COVID-19 Research integrity

Steve Jackson and the Moumen Troll

"I take issues of research integrity very seriously and shall of course review the concerns posted on PubPeer to establish whether there are any issues that need to be addressed." Stephen P Jackson.

Stephen P Jackson, Cambridge University professor and a major heavyweight in the field of DNA damage and cancer research worldwide, has trouble with another former postdoc. This time, Jackson Lab papers by Abdeladim Moumen were flagged on PubPeer. The man owns a biotech startup which currently provides all Morocco with proprietary COVID-19 kits.

The evidence in Moumen & Johnson papers, as flagged by Clare Francis, is heavy, and it looks like the second case of serious data falsification in the famous Cambridge lab.

In September 2018, I published the leaked news about the investigations into research fraud and bullying committed by Jackson’s former postdoc, Abderrahmane Kaidi. The University of Bristol sacked its lecturer, according to the documents I published later on it was over bullying of Kaidi’s lab members. Two papers from the Jackson lab were retracted in April 2019, one in Nature (Kaidi and Jackson 2013) and one in Science (Kaidi et al 2010), following an investigation by the University of Cambridge, which was referenced in a retraction notice:

The investigation concluded that the first author, Abderrahmane Kaidi, was responsible for the falsification of the data.”

Now same story, different postdoc?

The common lead author on the 3 papers from Jackson lab I will discuss below is Abdeladim Moumen. The Moroccan native did his PhD in the lab of Henri Buc at the Institut Pasteur in Paris, after his postdoc stint with Jackson Moumen became associate professor at the St George’s University in London, and in 2012 he returned to Morocco to works as a research director at the Moroccan Foundation for Advanced Science, Innovation and Research (MAScIR). Moumen also founded a MAScIR biotech spin-off, Moldiag, here its advertisement:

A success story, nothing to be ashamed of. And yet Moumen is not present in the group photo from 2017 Jackson Lab Reunion meeting, but Kaidi is grinning in the front, third to our left from Jackson (as disclaimer: also my ex-boss from Milan is there, second row right behind Jackson).

Source: Jackson Lab

Strange. Jackson lab reunions are big events sponsored by pharma industry like Astra Zeneca (who purchased Jackson’s company KuDOS) and a matter of huge prestige for all invited. If they are invited, that is. Jackson explained to me in an email:

If I remember correctly, Professor Moumen was invited to the reunion event, but was unable to attend.

Last year, Moumen’s company Moldiag produced a COVID-19 testing kit, the only one made in Morocco. For some reason, the governmental authorities were slow in approving those kits, which was presented as a scandal in local media. The oversight was swiftly fixed, in November 2020 Moldiag supplied the Moroccan public sector with a million of kits, and an advanced version was immediately approved. The company’s CEO Moumen was quoted:

The Covid-19 test was developed by the team at the Mascir medical biotechnology center in three weeks thanks to the experience accumulated over the past 10 years. In 2 months, we had a test ready and validated by Moroccan and foreign laboratories“.

I now wish to reassure everyone in Morocco that Moumen’s COVID-19 must be 1000% reliable, as his previous research from the Jackson lab proves. Like this Cell paper:

Abdeladim Moumen, Philip Masterson, Mark J. O’Connor, Stephen P. Jackson hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage Cell (2005) doi: 10.1016/j.cell.2005.09.032

Wow. Look at all these fake western blots, with their cloned gel bands, recycled several times! Is anything at all in that Cell paper which is not fake? There is even more, look at this dance of the fake gel bands:

Did you notice that some data from the 2005 paper was reused in a different Cell press publication four years later, with Jackson and Moumen as co-authors? That was done in collaboration with Galina Selivanova in Sweden, a Karolinska Institutet professor who was in 2016 subject to a misconduct investigation (as I previously reported), which ended with full acquittal for all 9 Karolinska professors involved.

Selivanova has 7 papers flagged on PubPeer, four received Errata declaring that these “do not change the validity of the data nor the conclusions from the experiments“. Also the following 2009 Jackson-Moumen collaboration was corrected right when it was first published, because “In the right panel of Figure 6A of this article, the splicing from non-neighboring lanes was not indicated“.

Martin Enge, Wenjie Bao, Elisabeth Hedström, Stephen P. Jackson, Abdeladim Moumen, Galina Selivanova MDM2-dependent downregulation of p21 and hnRNP K provides a switch between apoptosis and growth arrest induced by pharmacologically activated p53 Cancer Cell (2009) doi: 10.1016/j.ccr.2009.01.019 

Which in Elsevier’s corporate philosophy means there is no need to declare that a blot in Figure 4D was recycled from a different paper where it showed something else. The paper has even more issues. Two years ago, this evidence was posted:

Selivanova commented on PubPeer, also 2 years ago:

We acknowledge the lane splicing in Fig4B and offer to inform the journal about this, so that they can decide whether to offer a correction, in which the lanes are separated by a line.

