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Retraction Watch

Tracking retractions as a window into the scientific process

Papers on potential cancer drugs retracted for image manipulation

with 72 comments

ccr 9-13A group of researchers at the Einstein College of Medicine in the Bronx, New York has retracted two papers for image manipulation.

The retraction notices for “PM02734 (Elisidepsin) Induces Caspase-Independent Cell Death Associated with Features of Autophagy, Inhibition of the Akt/mTOR Signaling Pathway, and Activation of Death-Associated Protein Kinase” and “The Phosphatase Inhibitor Menadione (Vitamin K3) Protects Cells from EGFR Inhibition by Erlotinib and Cetuximab” say the same thing:

After an unidentified concerned reader made allegations of image mishandling in several figures, the authors requested that their medical school conduct an investigation as per its established protocol. The investigators concluded that there was enhancement of bands in some of the questioned figures and that the changes were subtle and seen only on special analysis. One of the coauthors, who since has returned to his home country, accepted full responsibility for the changes. He never mentioned the enhancements to any of the authors before manuscript submission. In no case would the conclusions from the experiments have been different if no alterations had been made. Independent repetition of key experiments by another senior investigator showed reproducibility of the major findings. In view of the reproducibility of the original data by a third party, the authors continue to stand by the conclusions of the article. However, because the submission did not meet the standards for manuscript submission to Clinical Cancer Research as described in the Instructions to Authors, the authors voluntarily retract this article. The authors apologize to the readers for the inconvenience that this oversight may have caused.

The menadione paper has been cited 5 times, according to Thomson Scientific’s Web of Knowledge, while the elisidepsin stud has been cited 15.

Roman Perez-Soler, who is first author on one of the papers and last author on the other, tells Retraction Watch that Yi-He Ling is the coauthor “who since has returned to his home country” and “accepted full responsibility for the changes.”

Both papers were funded by NIH grants, and Perez-Soler said the case had been referred to the Office of Research Integrity.

The menadione paper was also funded by Talon Therapeutics, the company developing the compound. PharmaMar, part of drug company Zeltia, funded part of the elisidepsin study. The company stopped development of elisidepsin (Irvalec) last year, saying the market wouldn’t be large enough.

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Written by Ivan Oransky

September 6, 2013 at 11:00 am

72 Responses

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  1. Looks like the western in figure 1 D is to blame. Duplication of lanes, with a little sneaky fiddling of the contrast.

    Ricky Connolly

    September 6, 2013 at 11:23 am

  2. If we go around, many phospho proteins Western blots will need corrections and retractions. When we blot for a protein, then detect it phosphorylated form the bands on the two blots are always very similar. We see the same orientation, the same general shape and the same irregularities in bands. If that is not the case the two blots are from different Western run defeating the purpose of the whole experiment

    Schmuck

    September 6, 2013 at 3:40 pm

  3. Another 2 papers where the authors shared with the retractions,

    1. Mol Pharmacol. 2008 Sep;74(3):793-806. http://www.ncbi.nlm.nih.gov/pubmed/18524889

    Figure 1.

    Figure 1F. Caspase 8 panel. Vertical change in background to left of bands in 24 h lane. It is supposed to be a time series.

    Figure 2.

    Figure 2A. BID panel. Please compare bands in lanes 1 and 2.
    Please compare bands in lanes 4 and 5.

    Figure 2B. TRAIL panel. Please compare 12, 24 and 48 hour lanes with 0,4 and 8 hour lanes.

    Figure 4.

    Figure 4D.
    Active BAX panel. Please compare 8 and 12 hour lanes.
    BAX panel. Please compare 8 and 12 hour lanes.

    Figure 5.

    Figure 5B.
    Please compare the lowest band in lane 3 of the left and right panels.
    Please compare the 2X band in lane 3 of the left and right panels.
    Please compare the 3X band in lane 3 of the left and right panels.
    Please compare the lowest band in lane 4 of the left and right panels.
    Please compare the 2X band in lane 4 of the left and right panels.
    Please compare the 3X band in lane 4 of the left and right panels.

    Figure 6.

    Figure 6E. Bottom panel. Vertical change in background between lanes 2 and 3 (see bottom of lanes).

    Figure 7.

    Figure 7B. Top panel. Vertical change in background between lanes 1 and 2.

    Figure 8.

    Figure 8C. Top panel. Please compare the BAX bands lanes 3 and 4.

    Figure 9.

    Figure 9C. BAX panel. Please compare bands lanes 1,2 and 4.

    Figure 10.

    Figure 10A. Beta-actin panel. Please compare bands lanes 4,5 and 6 with bands lanes 1,2 and 3 respectively.

    2. Mol Pharmacol. 2007 Aug;72(2):248-58. http://www.ncbi.nlm.nih.gov/pubmed/17456787

    Figure 2.

    Figure 2A. CyclinE panel. Please compare bands lanes 1 and 2.
    Please compare bands lanes 6 and 7.
    CDK2 panel. Please compare bands lanes 1 and 2.

    Figure 2C. Rb panel.
    Vertical, straight, light streak between upper bands lanes 1 and 2.
    Vertical change in background between upper and lower bands lane 2.
    Please compare upper bands lanes 2 and 3.

    p-RB(Ser-780 panel). Please compare lanes 1 and 2.
    Beta-actin panel. Please compare bands lanes 1 and 3.
    Please compare bands lanes 2 and 4.

    Figure 3.

    Figure 3A. p27KIP panel. Please compare bands lanes 4 and 5.

    Figure 4.

    Figure 4A. p27KIP panel. Please compare bands lanes 1,2 and 3.
    SKP-2 panel. Please compare bands lanes 1 and 2.
    Beta-Actin panel. Please compare bands lanes 1 and 3.
    Please compare bands lanes 2 and 4.

    Figure 5.

    Figure 5B. p27KIP panel. Vertical, straight changes in background between lanes 2 and 3 and between lanes 5 and 6.

    Figure 6.

    Figure 6A. p27KIP1 panel. Please compare lanes 5 and 6.
    Beta-actin panel. Vertical, straight change in background between lanes 5 and 6.

    Figure 7.

    Figure 7E and F. Multiple vertical changes in background.

    david hardman

    September 7, 2013 at 12:42 am

    • Wow! Just Wow!

      michaelhbriggs

      September 7, 2013 at 3:25 am

      • How credible is “changes were subtle and seen only on special analysis”?

