, Dannenberg and Kotha Subbaramaiah, appear on all nine. Subbaramaiah is now the Jack Fishman Professor of Cancer Prevention at Weill Cornell Medicine. 

The most extensive notice, for the 2009 paper “HDAC6 modulates Hsp90 chaperone activity and regulates activation of aryl hydrocarbon receptor signaling,” reads: 

This article has been withdrawn by the authors. The actin immunoblots in Fig. 2, A and B, are the same. Lanes 4 and 6 of the CYP1A1 and CYP1B1 panels in Fig. 3B are the same. Also in Fig. 3B, lanes 2 and 4 of the 18S rRNA panel are the same. The Hsp90 lanes are all the same in Fig. 6F. The control lanes in Fig. 6H were all reused in the control siRNA lanes. Additionally, the TSA lane for Hsp90 in Fig. 6H was reused in the HDAC6 siRNA lane. The first lane of the IP: Hsp90, IB: HDAC6 lane in Fig. 6I was reused in the TSA lane for Hsp90. The first lane in the input panel in Fig. 8F was reused in Fig. 8G. Additionally, lanes 2 and 3 of the input panel in Fig. 8G are duplicated. Lane 2 of the AhR panel in Fig. 8E was reused in the actin panel in Fig. 9D and in Subbaramaiah, K., et al. (2008) J. Biol Chem. 283, 33955–33968. In Fig. 9B, lanes 2 and 3 of the input are the same. Part of the input panel in Fig. 9C was reused in Subbaramaiah, K., et al. (2008) J. Biol. Chem. 283, 33955–33968. Parts of the actin panel in Fig. 9D were reused in Subbaramaiah, K., et al. (2008) J. Biol. Chem. 283, 33955–33968. The lanes in the p23 panel of Fig. S1A are the same. In Fig. S1B, lanes 3 and 4 of the Hsp90 panel are the same as well as lanes 1 and 2 of the AhR panel, lanes 1 and 2 of the actin panel, and lanes 3 and 4 of the actin panel. In Fig. S1C, the lanes in the XAP-2 panel are the same. In Fig. S1E, the first lane of the Hsp90 panel were reused in lanes 1 and 2 of the HDAC6 panel. Also in Fig. S1E, lane 3 of the Hsp90 panel was reused in lane 3 of the XAP-2 panel. In Fig. S2, the first lane of the Hsp90 panel was reused in lanes 4 and 6 of the same panel as well as in lane 4 of the IP: Hsp90, IB: AcK panel. Also in Fig. S2, the third lane of the Hsp90 panel was reused in lane 5 of the same panel as well as lane 6 of the IP: Hsp90, IB: AcK panel. Additionally, some portions of the IP: Hsp90, IB: AcK panel were reused in Subbaramaiah, K. et al. (2008) J. Biol. Chem. 283, 33955–33968. 

Dannenberg referred us to Weill media officials and his attorney, Bruce Singal, who specializes in research misconduct cases at the Boston firm of Barrett & Singal. Singal told us that Dannenberg: 

is cooperating fully, both with the JBC and with Weill Cornell, in making sure they get to the bottom of this. He certainly had nothing to do with generating the experiments [with the falsified data] and he had every reason to believe that the data were truthful and reliable.

Singal said Dannenberg became aware “a couple of months ago” from JBC about problems with the articles, and notified Weill Cornell officials at that time. Singal added that Weill is investigating the case, but would not identify a target of the inquiry: 

I’m not going to get into specifics.

Singal said he did not know if the U.S. Office of Research Integrity was looking into the matter. 

In a statement, Weill Cornell Medicine told Retraction Watch:

Weill Cornell Medicine is committed to the responsible conduct of research and promotes the highest ethical standards to foster scientific research that advances human health.  Our administration, faculty, students and staff share this responsibility and are required to follow our Policies and Procedures for Research Integrity.  Weill Cornell Medicine’s Office of Research Integrity (WCM’s ORI), overseen by our Senior Associate Dean for Research, ensures that all research is conducted in accordance with these policies and with federal, state, and institutional protocols.

WCM’s ORI was recently alerted by two faculty members that an academic journal had raised questions about their published articles.  In accordance with our outlined policies, WCM’s ORI commenced a faculty inquiry and forensic review of the research in question.  WCM’s ORI has taken and will continue to take all appropriate steps under our policy and federal regulations to fully investigate this matter.  The authors and their co-authors of the papers have decided to withdraw the articles from the journal.

If WCM’s ORI determines that there has been research misconduct, it will proactively notify appropriate academic journals and appropriate regulatory entities to ensure that the research record is fully corrected and the integrity of our research maintained. 