  • In regard to the potential duplication of images, we acknowledge that there are similarities between the images. Unfortunately, because of the people’s mobility between different jobs and countries since 2008, we no longer have access to the original data. Therefore we are unable to conclude if these are distinct blots or were the same with one being inadvertently mislabeled. We apologize for this.
  • Whatever the case, the induction of p53 and p21 by nutlin shown in Fig 4D have been observed by us and numerous other labs over many years, and these blots confirm what are well established facts about the p53/p21 response. Thus, whatever the case with the potential relatedness between the images, this does not alter the conclusion of our studies.

Because Selivanova was previously absolved in full by a Karolinska investigation, and the Elsevier journal Cancer Cell did not see the need to issue a second correction, the data manipulation was legalized. Retraction is not an option for a Cell press journal (read here and here).

The case is closed, forever and for all eternity, so I suppose Clare Francis shouldn’t have bothered submitting this new evidence, of the blots recycled from a Moumen-Jackson Cell 2005 paper, and also this:

Four figures at least in that Selivanova-Jackson copro-duction are manipulated. Expect exactly nothing from the publisher.

But let’s have a look at a third paper Moumen authored in Jackson’s lab.

Abdeladim Moumen, Christine Magill, Katherine L Dry, Stephen P. Jackson ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage Cell Cycle (2013) doi: 10.4161/cc.23592

 

One fake western blot with cloned gel bands, one more manipulated gel figure where a lane was slapped on? Are the conclusions affected by this?

After a reminder email, Jackson replied to me announcing action:

Thank you for your message below and for writing to me, making me aware of the recent PubPeer posts, which I had not seen before you brought them to my attention. I take issues of research integrity very seriously and shall of course review the concerns posted on PubPeer to establish whether there are any issues that need to be addressed.

The Cambridge professor added:

I have forwarded your email to the Director of the Gurdon Institute so that appropriate institutional due diligence can be undertaken.

Moumen did not reply when contacted via LinkedIn.

Original photos: King Faisal Prize, Le Matin.

Unsurprisingly, the shenanigans continued once Moumen set up his own lab in London:

Jogitha Selvarajah, Androulla Elia, Veronica A. Carroll, Abdeladim Moumen DNA damage-induced S and G2/M cell cycle arrest requires mTORC2-dependent regulation of Chk1 Oncotarget (2015) doi: 10.18632/oncotarget.2813

A Jackson Lab blot, reused?

Before we end, here something else indirectly related to the Jackson Lab.

One of the most successful Jackson mentees is Simon Boulton, senior group leader at The Crick in London. This is from Boulton’s own lab:

J. Ross Chapman, Patricia Barral, Jean-Baptiste Vannier, Valérie Borel, Martin Steger, Antonia Tomas-Loba, Alessandro A. Sartori, Ian R. Adams, Facundo D. Batista, Simon J. Boulton RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection Molecular Cell (2013) doi: 10.1016/j.molcel.2013.01.002

It looks like a falsified figure, where a gel was recycled in different experimental context. Luckily it’s Cell Press again, which closes the case before it can be opened.

The article was updated on 5.04.2021 to include additional evidence of data manipulation.


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13 comments on “Steve Jackson and the Moumen Troll

  1. BMC Cancer. 2011 Feb 21;11:79. doi: 10.1186/1471-2407-11-79.
    A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation
    Jane M Valentine 1, Sonia Kumar, Abdeladim Moumen

    Affiliation
    1DNA Damage Response Group, Basic Medical Science Department, St George’s University of London, Cranmer Terrace, London, UK.

    PMID: 21338495 PMCID: PMC3050855 DOI: 10.1186/1471-2407-11-79

    Pubpeer comment by Actinopolyspora Biskrensis.

    https://pubpeer.com/publications/F12829C57BC05986FD020E78B893ED

    Like

  2. Science. 2007 Dec 7;318(5856):1637-40. doi: 10.1126/science.1150034. Epub 2007 Nov 15.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430610/

    Orchestration of the DNA-damage response by the RNF8 ubiquitin ligase

    Nadine K Kolas 1, J Ross Chapman, Shinichiro Nakada, Jarkko Ylanko, Richard Chahwan, Frédéric D Sweeney, Stephanie Panier, Megan Mendez, Jan Wildenhain, Timothy M Thomson, Laurence Pelletier, Stephen P Jackson, Daniel Durocher