        How far did the investigators look?

        david hardman

        September 7, 2013 at 3:42 am

        • Another 2 papers sharing authors with the 2 retractions. This time about the molecule PS-341:-

          1. Clin Cancer Res. 2003 Mar;9(3):1145-54
          2. Mol Cancer Ther. 2002 Aug;1(10):841-9.

          1. Clin Cancer Res. 2003 Mar;9(3):1145-54. http://www.ncbi.nlm.nih.gov/pubmed/12631620
          Mechanisms of proteasome inhibitor PS-341-induced G(2)-M-phase arrest and apoptosis in human non-small cell lung cancer cell lines.
          Ling YH, Liebes L, Jiang JD, Holland JF, Elliott PJ, Adams J, Muggia FM, Perez-Soler R.
          Source

          Department of Oncology, Albert Einstein College of Medicine, 13200 Morris Park Avenue, Bronx, NY 10461, USA.

          Supported in part by NIH Grants CA50270 and U01 CA76642.

          Figure 5.

          Figure 5A. Please compare the Cyclin D and cdc2 panels.

          Actin panels. Please compare bands lanes 1 and 4.
          Please compare bands lanes 2 and 5.
          Please compare bands lanes 3 and 6.

          Figure 5B. Cyclin E panel. Please compare bands lanes 1 and 2.

          Figure 6.

          Please compare beta-actin panels in figures 6A and 6B.

          Figure 7.

          Figure 7C. Cyclin B1 panel. Please compare bands lanes 5 and 6.

          2. Mol Cancer Ther. 2002 Aug;1(10):841-9. http://www.ncbi.nlm.nih.gov/pubmed/12492117
          PS-341, a novel proteasome inhibitor, induces Bcl-2 phosphorylation and cleavage in association with G2-M phase arrest and apoptosis.
          Ling YH, Liebes L, Ng B, Buckley M, Elliott PJ, Adams J, Jiang JD, Muggia FM, Perez-Soler R.
          Source

          Department of Oncology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

          Supported in part by NIH Grants CA50270 and U01 CA76642

          Figure 7.

          PARP panel. Please compare bands lanes 6 and 7.

          Bcl-2 panel. Please compare bands lanes 2 and 5.
          Please compare bands lanes 3, 6 and 7.

          david hardman

          September 7, 2013 at 3:59 am

          • Well I don’t suppose you need any help finding these but I took a quick peep anyway. Very much enjoyed a figure in JBC (2003) 278, 33714 that I would like to share with you.

            http://www.ncbi.nlm.nih.gov/pubmed/12821677

            The figure is

            and is best observed blown right up till you can see the blacks of its pixels.

            Focus on Fig. 5C the 70 kDa line of bands. Observe that these all have sharp vertical shears. I am not sure how a whole gel’s worth of bands could all get this artefact during the experiment. It would be easy enough to do afterwards though.

            The direction of the shear and the space between shears can show interesting similarities. On this basis,

            Lanes 1 and 2 have a common origin

            Lane 4 appears to be a clone but has slightly different ends

            Lanes 7, 8 are paler versions of lanes 5, 6

            Lane 3 looks like a darker lane 5 with an addition to the left edge

            Lane 9 looks like a smeared version of lane 7

            So all the bands are related to at least one other band. Isn’t that nice for them!

            Have people noticed that this team have a prehistory in Texas at the MD Anderson? Probably just a coincidence.

            Scrutineer

            September 7, 2013 at 8:33 am

          • Additional observations Mol Cancer Ther. 2002 Aug;1(10):841-9.

            Figure 2.

            Please compare the bands in lanes 7 (Z-VAD) and 8 (AC-YVAD).

            Figure 5.

            Figure 5A. Vertical, straight change in signal between tops of lanes 1 and 2.
            Lane 1 does not have a visible well. Wells for lanes 2 and 3 are at the same level.
            Wells for lanes 4,5 and 6 a bitt higher up. Wells for lanes 7 and 8 at the same levels as the wells in lanes 2 and 3. Well for lane 9 higher up.

            david hardman

            September 8, 2013 at 11:49 am

  4. R Perez-Soler is one of the authors of a phase II clinical trail using bortezomib (PS-341).

    Lung Cancer. 2010 Apr;68(1):89-93. doi: 10.1016/j.lungcan.2009.05.009. Epub 2009 Jun 12.

    http://www.ncbi.nlm.nih.gov/pubmed/19524318

    Phase II study of the proteasome inhibitor bortezomib (PS-341, Velcade) in chemotherapy-naïve patients with advanced stage non-small cell lung cancer (NSCLC).
    Li T, Ho L, Piperdi B, Elrafei T, Camacho FJ, Rigas JR, Perez-Soler R, Gucalp R.
    Source

    Department of Oncology, Montefiore Medical Center & the Albert Einstein College of Medicine, Bronx, NY, United States.

    According to this trial “no objective response was observed”.

    One question is: how could the patients have given informed consent if there were several papers on bortezomib (PS-341) with irregularities on the page?

    R Perez-Soler is an author of Lung Cancer. 2010 Apr;68(1):89-93 and is also author of the 3 papers directly below (which have just been discussed) and he was in a position to look at the figures.

    1. Clin Cancer Res. 2003 Mar;9(3):1145-54.
    2. Mol Cancer Ther. 2002 Aug;1(10):841-9.
    3. J Biol Chem. 2003 Sep 5;278(36):33714-23.

    The obvious question is did he look at the figures?
    If so, did he communicate what he saw to the other authors of Lung Cancer. 2010 Apr;68(1):89-93?
    Of course, the other authors of that paper might have taken a look themselves.

    R Perez-Soler is senior author of Mol Cancer Ther. 2011 Nov;10(11):2029-30. doi: 10.1158/1535-7163.MCT-11-0745. http://www.ncbi.nlm.nih.gov/pubmed/22072812

    where the first sentence of text is:

    “This pivotal article by Ling et al. in the August 2002 issue of Molecular Cancer Therapeutics addressed the mechanism by which a novel proteasome inhibitor, PS341 (bortezomib), caused G2–M cell cycle arrest and apoptosis (1).”

    Reference 1 is Mol Cancer Ther. 2002 Aug;1(10):841-9.
    PS-341, a novel proteasome inhibitor, induces Bcl-2 phosphorylation and cleavage in association with G2-M phase arrest and apoptosis.
    Ling YH, Liebes L, Ng B, Buckley M, Elliott PJ, Adams J, Jiang JD, Muggia FM, Perez-Soler R.
    Source

    Department of Oncology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

    http://mct.aacrjournals.org/content/1/10/841.full

    Please see figure 7.

    http://mct.aacrjournals.org/content/1/10/841/F7.expansion.html

    PARP panel. Please compare bands lanes 6 and 7.
    Bcl-2 panel. Please compare bands lanes 2 and 5.
    Please compare bands lanes 3, 6 and 7.

