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).
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.
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
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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For Better Science 
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
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Additional problematic data BMC Cancer. 2011 Feb 21;11:79. doi: 10.1186/1471-2407-11-79.
Figure 2A.
Much more similar after 180 degree rotation and slight horizontal and horizontal re-sizing than expected.
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Many would be happy with 67 citations.
[HTML] A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation
JM Valentine, S Kumar, A Moumen – BMC cancer, 2011 – bmccancer.biomedcentral.com
The mammalian DNA-damage response (DDR) has evolved to protect genome stability and
maximize cell survival following DNA-damage. One of the key regulators of the DDR is p53,
itself tightly regulated by MDM2. Following double-strand DNA breaks (DSBs), mediators …
Cited by 67
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https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-11-79
Click on Authors name.
Jane M Valentine
DNA Damage Response Group, Basic Medical Science Department, St George’s University of London, Cranmer Terrace, London, UK
Outreach for Medicine, Department of Medical Education, School of Medicine, King’s College London, 4.20 Shepherd’s House, Guy’s Campus, London Bridge, London, UK
https://www.kcl.ac.uk/people/jane-valentine
Biography
Jane is a Senior Lecturer in Medical Education and Co-Director of King’s Extended Medical Degree Programme (EMDP). She is also Admissions Tutor for the EMDP, Chair of the MBBS Prizes Panel and an MBBS Senior Tutor. Jane is a keen advocate for diversity, equity and inclusion (DEI) within medical education. She has authored blogs, contributed to Parliamentary discussions and advised Government on social mobility, widening participation (WP) and access to the professions. Her academic interests are in curriculum development, teaching innovation – particularly the use of non-traditional teaching methods and environments – and DEI/WP-focused research.
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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.
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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?
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“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,
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“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.
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“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.
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Infinite improbability drive. Life imitates art! See 3 minutes.
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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
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“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.
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“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.
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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
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Correction to Cancer Cell . 2009 May 5;15(5):441-53.
3B in title of image.
A 2017 erratum ,mentions figures 2C and 3C, but not 2C.
https://www.cell.com/cancer-cell/fulltext/S1535-6108(17)30170-8
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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.
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2021 Editor’s Note for:
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.
Editor’s Note: 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, Yao Shi, Elisabeth Hedström, Per Kogner and Galina Selivanova
Clin Cancer Res September 1 2021 27 (17) 4943-4943; DOI:10.1158/1078-0432.CCR-21-2435
The editors are publishing this note to alert readers to a concern about this article (1): in Fig. 3D, the p21 and Noxa Western blots for SKN-DZ were accidentally duplicated as the PUMA and Noxa Western blots for SKN-BE(2). The SKN-DZ blots were correct, and the authors have additional SKN-BE(2) blots available for review upon request. The authors regret this error and stand by the conclusions in the article.
Reference
1.↵Burmakin M, Shi Y, Hedström E, Kogner P, Selivanova G. 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. Clin Cancer Res 2013;19:5092–103.
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More fool the Wellcome Trust! On the topic of the faked Cell paper (“hnRNPK”)!
St George’s has absorbed the money (“overhead costs”). Will like to keep it all quiet.
https://europepmc.org/grantfinder/grantdetails?query=pi%3A%22Moumen%2Ba%22%2Bgid%3A%22082609%22%2Bga%3A%22Wellcome%20Trust%22
Wellcome Trust
Funded by
Wellcome Trust
£ 142,873
Duration
01 Sep 2007 – 31 Mar 2011
Internal grant ID
082609
Grant DOI
10.35802/082609
Funding stream
Genetics, Genomics and Population Research
Grant type
Project Grant
Publications
All publications (1)
Free to read articles (1)
Regulation of hnRNP K and 4E-BP1 in response to DNA damage
Dr a Moumen | St George’s University of London
Abstract
This collaborative project will investigate mechanisms controlling two proteins that are involved in changes in gene regulation that occur when a cell’s DNA is damaged (e.g. by radiation or chemicals). Our recent work suggests that the concentrations of these proteins, called hnRNP K and 4E-BP1,change in response to DNA damage due to modifications in the structure of the proteins that influence the cell’s ability to destroy them. The key goals of the project will be to investigate the control of these structural changes, tocharacterise the molecules responsible and to establish the significance of these events for the ability of cells to react to DNA damage. We will also analyse possible interactions between the pathways controlled by hnRNPK and 4E-BP1 that may have important consequences for the ability of cells to react to DNA damage without harm to the organism as a whole.