Dannenberg has at least 60 papers that have been cited 100 or more times, according to Clarivate Analytics’ Web of Science. Subbaramaiah, who has not responded to our request for comment, is not far behind, with at least 41 articles that have tallied 100 or more citations. 

The names of some co-authors on the now-retracted articles might be familiar to some readers. For example, Clifford Hudis, the CEO of the American Society of Clinical Oncology, was among the authors of “Cyclooxygenase-2-derived prostaglandin E2 stimulates Id-1 transcription,” from 2008.

Another notable, Jon Sudbo, the first author of the 2005 Lancet article, which the journal retracted in 2006 after investigators determined that Sudbo had fabricated data from 900 patients in the paper.

Like Retraction Watch? You can make a tax-deductible contribution to support our work, follow us on Twitter, like us on Facebook, add us to your RSS reader, or subscribe to our daily digest. If you find a retraction that’s not in our database, you can let us know here. For comments or feedback, email us at team@retractionwatch.com.

16 thoughts on “Prominent cancer researcher loses nine papers, making 10”

  1. 2 thoughts:

    “Singal said Dannenberg became aware “a couple of months ago” from JBC about problems with the articles, and notified Weill Cornell officials at that time.” Dannenberg could have read the numerous PubPeer threads on his papers beginning 2 years ago. Don’t see any of his papers with author comments, so maybe he didn’t.

    “Singal said he did not know if the U.S. Office of Research Integrity was looking into the matter.” One would hope so, although maybe they don’t always notify individual targets of investigations.

    1. To Regret: Since WCM’s response quoted here stated “WCM’s ORI commenced a faculty inquiry and . . . will continue to take all appropriate steps under our policy and federal regulations to fully investigate this matter” and since the two J. Biol Chem. papers linked here cited support from a federal NIH NCI grant, WCM would be obligated to inform the federal Office of Research Integrity (ORI) if a WCM investigation is initiated and later obligated to send its report to the federal ORI on its conclusions.

      The federal ORI itself does not initiate its own “investigations” — instead, ORI waits for the institutional investigation report, and then ORI initiates its own oversight review, notifying the respondent of the institutional investigation if ORI decides that a research misconduct finding and federal administrative actions may be pursued by ORI itself.

  2. “Our administration, faculty, students and staff share this responsibility and are required to follow our Policies and Procedures for Research Integrity. Weill Cornell Medicine’s Office of Research Integrity (WCM’s ORI), overseen by our Senior Associate Dean for Research, ensures that all research is conducted in accordance with these policies and with federal, state, and institutional protocols.”

    Does that apply here?

    Blood. 2006 Apr 15;107(8):3295-302. Epub 2005 Dec 27.
    NF-kappaB is essential for the progression of KSHV- and EBV-infected lymphomas in vivo.
    Keller SA1, Hernandez-Hopkins D, Vider J, Ponomarev V, Hyjek E, Schattner EJ, Cesarman E.
    Author information
    1
    Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, 1300 York Ave, New York, NY 10021, USA.

    Figure 3A.
    https://pubpeer.com/publications/2CF0AD15767F7E22A39DEDC78E40D0#1

    1. “Our administration, faculty, students and staff share this responsibility and are required to follow our Policies and Procedures for Research Integrity. Weill Cornell Medicine’s Office of Research Integrity (WCM’s ORI), overseen by our Senior Associate Dean for Research, ensures that all research is conducted in accordance with these policies and with federal, state, and institutional protocols.”

      Again, does that apply here?

      J Immunol. 2003 Nov 15;171(10):5034-41.
      Reprogramming of IL-10 activity and signaling by IFN-gamma.
      Herrero C1, Hu X, Li WP, Samuels S, Sharif MN, Kotenko S, Ivashkiv LB.
      Author information
      1
      Department of Medicine, Hospital for Special Surgery, Weill Graduate School of Medical Sciences of Cornell University, New York, NY 10021, USA.

      Figure 3.
      https://pubpeer.com/publications/76685C1CD74576DA75194360EC9154#5

      or here?

      Proc Natl Acad Sci U S A. 2005 Jul 19;102(29):10267-72. Epub 2005 Jul 6.
      Inhibition of IFN-alpha signaling by a PKC- and protein tyrosine phosphatase SHP-2-dependent pathway.
      Du Z1, Shen Y, Yang W, Mecklenbrauker I, Neel BG, Ivashkiv LB.
      Author information
      1
      Graduate Program in Immunology, Weill Graduate School of Medical Sciences of Cornell University, New York, NY 10021, USA.