    This in paper number 2 in comment “david hardman September 7, 2013 at 3:59 am”

    david hardman

    September 7, 2013 at 9:30 am

    • In reply to Scrutineer September 7, 2013 at 8:33 am

      “Have people noticed that this team have a prehistory in Texas at the MD Anderson? Probably just a coincidence.”

      On the drug PS-341 there is

      Clin Cancer Res. 2004 May 1;10(9):3207-15. http://www.ncbi.nlm.nih.gov/pubmed/?term=15131062

      Induction of cell cycle arrest and apoptosis by the proteasome inhibitor PS-341 in Hodgkin disease cell lines is independent of inhibitor of nuclear factor-kappaB mutations or activation of the CD30, CD40, and RANK receptors.
      Zheng B, Georgakis GV, Li Y, Bharti A, McConkey D, Aggarwal BB, Younes A.
      Source

      Departments of Lymphoma/Myeloma, Bioimmunotherapy, and Cancer Biology, M. D. Anderson Cancer Center, Houston, Texas 77030, USA.

      Figure 5.

      L-428 section of panels. Please compare the caspase-3 and cleaved PARP panels.
      Please compare the KM-H2 BID panel with a horizontal mirror image of the L-428 BID panel.

      Figure 6.

      Figure 6A. Please compare the HD-MyZ and HD-LM Phospho-p53 (ser15) panels.
      Please compare the HD-MyZ and HD-LM Total p53 panels.

      david hardman

      September 7, 2013 at 9:43 am

      • Home foudn for Clin Cancer Res. 2004 May 1;10(9):3207-15

        http://pubpeer.com/publications/1AAA8FC9FADEBD1D995538D146F5CF

        david hardman

        September 7, 2013 at 12:02 pm

      • How extraordinary!

        That Fig. 6 is such a tease that I have totally neglected today’s “hard” Sudoku puzzle in the Guardian!

        Working out how the various slices are related is going to offer hours of fun.

        In both of your examples (which represent different cell lines so cannot be re-probes of the same blot), the limp, flaccid right-most lane is an instant give away. I’m not sure what to make of it, but there is a tendency in many of the gel slices for the right side lanes to be so much more wonky than their counterparts on the left side. Does the rotation of the Earth skew gel electrophoresis?

        Anyway the MD Anderson has for many years been the best cancer hospital in the world

        http://www.mdanderson.org/newsroom/news-releases/2012/ut-md-anderson-named-nation-s-top-hospital-for-cancer-in-u-s-news-world-report-survey.html

        Which is probably why the Houston Chronicle likes to try to keep them on the straight and narrow path

        http://blog.chron.com/sciguy/2012/06/m-d-anderson-president-goes-on-cnbc-extols-his-own-company/

        Whether it is important to be numero uno or not, it is good to know that, for at least 18 months, the world’s best cancer hospital has been investigating one of the PIs responsible for Fig. 6

        http://retractionwatch.wordpress.com/2012/01/31/md-anderson-investigating-researcher-bharat-aggarwal-over-images/

        The 451 comments on that report, still fall short of the >500 articles produced by the prolific Aggarwal. RW enthusiasts will know that despite being threatened of legal action, RW keeps track of developments such as the expressions of concern by Blood in May this year:

        http://retractionwatch.wordpress.com/?s=aggarwal

        Scrutineer

        September 7, 2013 at 7:37 pm

        • In reply to Scrutineer September 7, 2013 at 7:37 pm

          On the topic of “hard” Sudoku puzzles:

          Blood. 2012 Apr 26;119(17):4017-25. doi: 10.1182/blood-2011-01-331421. Epub 2012 Mar 9.
          The pan-deacetylase inhibitor panobinostat induces cell death and synergizes with everolimus in Hodgkin lymphoma cell lines.
          Lemoine M, Derenzini E, Buglio D, Medeiros LJ, Davis RE, Zhang J, Ji Y, Younes A.
          Source

          Department of Lymphoma and Myeloma, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA.

          Figure 6.

          Figure 6A. Please compare the L-248 GLUT1 panel figure 6A with the HDLM-2 pTSC2 panel figure 3B.

          Figure 3.

          david hardman

          September 8, 2013 at 5:26 am

          • Mostly the same authors from the same institute, the year before.

            Blood Cancer J. 2011 Dec;1(12):e46.
            The JAK inhibitor AZD1480 regulates proliferation and immunity in Hodgkin lymphoma.
            Derenzini E, Lemoine M, Buglio D, Katayama H, Ji Y, Davis RE, Sen S, Younes A.

            Fig. 2C HD-LM2 and L-428 Caspase 9 slices are different exposures of the same image. The lower bands look to have been spliced into the gels due to the horizontal lines (especially clear in lane 4, above and below the band) and the different band morphology.

            in all four Caspase 3 slices, there are one or two lower bands in the 3rd and 4th columns. These do not have the same shapes as the bands above but they do have a pale splice edge above the band indicating that they have been spliced into the gel.

            Fig. 5C the Donor panel of Aurora A and B appear to be identical except for different crops and intensities. So do the pHistoneH3 and HistoneH3. Even allowing for reprobing the same gel, should they be this similar? And since these slices don’t have any bands in them, how do we even know that these are the correct parts of gels?

            Fig. 5D Histone H3 and pHistone H3 look to be identical apart from intensity changes. This includes the light patches where transfer is poor (airbubbles under the membrane). Because of the charge alteration, pH3 should run slightly differently during electrophoresis so there should be a slight difference in the location of pH3 relative to H3 in the gel. But here there isn’t.

            Scrutineer

            September 8, 2013 at 11:11 am

        • Is inquiry in Aggarwal’s case over or not?

          Piggy

          September 10, 2013 at 9:43 am

          • I think this would be very obvious if it had happened. It has been over a year but if they are doing a thorough job, they have some 500 papers to go through (maybe a bit less, I am not sure how many he had before moving to the MD Anderson). Of which 65 are already reported to have interesting figures as all laid out on Juiichi Jigen’s special page.

            http://md-anderson-cc.blogspot.com

            Hommage a Aggarwal

            Scrutineer

            September 11, 2013 at 5:56 am

      • David, I have to say that this is becoming remarkably fascinating. Is there more to discover? (Er, should that be more to “uncover”?)