    Affiliation

    Nadine K. Kolas,1,* J. Ross Chapman,2,* Shinichiro Nakada,1,* Jarkko Ylanko,1,3 Richard Chahwan,2 Frédéric D. Sweeney,1,3 Stephanie Panier,1 Megan Mendez,1 Jan Wildenhain,1 Timothy M. Thomson,4 Laurence Pelletier,1,3 Stephen P. Jackson,2,§ and Daniel Durocher1,3,§

    Author information Copyright and License information Disclaimer
    1Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, M5G 1X5, Ontario, Canada

    2The Wellcome Trust and Cancer Research UK Gurdon Institute, and the Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK

    3Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada

    4Department of Molecular and Cellular Biology, Instituto de Biología Molecular de Barcelona c. Jordi Girona 18-2608034 Barcelona, Spain

    §Address correspondence to:

    Daniel Durocher, Ph.D., Centre for Systems Biology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Room 1073, 600 University Avenue, Toronto, ON, CANADA, Tel: 416-586-4800 ext. 2544, Fax: 416-586-8869, e-mail: ac.no.irhsm@rehcorud

    Stephen P. Jackson, Ph.D., The Wellcome Trust and Cancer Research, UK Gurdon Institute, Tennis Court Road, Cambridge, CB2 1QN, UNITED KINGDOM, Tel: +44 (0)1223 334088, Fax: +44 (0)1223 334089, email: ku.ca.mac.nodrug@noskcaj.s
    *These authors contributed equally to this work

    PMID: 18006705 PMCID: PMC2430610 DOI: 10.1126/science.1150034

    Problematic data figure 3D. Much more similar than expected.

    Like

  3. Mol Cell. 2015 Aug 6;59(3):462-77. doi: 10.1016/j.molcel.2015.06.007. Epub 2015 Jul 9.
    BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks

    Martin R Higgs 1, John J Reynolds 1, Alicja Winczura 2, Andrew N Blackford 2, Valérie Borel 3, Edward S Miller 1, Anastasia Zlatanou 1, Jadwiga Nieminuszczy 2, Ellis L Ryan 1, Nicholas J Davies 1, Tatjana Stankovic 1, Simon J Boulton 3, Wojciech Niedzwiedz 2, Grant S Stewart 4

    Affiliations
    1
    School of Cancer Sciences, University of Birmingham, Birmingham B15 2TT, UK.
    2
    The Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
    3
    The Francis Crick Institute, Clare Hall Laboratories, South Mimms, Herts EN6 3LD, UK.
    4
    School of Cancer Sciences, University of Birmingham, Birmingham B15 2TT, UK. Electronic address: g.s.stewart@bham.ac.uk.
    PMID: 26166705 DOI: 10.1016/j.molcel.2015.06.007

    Problematic data figures 5A and 6G. Legend figure 5A states “The blots originate from a single gel.
    A white line denotes removal of the superfluous lanes”,
    yet in figure 5G there are no splices in the BODL1 panel. There is nowhere for the “superfluous lanes”.

    What lanes have been removed if 6G is unspliced?

    Like

  4. “Abdeladim Moumen, Philip Masterson, Mark J. O’Connor, Stephen P. Jackson hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage Cell (2005) doi: 10.1016/j.cell.2005.09.032”

    Figure 7A. Much more similar after 180 degree rotation than expected,

    https://imgur.com/UnMLkeg

    Like

    • “Abdeladim Moumen, Philip Masterson, Mark J. O’Connor, Stephen P. Jackson hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage Cell (2005) doi: 10.1016/j.cell.2005.09.032”

      Figures 4A and 7A much more similar than expected.

      Like

  5. “Martin Enge, Wenjie Bao, Elisabeth Hedström, Stephen P. Jackson, Abdeladim Moumen, Galina Selivanova MDM2-dependent downregulation of p21 and hnRNP K provides a switch between apoptosis and growth arrest induced by pharmacologically activated p53 Cancer Cell (2009) doi: 10.1016/j.ccr.2009.01.019 ”

    Fine detail.
    Data in 1. Cancer Cell. 2009 Mar 3;15(3):171-83. doi: 10.1016/j.ccr.2009.01.01 from 2.Cell. 2005 Dec 16;123(6):1065-78.

    Figure 4D Cancer Cell. 2009 Mar 3;15(3):171-83 much more similar to figure 7A Cell. 2005 Dec 16;123(6):1065-78, 
    even though the experiments are different.