      Figure 6F.
      https://pubpeer.com/publications/81108B3D24951D92669B45BC69FF9B#2

      Figure 1.
      https://pubpeer.com/publications/81108B3D24951D92669B45BC69FF9B#3

      or here?

      J Immunol. 2008 Jun 15;180(12):8057-65.
      IFN-gamma and STAT1 arrest monocyte migration and modulate RAC/CDC42 pathways.
      Hu Y1, Hu X, Boumsell L, Ivashkiv LB.
      Author information
      1
      Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY 10021, USA.

      https://pubpeer.com/publications/22158510422A7662F03042B8A8D864#2

  3. Cancer Discov. 2014 Sep;4(9):1022-35. doi: 10.1158/2159-8290.CD-14-0098. Epub 2014 Jul 31.
    Cell-cycle reprogramming for PI3K inhibition overrides a relapse-specific C481S BTK mutation revealed by longitudinal functional genomics in mantle cell lymphoma.
    Chiron D1, Di Liberto M1, Martin P2, Huang X1, Sharman J3, Blecua P4, Mathew S1, Vijay P5, Eng K5, Ali S6, Johnson A7, Chang B8, Ely S1, Elemento O4, Mason CE4, Leonard JP2, Chen-Kiang S9.
    Author information
    1
    Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York.
    2
    Department of Medicine, Weill Cornell Medical College, New York, New York.
    3
    Willamette Valley Cancer Institute and Research Center/US Oncology Research, Springfield, Oregon.
    4
    Department of Physiology and Biophysics, Weill Cornell Medical College, New York, New York. Institute for Computational Biomedicine, Weill Cornell Medical College, New York, New York.
    5
    Department of Physiology and Biophysics, Weill Cornell Medical College, New York, New York. Tri-Institutional Training Program in Computational Biology and Medicine, Weill Cornell Medical College, New York, New York.
    6
    Foundation Medicine, Inc., Cambridge, Massachusetts.
    7
    Ohio State University, Columbus, Ohio.
    8
    Pharmacyclics, Sunnyvale, California.
    9
    Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Medical College, New York, New York. sckiang@med.cornell.edu

    Figure 3A.
    https://pubpeer.com/publications/4DDFC6377127F3E4BC45A8E63C2266#1

    Figures 3C and 6B.
    https://pubpeer.com/publications/4DDFC6377127F3E4BC45A8E63C2266#2

    2019 correction.
    https://cancerdiscovery.aacrjournals.org/content/9/11/1629.long

    In the original version of this article (1), the actin signal for Pt 8 Ib1 in Fig. 3A was an accidental duplication of the actin signal for Pt 6 r_Ib in the adjacent lane. This figure has now been amended with the correct actin signal for Pt 8 Ib1. The corresponding actin loading control for BTK-pY223 blot (derived from a different gel than the other Western blots in Fig. 3A) is now also included. Dotted lines to indicate joining of lanes that were not continuous in the original Western blots have been added to Fig. 3A and C. The same actin signal for r_IbBM is intentionally presented in Figs. 3C and 4B because the same blot was used in the assembly of each panel. The figures and figure legends have been corrected in the latest online HTML and PDF versions of the article. The authors regret these errors and omissions.

  4. Blood. 2007 Jan 15;109(2):729-39. Epub 2006 Sep 7.
    Hodgkin lymphoma cells express TACI and BCMA receptors and generate survival and proliferation signals in response to BAFF and APRIL.
    Chiu A1, Xu W, He B, Dillon SR, Gross JA, Sievers E, Qiao X, Santini P, Hyjek E, Lee JW, Cesarman E, Chadburn A, Knowles DM, Cerutti A.
    Author information
    1
    Department of Pathology and Laboratory Medicine, Weill Medical College, Cornell University, 1300 York Ave, Rm C-410, New York, NY 10021, USA.

    Figure 5A.
    https://pubpeer.com/publications/6F8061D70C33EA7D14013FCF2015AB#17

    Figure 5C.
    https://pubpeer.com/publications/6F8061D70C33EA7D14013FCF2015AB#20

    Figure 3C.
    https://pubpeer.com/publications/6F8061D70C33EA7D14013FCF2015AB#21

  5. J Virol. 2009 May;83(9):4308-15. doi: 10.1128/JVI.02196-08. Epub 2009 Feb 18.
    Role of defective Oct-2 and OCA-B expression in immunoglobulin production and Kaposi’s sarcoma-associated herpesvirus lytic reactivation in primary effusion lymphoma.
    Di Bartolo DL1, Hyjek E, Keller S, Guasparri I, Deng H, Sun R, Chadburn A, Knowles DM, Cesarman E.
    Author information
    1
    Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065, USA.