        The proteasome inhibitor Bortezomib (aka PS-341, Velcade) is being used to treat multiple myeloma. It appears that those cancerous cells are unusually sensitive to proteasome inhibition. A minority of around 15% of myeloma patients response extremely well to the treatment, but most seem to have some benefit. I’m not a cancer expert, but from what I can see this has been a most important development for myeloma patients.

        Clearly, it is then important for cancer researchers to study whether other cell types are comparably sensitive to proteasome inhibition.

        The immediate problem is though, that like all anti-cancer drugs, proteasome inhibitors are poisons. The human genome encodes hundreds of ubiquitin ligase systems that selectively target proteins for proteasomal destruction depending on signals that the given cell is processing. Some of these are critical for cell cycle and so are obvious targets for anti-cancer drugs. Others may be critical to the normal functioning of certain cell types. The right inhibitor dose might have useful therapeutic properties, but too high a dose will disrupt cell regulation across the board. And it is already clear that different cell types aren’t all comparably sensitive to proteasome inhibitors.

        So are there other cancers besides myeloma that might be treatable with proteasome inhibitors? Self evidently, it is highly desirable to find this out. Unfortunately figure fabrications in the articles studying proteasome-inhibited cancer cells in tissue culture are not going to help us get to the answer. Have there already been Phase II trials that have failed which were based upon evidence supplied by such articles?

        Scrutineer

        September 7, 2013 at 7:42 pm

        • In reply to Scrutineer September 7, 2013 at 7:42 pm

          “Have there already been Phase II trials that have failed which were based upon evidence supplied by such articles?”

          1. Clin Cancer Res. 2003 Mar;9(3):1145-54.
          2. Mol Cancer Ther. 2002 Aug;1(10):841-9.
          3. J Biol Chem. 2003 Sep 5;278(36):33714-23.
          4. Clin Cancer Res. 2004 May 1;10(9):3207-15.

          are becoming like the bricks. No citation is not evidence that they were not influential.

          In a recent review, Mol Cancer Ther. 2011 Nov;10(11):2029-30. doi: 10.1158/1535-7163.MCT-11-0745. http://www.ncbi.nlm.nih.gov/pubmed/22072812

          the first sentence of text is:

          “This pivotal article by Ling et al. in the August 2002 issue of Molecular Cancer Therapeutics addressed the mechanism by which a novel proteasome inhibitor, PS341 (bortezomib), caused G2–M cell cycle arrest and apoptosis (1).”

          Reference 1 is Mol Cancer Ther. 2002 Aug;1(10):841-9.

          Candidates for Phase II trials that have failed which were based upon evidence supplied by such articles are:-

          1. Lung Cancer. 2010 Apr;68(1):89-93. doi: 10.1016/j.lungcan.2009.05.009. Epub 2009 Jun 12.
          Phase II study of the proteasome inhibitor bortezomib (PS-341, Velcade) in chemotherapy-naïve patients with advanced stage non-small cell lung cancer (NSCLC).
          Li T, Ho L, Piperdi B, Elrafei T, Camacho FJ, Rigas JR, Perez-Soler R, Gucalp R.
          Source

          Department of Oncology, Montefiore Medical Center & the Albert Einstein College of Medicine, Bronx, NY, United States.

          “No objective response was observed.”

          2. J Thorac Oncol. 2012 Jun;7(6):1032-40. doi: 10.1097/JTO.0b013e31824de2fa.
          Phase-I/II study of bortezomib in combination with carboplatin and bevacizumab as first-line therapy in patients with advanced non-small-cell lung cancer.
          Piperdi B, Walsh WV, Bradley K, Zhou Z, Bathini V, Hanrahan-Boshes M, Hutchinson L, Perez-Soler R.
          Source

          Department of Oncology, Montefiore Medical Center, Albert Einstein College of Medicine Bronx, NY 10461, USA.

          Is it standard to conduct clinical trials of a drug in combination with other drugs if with the drug there was no objective response?

          3. J Thorac Oncol. 2012 Sep;7(9):1466-70.
          Phase II clinical trial of first or second-line treatment with bortezomib in patients with malignant pleural mesothelioma.
          Fennell DA, McDowell C, Busacca S, Webb G, Moulton B, Cakana A, O’Byrne KJ, Meerbeeck JV, Donnellan P, McCaffrey J, Baas P.
          Source

          Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester, United Kingdom.

          “Bortezomib monotherapy exhibits insufficient activity to warrant further investigation in unselected patients with mesothelioma.”

          4. Head Neck. 2013 Jul;35(7):942-8. doi: 10.1002/hed.23046. Epub 2012 Jul 13.

          http://www.ncbi.nlm.nih.gov/pubmed/22791234

          Phase II 2-arm trial of the proteasome inhibitor, PS-341 (bortezomib) in combination with irinotecan or PS-341 alone followed by the addition of irinotecan at time of progression in patients with locally recurrent or metastatic squamous cell carcinoma of the head and neck (E1304): a trial of the Eastern Cooperative Oncology Group.
          Gilbert J, Lee JW, Argiris A, Haigentz M Jr, Feldman LE, Jang M, Arun P, Van Waes C, Forastiere AA.
          Source

          Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.

          “The bortezomib-based regimens evaluated in this study have minimal activity in recurrent or metastatic head and neck cancer.”

          5. Int J Gynecol Cancer. 2012 Jun;22(5):792-800. doi: 10.1097/IGC.0b013e318251051a.
          An open-label phase 2 study of twice-weekly bortezomib and intermittent pegylated liposomal doxorubicin in patients with ovarian cancer failing platinum-containing regimens.
          Parma G, Mancari R, Del Conte G, Scambia G, Gadducci A, Hess D, Katsaros D, Sessa C, Rinaldi A, Bertoni F, Vitali A, Catapano CV, Marsoni S, van de Velde H, Colombo N.
          Source

          Division of Gynaecology, Istituto Europeo di Oncologia (IEO), Milan, Italy.

          “The combination of bortezomib and PLD was well tolerated, but the antitumor activity is insufficient to warrant further investigation in ovarian cancer.”

          6. Anticancer Res. 2012 Mar;32(3):1027-31.
          Phase II study of panobinostat and bortezomib in patients with pancreatic cancer progressing on gemcitabine-based therapy.
          Wang H, Cao Q, Dudek AZ.
          Source

          Division of Hematology, Oncology and Transplantation, University of Minnesota Medical School, Minneapolis, MN, USA.