    Like

  6. Oncotarget. 2015 Jan; 6(1): 427–440.Published online 2014 Nov 15. doi: 10.18632/oncotarget.2813PMCID: PMC4381605PMID: 25460505

    DNA damage-induced S and G2/M cell cycle arrest requires mTORC2-dependent regulation of Chk1

    Jogitha Selvarajah,1 Androulla Elia,1 Veronica A. Carroll,#1 and Abdeladim Moumen#2Jogitha Selvarajah,1 Androulla Elia,1 Veronica A. Carroll,#1 and Abdeladim Moumen#2

    Author information 1 Cardiovascular and Cell Sciences Research Institute, St George’s University of London, Cranmer Terrace, UK
    2 Division of Medical Biotechnology, MAscIR Institution, Rabat, Morocco

    1 Cardiovascular and Cell Sciences Research Institute, St George’s University of London, Cranmer Terrace, UK2 Division of Medical Biotechnology, MAscIR Institution, Rabat, Morocco#Contributed equally.Correspondence to:Veronica A. Carroll, ku.ca.lugs@llorracvAbdeladim Moumen, 

    Figure 2C. Much more similar to figure 1B Cell Cycle 12:4, 698–704 (2013) than expected,
    even though the experiments are different.

    FYI:
    Cell Cycle. 2013 Feb 15; 12(4): 698–704.
    doi: 10.4161/cc.23592
    PMCID: PMC3594270
    PMID: 23343766
    ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage

    Abdeladim Moumen, 1 , † Christine Magill, 2 Katherine L. Dry, 2 and Stephen P. Jackson 2 ,*

    Author information
    1DNA Damage Response Group; Basic Medical Science Department; St. George’s University of London; London, UK
    2The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry; Cambridge University; Cambridge, UK
    †Current affiliation: Moroccan Foundation for Advanced Science, Innovation and Research; Rabat Design Center; Rabat, Morocco
    *Correspondence to: Stephen P. Jackson, Email: *Correspondence to: Stephen P. Jackson, Email: s.jackson@gurdon.cam ac.uk

    Pubpeer comments for Cell Cycle. 2013 Feb 15; 12(4): 698–704.

    https://pubpeer.com/publications/FEF5B43E894DD798B17122C43281E8

    Like

  7. “Abdeladim Moumen, Philip Masterson, Mark J. O’Connor, Stephen P. Jackson hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage Cell (2005) doi: 10.1016/j.cell.2005.09.032”

    Figure 1E. Much more similar after vertical stretch than expected.

    Like

  8. “Martin Enge, Wenjie Bao, Elisabeth Hedström, Stephen P. Jackson, Abdeladim Moumen, Galina Selivanova MDM2-dependent downregulation of p21 and hnRNP K provides a switch between apoptosis and growth arrest induced by pharmacologically activated p53 Cancer Cell (2009) doi: 10.1016/j.ccr.2009.01.019 ”

    Data figure 4D, right set of panels becoming more problematic.
    Much more similar than expected, although all 3 cell types are different.

    Like

  9. Cancer Cell . 2009 May 5;15(5):441-53. doi: 10.1016/j.ccr.2009.03.021.

    Ablation of key oncogenic pathways by RITA-reactivated p53 is required for efficient apoptosis

    Vera V Grinkevich 1, Fedor Nikulenkov, Yao Shi, Martin Enge, Wenjie Bao, Alena Maljukova, Angela Gluch, Alexander Kel, Olle Sangfelt, Galina Selivanova

    Affiliation
    1Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 17177, Stockholm, Sweden.
    PMID: 19411072 DOI: 10.1016/j.ccr.2009.03.021

    Figure 3B. The HCT116 pSer473Akt and Akt panels do not look like they come from the same blot, whereas the HCT118 TP53-/- pSer473Akt and Akt panels look like they come from the same blot.

    A 2017 erratum ,mentions figures 2C and 3C, but not 2B.
    https://www.cell.com/cancer-cell/fulltext/S1535-6108(17)30170-8

    Like

  10. Clin Cancer Res. 2013 Sep 15;19(18):5092-103. doi: 10.1158/1078-0432.CCR-12-2211.

    Dual targeting of wild-type and mutant p53 by small molecule RITA results in the inhibition of N-Myc and key survival oncogenes and kills neuroblastoma cells in vivo and in vitro

    Mikhail Burmakin  1 , Yao Shi, Elisabeth Hedström, Per Kogner, Galina Selivanova

    Affiliation 1 Authors’ Affiliations:

    Department of Microbiology, Tumour and Cell biology (MTC); and Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.

    PMID: 23864164 DOI: 10.1158/1078-0432.CCR-12-2211

    Problematic data figure 3D. Much more similar and different than expected.

    Like

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