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How long does it take for the director of the Gurdon Institute, Cambridge, England, to review the problematic data, then write to Cell and Cancer Cell (same Augean stable) and Cell Cycle, insisting on the retraction of all 3 papers for image manipulation and using same data to represent different experiments?
April, May, June…July, August (holidays)…Christmas 2021…Easter 2022….?
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Christmas 2021 is imminent and the director of the Gurdon Institute has still not retracted Cell. 2005 Dec 16;123(6):1065-78.
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Quite a lot of pollution (citations) of the scientific record. University of Cambridge is very “woke”. Do something about the environment!
Thought control.
https://www.rt.com/uk/524774-cambridge-university-report-microaggressions/
When it comes to the scientific record it couldn’t give a toss!
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=moumen+jackson&btnG=
[HTML] hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage
A Moumen, P Masterson, MJ O’Connor, SP Jackson – Cell, 2005 – Elsevier
In response to DNA damage, mammalian cells trigger the p53-dependent transcriptional
induction of factors that regulate DNA repair, cell-cycle progression, or cell survival. Through
differential proteomics, we identify heterogeneous nuclear ribonucleoprotein K (hnRNP K) …
Cited by 323 Related articles All 12 versions
[HTML] MDM2-dependent downregulation of p21 and hnRNP K provides a switch between apoptosis and growth arrest induced by pharmacologically activated p53
M Enge, W Bao, E Hedström, SP Jackson, A Moumen… – Cancer cell, 2009 – Elsevier
We have previously identified the p53-reactivating compound RITA in a cell-based screen.
Here, using microarray analysis, we show that the global transcriptional response of tumor
cells to RITA is p53 dependent. Pathway analysis revealed induction of the p53 apoptosis …
Cited by 169 Related articles All 9 versions
ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage
A Moumen, C Magill, K Dry, SP Jackson – Cell cycle, 2013 – Taylor & Francis
Previous work has established that heterogeneous nuclear ribonucleoprotein K (hnRNP K)
is stabilized in an ATM-dependent manner in response to DNA damage and acts as a
cofactor for p53-mediated transcription. Here, we show that in response to DNA damage …
Cited by 54 Related articles All 6 versions
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I think as Failed Scientists our opinion may not matter. Even that Leader of the Fraudatorium Augustine Choi is back tweeting about how great he and that scandalous dump he works for (Weill-Cornell) are. I love the way he is always shilling for his wife.
https://twitter.com/augustinemkchoi?lang=en
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“our opinion may not matter”.
At least we can a have a good laugh!
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Augustine Choi is not the same person as Abdeladim Moumen, or Stephen Jackson.
Let’s see what happens in this case. Cambridge University and St George’s University may hold different standards than Cornell University.
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Cool! A test using the scientific method!
Zeb hypothesizes that the british educational insitutions are more likely to punish rogue faculty than american institutions. Sure, this is on data point, but could eventually lead to a publication in a high impact factor journal. Remember, if it cant get into a high impact factor journal, it must be bad science, so the goal here is get more rogue faculty outed by Schneider so we have enough data points for a high impact factor journal.
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” Jackson Moumen became associate professor at the St George’s University in London”
St George’s University is a realively large and sophisticated employer. It should still have records of the candidates that applied for that associate prorfessor position.
St Geroge’s University should now offer that position to the person second on that list.
St George’s University is woke, it should put things right.
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Reply to NMH, the failed scientist and incel
July 18, 2021
” goal here is get more rogue faculty outed by Schneider so we have enough data points for a high impact factor journal.”
Yup.
To date there is preliminary evidence that unviersities Scotland may be more likely to take action than universities in England, or Wales.
For example Irina Stencheva was fired by the University of Edinburgh,
https://forbetterscience.com/2018/06/18/edinburgh-breaks-silence-to-announce-stancheva-retractions/
yet, Sarah Martin, who a comparable number of problematic publications remains in post at the Barts Cancer Institute, London.
https://www.bartscancer.london/staff/dr-sarah-martin/
Problematic papers.