          “Treatment of advanced pancreatic cancer with bortezomib in combination with panobinostat is not supported by our clinical study.”

          david hardman

          September 8, 2013 at 1:05 am

          • Well David, you demonstrate whether we should question if cancer research is in safe hands.
            Many other cancer experts will have reviewed and no doubt cited these papers – did everyone miss these ‘errors’ or ‘irregularities’?

            Are these isolated cases or the tip of an iceberg?

            Stewart

            September 8, 2013 at 1:59 pm

        • Reply to Scrutineer September 8, 2013 at 11:11 am

          Same senior author, same institute.

          Blood. 2012 Jul 12;120(2):347-55. doi: 10.1182/blood-2011-07-369397. Epub 2012 May 30.
          Essential role of TAK1 in regulating mantle cell lymphoma survival.
          Buglio D, Palakurthi S, Byth K, Vega F, Toader D, Saeh J, Neelapu SS, Younes A.
          Source

          Department of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA.

          Figure 2.

          Figure 2A. Please compare the Jeko-1 and SP53 beta actin panels.

          Figure 2C. Please compare the Mino and SP53 RPMI panels.

          Please pay attention to the outliers to the left of the clouds in the lower left corner,

          and to the right of the upper part of the clouds.

          Figure 5.

          Figure 5A. Please compare the bands in the right 4 lanes of the Jeko-1 and Mino TAK1 panels.

          The bands in the zero lanes of the Jeko-1 and Mino panels are much darker than the other bands.

          The band in the zero lane of the Jeko-1 lane is almost geometrical.

          Please compare the bands in the Jeko-1 and Mino NFKB p65 nuclear panels.

          Please compare the bands in the right 3 lanes of the Jeko-1 NFKB p65 nuclear panel with vertically compressed versions of the

          bands in the right 3 lanes of the Mino NFKB p65 nuclear panel.

          Figure 5B. Cleaved caspase 3 panels.

          Please compare the lower bands in lanes 4 and 5 in the Jeko-1 panel with the lower bands in lanes 4 and 5 in the SP53 panel.

          Figure 6.

          Figure 6A. Beta actin panels. Please compare the case 1 and case 2 beta actin panels.

          david hardman

          September 8, 2013 at 11:58 am

      • David, thanks for showing us that nice Figure 6.

        Although not directly related to the authors of the original topic, it’s just funny.

        Yes, the p53-panels are identical although different experiments are purported. The funny thing is, they are right next to each other. And there has not even been an attempt to obfuscate the fact that the bands are identical.

        It is so up-front and obvious. The real scandal is that this has not been detected by the reviewers. If you have to turn images around, if only parts of images are identical, if you have to change contrast or other image settings to really see it, if the duplicated images are in Fig 1 and in Fig 12, then I can understand if reviewers miss image duplications and stuff. But here the duplicated images are right next to each other. You can see it right away, first look.

        genetics

        September 10, 2013 at 6:32 am

        • Are many of these panels just different exposures of the same blots? Look at the Tak1 blots?

          enzo

          September 21, 2013 at 10:27 am

          • In reply to enzo September 21, 2013 at 10:27 am

            Figure 5 Blood. 2012 Jul 12;120(2):347-55.

            Figure 5A. Different exposures of the same thing would explain the high degree of similarity between the right 4 lanes of the Jeko-1 and Mino TAK1 panels.

            david hardman

            September 21, 2013 at 10:38 am

      • Continuation david hardman September 7, 2013 at 9:43 am

        2014 correction of figures 5A and 6A in Clin Cancer Res. 2004 May 1;10(9):3207-15.

        http://clincancerres.aacrjournals.org/content/20/11/3044

        david hardman

        June 2, 2014 at 5:38 am

  5. As well as the above litany of image manipulation, am I right in my interpretation of the quote from Roman Perez-Soler?

    Yi-He Ling is the coauthor “who since has returned to his home country” and “accepted full responsibility for the changes.”

    My reading is that Roman Perez-Soler is formally stating that this was all Yi-He Ling’s doing? If so, this is a lot worse than dozens of papers with manipulated/falsified images. Pass the blame, if there isn’t a convenient underling, a co-author (so equal responsibility, surely?) who has “gone home” will do nicely.

    Moreover, such a use of language panders to all sorts of racist stereotypes and leaves the “home” side feeling comfortable to continue in their rotten ways.

    Or have I got this wrong?

    ferniglab

    September 9, 2013 at 4:11 am

    • The buck stops there in the far far away land

      Schmuck

      September 9, 2013 at 6:19 pm

    • Rest assure, you got nothing wrong……

      I was thinking the same thing. How blatantly shameless can one be? Hey, I mean, Perez-Soler was FIRST author and SENIOR/CORRESPONDING author of the menadione paper and SENIOR/CORRESPONDING author on the other one. The first author needs to know the original blots of every band in the paper. IMHO the senior author as well, although we all know that this is often not the case.

      So PIs and senior authors putting the blame solely on the first author, that’s the usual stuff we see all the time. The higher ranking the PI is, the more often one seems to see this pattern.

      But here we have a paper with first and corresponding author in one person. And this person has the guts to tell us it’s completely the fault of someone else who is not in the country anymore? Wow…..

      genetics

      September 10, 2013 at 5:25 am

      • Hmmm, interesting, so the suggestion is that it is time for a new entry into the “Thesaurus of euphemisms”?

        http://ferniglab.wordpress.com/2013/05/05/thesaurus-of-euphemisms/

        One might even write a post on the decline of the “Officer Class”, to consider why those in charge and responsible for hitting the iceberg head for the lifeboat, leaving the passengers and vulnerable to go down with the ship… Maybe science needs something akin to maritime investigations, where it is assumed, correctly, that those in charge have a primary responsibility, regardless or circumstances.

        ferniglab

        September 10, 2013 at 5:40 am

  6. Retraction unrelated authors, same journal.

    http://clincancerres.aacrjournals.org/content/19/18/5256.full

    “The authors wish to retract the article titled “Critical Role of Notch Signaling in Osteosarcoma Invasion and Metastasis,” which was published in the May 15, 2008, issue of Clinical Cancer Research (1).

    “Many years after this article was published” (it is now only 5 years 4 months later) might be another entry for the thesaurus.

    david hardman

    September 21, 2013 at 4:40 am

  7. “However, because the submission did not meet the standards for manuscript submission to Clinical Cancer Research as described in the Instructions to Authors, the authors voluntarily retract this article.”