    Figure 3.
    https://pubpeer.com/publications/2EE5DEE2FB1D0B985565FABDA9B20E#1

  6. J Immunol. 2000 Jul 15;165(2):830-9.
    B cell receptor engagement and T cell contact induce Bcl-6 somatic hypermutation in human B cells: identity with Ig hypermutation.
    Zan H1, Li Z, Yamaji K, Dramitinos P, Cerutti A, Casali P.
    Author information
    1
    Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University, New York, NY 10021, USA.

    Figure 2A.
    https://pubpeer.com/publications/F6651B803E1E0886D0DAC74DB0A6A2#2

  7. J Biol Chem. 1998 Aug 21;273(34):21875-82.Resveratrol inhibits cyclooxygenase-2 transcription and activity in phorbol ester-treated human mammary epithelial cells.Subbaramaiah K1, Chung WJ, Michaluart P, Telang N, Tanabe T, Inoue H, Jang M, Pezzuto JM, Dannenberg AJ.Author information1Department of Medicine, Department of Surgery, at Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

    Figure 8. Much more similar than you would expect.

    See: https://imgur.com/W68p6JB

  8. “is cooperating fully, both with the JBC and with Weill Cornell, in making sure they get to the bottom of this. He certainly had nothing to do with generating the experiments [with the falsified data] and he had every reason to believe that the data were truthful and reliable.”

    “cooperating fully” sounds like plea bargaining.

  9. Cancer Prev Res (Phila). 2013 Sep;6(9):886-97. doi: 10.1158/1940-6207.CAPR-13-0140. Epub 2013 Jul 23.

    Dietary Polyphenols Suppress Elevated Levels of Proinflammatory Mediators and Aromatase in the Mammary Gland of Obese Mice
    Kotha Subbaramaiah 1, Erika Sue, Priya Bhardwaj, Baoheng Du, Clifford A Hudis, Dilip Giri, Levy Kopelovich, Xi Kathy Zhou, Andrew J Dannenberg
    Affiliation
    1
    Department of Medicine, Weill Cornell Medical College, 525 East 68th St, Room F-206, New York, New York 10065, USA. ksubba@med.cornell.edu

    Problematic data.

    Much more similar than expected within each figure below.

    Figure 1D.
    See: https://imgur.com/8qXztuo

    Figure 2D.
    See: https://imgur.com/ubBrDfl

    Figure 3D.
    See: https://imgur.com/k2gl46f

    Figure 6C.
    See: https://imgur.com/aYqj0fU

  10. Where were the peer reviewers? Don’t such articles undergo scientific and editorial scrutiny before publishing? And if fraud was intended, why would authors re-use figures? Being pictorial, they are obviously most visible and detectable of all the ways that data might be faked. Something is missing from this story.

  11. 2021 retraction for:
    Cancer Discov . 2012 Apr;2(4):356-65. doi: 10.1158/2159-8290.CD-11-0241. Epub 2012 Jan 27.
    Increased levels of COX-2 and prostaglandin E2 contribute to elevated aromatase expression in inflamed breast tissue of obese women
    Kotha Subbaramaiah 1, Patrick G Morris, Xi Kathy Zhou, Monica Morrow, Baoheng Du, Dilip Giri, Levy Kopelovich, Clifford A Hudis, Andrew J Dannenberg
    Affiliations expand
    PMID: 22576212
    PMCID: PMC3398487 DOI: 10.1158/2159-8290.CD-11-0241

    2021 retraction. https://cancerdiscovery.aacrjournals.org/content/11/5/1306

    This article (1) has been retracted at the request of the authors based upon evidence of data falsification or fabrication in Figs. 2B, 4C, and 5H. An Editor’s Note had previously been issued (2). A copy of this Retraction Notice was sent to the last known e-mail addresses for the 9 authors. Eight authors (Kotha Subbaramaiah, Patrick G. Morris, Xi Kathy Zhou, Monica Morrow, Dilip Giri, Levy Kopelovich, Clifford A. Hudis, and Andrew J. Dannenberg) agreed to the retraction; one author (Baoheng Du) did not respond. The authors apologize to the scientific community and deeply regret any inconveniences or challenges resulting from the publication and subsequent retraction of this article.

    References 1.↵Subbaramaiah K, Morris PG, Zhou XK, Morrow M, Du B, Giri D, et al. Increased levels of COX-2 and prostaglandin E2 contribute to elevated aromatase expression in inflamed breast tissue of obese women. Cancer Discov 2012;2:356–65.

    2.↵Editor’s Note: Increased levels of COX-2 and prostaglandin E2 contribute to elevated aromatase expression in inflamed breast tissue of obese women. Cancer Discov 2019;9:1142.

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.