Sarah Martin (without Alan Ashworth):
https://pubpeer.com/publications/2759A34758691741B87D49DFB05C3E
https://pubpeer.com/publications/8E38ECD6759C2479400E4306A749EB
https://pubpeer.com/publications/C961F8BD02A1C6B26EDD0358BEE8FC
Sarah Martin with Alan Ashworth:
https://pubpeer.com/publications/22A0D80CF891EEFEB7C23332484780
https://pubpeer.com/publications/CECD3E767BD0AFA9DDB1BA919F663F
https://pubpeer.com/publications/261D475F6640FC59C9A867EC7F5DD2
https://pubpeer.com/publications/67F39E13B7C8B51E8F8F34D70AFF84
Similarly QMUL, London has decided to take no action against Prof Thomas T MacDonald.
https://www.qmul.ac.uk/blizard/all-staff/profiles/tom-macdonald.html
Professor Tom MacDonald, PhD FRCPath FMedSci
“He has served on many grant awarding panels and advisory groups and is currently a member of the review panel of NC3R’s, Action Medical Research, was a past member of PSMB at MRC (2007-11) and chairs the MRC non-clinical training panel, sits on the MRC training and careers panel, chairs the Mason Medical Foundation Awards panel and also chairs the Kings Health Partners Awards Panel. He is a co-investigator on an MRC Programme with Graham Lord from Kings College and receives support from Glaxo Smith Kline in the UK and USA, Janssen Pharmaceuticals, Grunenthal, VH2 and Topivert to develop new molecules to treat inflammatory bowel disease.”
Impressive Pubpeer record:
https://pubpeer.com/publications/672F4F8A70BFBC3BE050D774C71488
https://pubpeer.com/publications/03ED65961D0E5B83FEAC28BBD5BD4D
https://pubpeer.com/publications/7F8A877887CF4CA7CA96B10A75674D
https://pubpeer.com/publications/9D805B95C0D61C5C559B350ED10869
https://pubpeer.com/publications/65E51DC922E5C8D1853A284C81652E
https://pubpeer.com/publications/955A28B11F388331A0A51B0E03C4BB
https://pubpeer.com/publications/798054ACD94648BB3748E20D75B1EE
https://pubpeer.com/publications/4861C25530B30ABEE6AA025C746C3C
https://pubpeer.com/publications/EED4F09DE9438C380E169D4EC96E98
https://pubpeer.com/publications/E4C7771CBD8F9F54EEAB54CB39905A
https://pubpeer.com/publications/A98514FE2714F2F8063CED78D8516B
https://pubpeer.com/publications/8482F49638E7E61D86CD257354FAE4
https://pubpeer.com/publications/8F7F07118764E28B1F6F59B0D2B25B
https://pubpeer.com/publications/7063BE20879224A9DFA37D198D8639
https://pubpeer.com/publications/6ED16FD333575E90EF97F2B85FB81B
https://pubpeer.com/publications/3BD205655E0AB5927B48AB9B8DE393
https://pubpeer.com/publications/57FF58D9434D8A758AD55DDF168DEE
https://pubpeer.com/publications/90E0BB37F60D3AFBD7E66AFF778513
https://www.scotsman.com/news/university-dundee-scientist-resigns-after-research-misconduct-1458779
Robert Ryan resigned from the University of Dundee in 2017.
https://retractionwatch.com/2018/08/09/glasgow-professor-leaves-post-amidst-multiple-retractions/
Professor Fiona Lyall left her post at the University of Glasgow after 3 retractions.
England does score two back,
Eric Lam was fired from Imperial College London.
https://retractionwatch.com/2021/05/28/imperial-college-london-researcher-fired-for-research-misconduct/
https://forbetterscience.com/2018/11/22/eric-lam-shady-research-at-imperial-to-cure-breast-cancer/
Univeristy of Bristol fired Abderrahmane Kaidi
https://forbetterscience.com/2018/09/17/abder-kaidi-fraud-and-bullying-scandal-unravelling/
I make that Scotland 3:-
Irina Stancheva,
Robert Ryan,
Finoa Lyall
England 2:-
Eric Lam
Abderrahmane Kaidi
What you have to take into account is the populations of Scotland and England.
Population Scotland
https://www.nrscotland.gov.uk/statistics-and-data/statistics/scotlands-facts/population-of-scotland
5,466,000
Popoulation England.
https://www.visitnorthwest.com/essential/population-england/
56,550,000
i.e. more than 10 times the population of Scotland.
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Irina Stancheva is Bulgarian. Lam is Chinese. Kaidi is Arab. Ryan was tenure-track, Irish and lost EMBO grant.