    Editor-in-chief of Clinical Cancer Research

    http://clincancerres.aacrjournals.org/site/misc/edboard.xhtml

    on Pubpeer

    https://pubpeer.com/publications/17510321

    https://pubpeer.com/publications/12097303

    https://pubpeer.com/publications/12517770

    https://pubpeer.com/publications/14559802

    https://pubpeer.com/publications/11086072

    https://pubpeer.com/publications/12480690

    david hardman

    October 20, 2013 at 4:43 am

  8. A retraction from Anderson

    http://bloodjournal.hematologylibrary.org/content/early/2010/10/20/blood-2009-11-253294

    Anyone know of more in the pipeline?

    Stewart

    October 21, 2013 at 2:11 pm

    • Another Retraction by Anderson!

      http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2008.07114.x/pdf

      Should this have its own thread?

      Stewart

      October 21, 2013 at 2:13 pm

      • Another one from Anderson!

        This time there was an erratum first, then a suggestion experiments were being repeated with promising results, then a retraction

        http://bloodjournal.hematologylibrary.org/content/113/18/4309

        It there a pattern developing here?

        Stewart

        October 21, 2013 at 2:18 pm

        • Barts Cancer Institute sponsors Professor Kenneth C. Anderson’s plenary lecture at the NCRI Conference 2012.

          Please see the comments. Maybe some new papers to look at.

          david hardman

          October 21, 2013 at 2:52 pm

          • Continuation: david hardman October 21, 2013 at 2:52 pm

            Based on comment in Youtube.

            Proc Natl Acad Sci U S A. 2008 Jan 29;105(4):1285-90.

            Jinushi M, Vanneman M, Munshi NC, Tai YT, Prabhala RH, Ritz J, Neuberg D, Anderson KC, Carrasco DR, Dranoff G.

            Figure 5. Please compare the left Bortezomid CHK-2 (pT68) panel and the left Dex CHK-2 (pT68) panel.

            Please compare the right Dex CHK-2 panel with the left 4 lanes of the Dex ATM panel, and
            the left 4 lanes of the left Bortezomib CKK-2 panel.

            david hardman

            October 21, 2013 at 3:05 pm

  9. Cancer Cell. 2007 Apr;11(4):349-60.
    The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.
    Carrasco DR, Sukhdeo K, Protopopova M, Sinha R, Enos M, Carrasco DE, Zheng M, Mani M, Henderson J, Pinkus GS, Munshi N, Horner J, Ivanova EV, Protopopov A, Anderson KC, Tonon G, DePinho RA.

    Source
    Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, and Department of Pathology, Brigham and Women’s Hospital, Boston, MA 02115, USA.

    PMID: 17418411

    Figure 2.

    Figure 2B. Please compare WT 16Kb bands lanes S.9 and S.10.

    Figure 2C. Ponceau panel. Please compare bands lanes 2,3,4, 5 and 6.

    david hardman

    October 21, 2013 at 3:11 pm

    • Figures 2B bands from S8 and S9: WT 16Kb: They are identical.

      Figure 2C, ponceau. Bands from lanes 2 and 4 are identical. Bands from lanes 4, 5 and 6 are identical.

      stewart

      October 21, 2013 at 4:58 pm

      • Correction, 3, 5 and 6 are identical.

        stewart

        October 21, 2013 at 5:00 pm

        • I’ll meet you both on the partial lane duplication (with one added lower band) in S.8 and S.9. Good spot this!

          Then I’ll raise you both on Fig. 2C: Yes, bands 2-6 are the same (apart from rotation and intensity, we all agree). But, in addition, bands 1 and 6 exhibit common ancestry (apart from rotation and intensity). And now you can’t raise me because there aren’t any bands left ;-)

          Scrutineer

          November 25, 2013 at 3:32 pm

          • Another problematic publication from the Albert Einstein College of Medicine.

            Stem Cell Res Ther. 2010 Mar 15;1(1):6. doi: 10.1186/scrt6.
            Switching of mesodermal and endodermal properties in hTERT-modified and expanded fetal human pancreatic progenitor cells.
            Cheng K1, Follenzi A, Surana M, Fleischer N, Gupta S.
            Author information
            1Hepatology Division, Department of Medicine, Albert Einstein College of Medicine, Ullmann Bldg, Rm 625, 1300 Morris Park Avenue, Bronx, NY 10461, USA.

            This work was supported in part by NIH grants P01 DK52956, P20 GM075037, R01 DK46952, R01 DK071111, P30 DK41296 and P30 CA13330.

            Figure 3.

            Figure 3c.

            Right set panels.

            TGF-alpha panel. Please compare signal lanes 1 and 3, paying attention to dark spots in the background.

            TGF-beta panel. Please compare signal lanes 1 and 3, paying attention to dark spots in the background.

            TGF-beta1 panel. Please compare signal lanes 1 and 3.

            Please compare TGF-beta2 and TGF-beta1R panels.

            TGF-beta2R panel. Please compare signal lanes 1 and 3.

            GAPDH panel. Please compare signal lanes 2 and 4, paying attention dark spots below mid-right of bands near floor of panel.
            Also, please compare lanes 1 and 3.

            Left set panels.

            GATA-2 panel. Please compare signal lanes 4,5 and 6.

            GATA-6 panel. Please compare signal lanes 1 and 3.

            ISL-1 panel. Please compare signal lanes 1 and 4.

            Figure 5.

            Figure 5d.
            Glucagon panel. Vertical change background between lanes 1 and 2.

            PC1/3 panel. Vertical change background between lanes 3 and 4.
            No vertical changes background in Insulin, hPdx1, rPdx1 or GAPDH panels.

            Comparison between differentially spliced panels is problematic.

            david hardman

            May 27, 2014 at 10:20 am

            • Thank you Dr Hardman!

              Ken Anderson is one of the, if not THE, biggest players in Cancer Research in the world.

              Stewart

              May 27, 2014 at 2:04 pm

              • Hepatology. 2006 Aug;44(2):410-9.
                Immunosuppression using the mTOR inhibition mechanism affects replacement of rat liver with transplanted cells.
                Wu YM1, Joseph B, Gupta S.
                Author information

                1Marion Bessin Liver Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

                Supported in part by NIH grants R01 DK46952, P30-DK41296, and 2P01-DK52956.

                http://onlinelibrary.wiley.com/doi/10.1002/hep.21277/pdf

                Figure 6.

                MIP2 panel. Vertical changes in background between lanes 2 and 3, and between lanes 4 and 5, but not between lanes 1 and 2, and not between lanes 6 and 7.

                CINC panel. Vertical, straight, grey streak/vertical change between lanes 1 and 2, and between lanes 6 and 7.

                TNF-alpha panel. Vertical change background between lanes 1 and 2. Vertical step in level of panel between lanes 1 and 2.

                Actin panel. Band lane 2 has vertical, light streak at left edge.

                Differential splicing makes comparison between panels problematic.

                david hardman

                May 27, 2014 at 3:03 pm

                • J Biol Chem. 2000 Aug 25;275(34):26050-7.
                  KATP channels regulate mitogenically induced proliferation in primary rat hepatocytes and human liver cell lines. Implications for liver growth control and potential therapeutic targeting.
                  Malhi H1, Irani AN, Rajvanshi P, Suadicani SO, Spray DC, McDonald TV, Gupta S.
                  Author information
                  1Marion Bessin Liver Research Center, the Cancer Research Center, and the Departments of Medicine and Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
                  http://www.jbc.org/content/early/2000/06/20/jbc.M001576200
                  Figure 3.
                  http://www.jbc.org/content/275/34/26050/F3.large.jpg
                  Figure 3B. SUR1 panel. Vertical step in level top of panel between lanes 1 and 2.
                  There are only 5 lanes.
                  Please compare signal lane 1 SUR1 panel and signal lane 1 Actin panel.

                  david hardman

                  May 28, 2014 at 2:08 am

            • Stem Cell Res Ther. 2010 Mar 15;1(1):6. doi: 10.1186/scrt6.

              now at Pubpeer.

              https://pubpeer.com/publications/20504287

              david hardman

              May 28, 2014 at 11:07 am

              • J Cell Sci. 2008 Apr 1;121(Pt 7):1002-13

                at Pubpeer: https://pubpeer.com/publications/18319302

                For reference:

                J Cell Sci. 2008 Apr 1;121(Pt 7):1002-13. doi: 10.1242/jcs.019315. Epub 2008 Mar 4.
                Phenotype reversion in fetal human liver epithelial cells identifies the role of an intermediate meso-endodermal stage before hepatic maturation.
                Inada M1, Follenzi A, Cheng K, Surana M, Joseph B, Benten D, Bandi S, Qian H, Gupta S.
                Author information

                1Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.

                david hardman

                May 28, 2014 at 12:31 pm

                • Hepatology. 2006 Aug;44(2):410-9

                  now at Pubpeer.

                  https://pubpeer.com/publications/16871590

                  david hardman

                  May 28, 2014 at 4:53 pm

                  • J Clin Invest. 2008 Mar;118(3):935-45

                    at Pubpeer.

                    https://pubpeer.com/publications/2C093420143131124E4B20672C3FB4

                    For reference:

                    J Clin Invest. 2008 Mar;118(3):935-45. doi: 10.1172/JCI32748.
                    Transplanted endothelial cells repopulate the liver endothelium and correct the phenotype of hemophilia A mice.
                    Follenzi A1, Benten D, Novikoff P, Faulkner L, Raut S, Gupta S.
                    Author information

                    1Department of Pathology, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, New York, New York 10461, USA.

                    david hardman

                    May 29, 2014 at 4:14 am

                    • Am J Pathol. 2008 Sep;173(3):856-64

                      at Pubpeer https://pubpeer.com/publications/18688024

                      Am J Pathol. 2008 Sep;173(3):856-64. doi: 10.2353/ajpath.2008.080096. Epub 2008 Aug 7.
                      Elevated expression of the miR-17-92 polycistron and miR-21 in hepadnavirus-associated hepatocellular carcinoma contributes to the malignant phenotype.
                      Connolly E1, Melegari M, Landgraf P, Tchaikovskaya T, Tennant BC, Slagle BL, Rogler LE, Zavolan M, Tuschl T, Rogler CE.
                      Author information

                      1Marion Bessin Liver Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

                      david hardman

                      May 30, 2014 at 11:29 am

                    • J Biol Chem. 2007 Nov 2;282(44):31900-8

                      at Pubpeer https://pubpeer.com/publications/17848570

                      Shared author with J Clin Invest. 2008 Mar;118(3):935-45 also work on liver cells.

                      J Biol Chem. 2007 Nov 2;282(44):31900-8. Epub 2007 Sep 11.
                      Role of MAPK phosphatase-1 in sustained activation of JNK during ethanol-induced apoptosis in hepatocyte-like VL-17A cells.
                      Venugopal SK1, Chen J, Zhang Y, Clemens D, Follenzi A, Zern MA.
                      Author information

                      1Department of Internal Medicine, Transplant Research Program, UC Davis Medical Center, Sacramento, California 95817, USA.

                      david hardman

                      May 30, 2014 at 11:39 am

  10. Proc Natl Acad Sci U S A. 1998 Jan 6;95(1):310-5

    at Pubpeer https://pubpeer.com/publications/9419372

    Proc Natl Acad Sci U S A. 1998 Jan 6;95(1):310-5.
    Liver repopulation with xenogenic hepatocytes in B and T cell-deficient mice leads to chronic hepadnavirus infection and clonal growth of hepatocellular carcinoma.
    Petersen J1, Dandri M, Gupta S, Rogler CE.
    Author information

    1Marion Bessin Liver Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

    david hardman

    May 30, 2014 at 11:34 am

  11. Exp Cell Res. 2013 Aug 15;319(14):2266-74

    at Pubpeer https://pubpeer.com/publications/35AE81DBE3A6A9383268F8131917A1

    Exp Cell Res. 2013 Aug 15;319(14):2266-74. doi: 10.1016/j.yexcr.2013.06.008. Epub 2013 Jun 24.
    Bone-derived mesenchymal stromal cells from HIV transgenic mice exhibit altered proliferation, differentiation capacity and paracrine functions along with impaired therapeutic potential in kidney injury.

    Kang Cheng a , Partab Rai a, Xiqian Lan a , Andrei Plagov a, Ashwani Malhotra a, Sanjeev Gupta b,
    Pravin C. Singhal a, *.
    a Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhassett, NY, USA
    b Departments of Medicine and Pathology, Marion Bessin Liver Research Center, Diabetes Center, Cancer Center, Ruth L. and David S. Gottesman
    Institute for Stem Cell and Regenerative Medicine Research, Institute for Clinical and Translational Research, Albert Einstein College of Medicine,Bronx, NY, USA

    david hardman

    May 30, 2014 at 12:16 pm

    • Hepatology. 2009 Oct;50(4):1194-203. doi: 10.1002/hep.23120.
      Hepatic targeting and biodistribution of human fetal liver stem/progenitor cells and adult hepatocytes in mice.
      Cheng K1, Benten D, Bhargava K, Inada M, Joseph B, Palestro C, Gupta S.
      Author information

      1Marion Bessin Liver Research Center, Diabetes Research Center, and Cancer Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

      Supported in part by National Institutes of Health Grants R01 DK46952, R01DK 071111, and P30 DK41296.

      http://onlinelibrary.wiley.com/doi/10.1002/hep.23120/pdf

      Please go to 200%.

      Figure 5A. GAPDH panel. Vertical, straight, grey streak/vertical change background between lanes 5 and 6.
      Please compare bands and background in lane 4 (Heart) and lane 6 (Intestine).

      Figure 5B. 1h GAPDH panel. Please compare lane 6 (Intestine) with horizontal mirror image lane 5 (Kidney).

      1wk CMT1A panel. Subtle, vertical, straight change in background between lanes 4,5 and 6.
      Please compare lane 4 (Heart) with darker version lane 5 (Kidney), paying attention to the pattern of light and dark in the background.
      For example, in the upper left corner of both lanes there is a cluster of dark streaks, and in the lower left corner of each lane there is a light streak that looks like the number “2”.

      1wk GAPDH panel. Please compare lane 1 (Liver) and lane 4(Heart), paying attention to the light defects in the grey band just above the main dark band.

      david hardman

      June 1, 2014 at 3:18 am

  12. Hepatology. 2009 Sep;50(3):815-24. doi: 10.1002/hep.23060.
    Long-term reduction of jaundice in Gunn rats by nonviral liver-targeted delivery of Sleeping Beauty transposon.
    Wang X1, Sarkar DP, Mani P, Steer CJ, Chen Y, Guha C, Chandrasekhar V, Chaudhuri A, Roy-Chowdhury N, Kren BT, Roy-Chowdhury J.
    Author information

    1Department of Medicine, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx 10461, NY, USA.

    National Institutes of Health grants: RO1DK46057(toJ.R.C.), RO1DK39137(toN.R.C.), R01DK064670(toC.G.),
    Liver Pathobiology and Gene Therapy Core Center P30 DK41296 (Albert Einstein College of Medicine).

    http://onlinelibrary.wiley.com/doi/10.1002/hep.23060/pdf

    Figure 4A. Please go to 300%. Background is dark, but to see the contrast better simply bring the computer screen upright.

    Vertical, straight change in background between lanes 9 and 10.

    Dark rectangle between 25% and 80% the way up lane 10.

    Dark rectangle between 25% and 75% the way up lane 11. 214 b.p. band in lane 11 in darker than general background.

    Near rectangle of smoother than general background at 214 b.p. level lane 6.

    david hardman

    June 1, 2014 at 11:58 am

  13. Hepatology. 2005 Nov;42(5):1118-26.
    Gadd45beta is induced through a CAR-dependent, TNF-independent pathway in murine liver hyperplasia.

    Author information.

    1 . Amedeo Columbano1,§,*, Giovanna M. Ledda-Columbano1, Monica Pibiri1,Costanza Cossu1,Marta Menegazzi2,David D. Moore3,Wendong Huang3,Jianmin Tian4 and Joseph Locker4
    Author Information

    1.Department of Toxicology, Oncology and Molecular Pathology Unit, University of Cagliari, Italy
    2. Department of Neuroscience, Biological Chemistry Unit, University of Verona, Italy
    3. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX
    4. Department of Pathology, Albert Einstein College of Medicine, Bronx, NY.

    Supported by RO1 DK46546 and UI9DK62434 (D.D.M.) of the National Institutes of Health

    Original article:

    http://onlinelibrary.wiley.com/doi/10.1002/hep.20883/pdf

    Please compare TCPOBOP WT CyP2b10 panel figure 3 with slightly fuzzier, lighter version of 180 degree rotation TCPOBOP TNFR1-/- CyP2b10 panel figure 1.

    Please compare TCPOBOP WT Gadd45beta panel figure 3 with
    TNFR1-/- lanes TCPOBOP Gadd45beta panel figure 1.

    Please compare CAR-/- Gadd45beta panel figure 3 with left 3 lanes CONTROL Gadd45beta panel figure 3, paying attention to the dark spot about one quarter the way up the leftmost lanes.

    Please compare the TCPOBOP WT Cyclin D1 panel figure 3 with 180 degree rotation
    TCPOBOP TNFR1-/- lanes Cyclin D1 panel figure 1.

    At Pubpeer: https://pubpeer.com/publications/4CEFC3E85E129F70A2B447E43D616A

    david hardman

    June 2, 2014 at 10:35 am

  14. Parasitol Res. 2013 Apr;112(4):1417-25.

    Comments at Pubpeer: https://pubpeer.com/publications/DB6B2ED4E4FD870763A4BB0D36A6DC

    Please see imgur image: http://i.imgur.com/jZyJHo3.jpg

    Parasitol Res. 2013 Apr;112(4):1417-25. doi: 10.1007/s00436-012-3271-5. Epub 2013 Feb 13.
    Identification of a functional prostanoid-like receptor in the protozoan parasite, Trypanosoma cruzi.
    Mukherjee S1, Sadekar N, Ashton AW, Huang H, Spray DC, Lisanti MP, Machado FS, Weiss LM, Tanowitz HB.
    Author information

    1Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY, USA.

    David Hardman

    June 13, 2014 at 4:53 am

  15. J Biol Chem. 2005 Jun 24;280(25):24085-94.

    Comments at Pubpeer: https://pubpeer.com/publications/15843370

    J Biol Chem. 2005 Jun 24;280(25):24085-94. Epub 2005 Apr 18.
    The adipocyte as an important target cell for Trypanosoma cruzi infection.
    Combs TP1, Nagajyothi, Mukherjee S, de Almeida CJ, Jelicks LA, Schubert W, Lin Y, Jayabalan DS, Zhao D, Braunstein VL, Landskroner-Eiger S, Cordero A, Factor SM, Weiss LM, Lisanti MP, Tanowitz HB, Scherer PE.
    Author information

    1Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

    David Hardman

    June 13, 2014 at 4:57 am


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