Most others you name are English or at least British. Hope this helps to figure out what goes on.
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Augustine Choi is Korean with a big-ass pubpeer record (along with annoying tweeting), and he still has his job. Therefore, Schneider, your putative “recent immigrant hypothesis” has been falsified! Science proves it’s self correcting indeed.
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In America, as long as you are not Black, your ethnicity doesn’t matter. Just bring in money. When you fail, you go.
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England: Sarah Martin is Irish (foreign), not the same thing as British. Nothing happens.
Scotland: Robert Rayn, Irish (foreign), not the same as British, resigned.
Scotland: Irina Stancheva, Bulgariian (foreign), fired.
I mention that to show that it is more to do with Scotland vs England, not the backgrounds of the researchers.
One interpretation is that Scotland pays more attention to the data, whereas England pays less attention to the data.
Scotland less impressed by aristocracy, England more impressed by aristocracy.
There is all of this, where England does not pay attention to the data:
https://forbetterscience.com/2021/02/10/the-english-science-supremacy/
https://forbetterscience.com/2021/05/03/kristian-helin-gets-the-perfect-job/
https://forbetterscience.com/2019/09/05/david-latchman-uncensored/
https://www.theguardian.com/education/2020/feb/01/david-latchman-geneticist-should-resign-over-his-team-science-fraud
https://www.theguardian.com/science/2019/jul/01/research-misconduct-claim-upheld-against-former-head-of-ucl-lab
https://www.buzzfeednews.com/article/peteraldhous/a-uk-university-knew-of-problems-in-a-top-geneticists-lab
Perhaps Scotland’s smaller population/scientific establishment means that by chance such monstrous agglomerations do not exist, or have yet to ben found, but at present there are no Scottish equivalents.
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What have Moomin trolls done to desrve this?
Are there any Moomin trolls on record exhibiting this type of behavour?
If you are not careful Moomin trolls will be tarred with the same brush!
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“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”
Is there something the matter with “hnRNP K”?
Nucleic Acids Res . 2004 Oct 14;32(18):5553-69. doi: 10.1093/nar/gkh876. Print 2004.
Protein kinase CK2 phosphorylation regulates the interaction of Kaposi’s sarcoma-associated herpesvirus regulatory protein ORF57 with its multifunctional partner hnRNP K
Poonam Malik 1, J Barklie Clements
Affiliation
1Division of Virology, Institute of Biomedical and Life Sciences, University of Glasgow, Church Street, Glasgow, G11 5JR, Scotland, UK.
PMID: 15486205 PMCID: PMC524287 DOI: 10.1093/nar/gkh876
Problematic data figure 6C. Much more similar than expected.
Problematic data figure 8. Much more similar and different than expected.
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Data in Nucleic Acids Res. 2004; 32(18): 5553–5569 very similar to data in J Gen Virol . 2004 Aug;85(Pt 8):2155-2166.
Much more similar than expected.
FYI:
J Gen Virol. 2004 Aug;85(Pt 8):2155-2166. doi: 10.1099/vir.0.79784-0.
Functional co-operation between the Kaposi’s sarcoma-associated herpesvirus ORF57 and ORF50 regulatory proteins
Poonam Malik 1, David J Blackbourn 1, Ming Fei Cheng 2, Gary S Hayward 2, J Barklie Clements 1
Affiliations
1Division of Virology, Institute of Biomedical and Life Sciences, University of Glasgow, Church Street, Glasgow G11 5JR, UK.
2Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, USA.
PMID: 15269354 DOI: 10.1099/vir.0.79784-0
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https://www.researchgate.net/profile/Poonam-Malik-3
Poonam Malik
The University of Edinburgh | UoE · Usher Institute
MBA (Edinb); PhD (Glas); MSc (IVRI), BSc (DEI); FRSB
Protein kinase CK2 phosphorylation regulates the interaction of Kaposi’s sarcoma-associated herpesvirus regulatory protein ORF57 with its multifunctional partner hnRNP K
Feb 2004
Poonam Malik
J Barklie Clements
ORF57 protein of Kaposi’s sarcoma-associated herpesvirus has a counterpart in all herpesvirus of mammals and birds and regulates gene expression at transcriptional and post-transcriptional levels. ORF57 was capable of self-interaction and bound a rapidly migrating form of heterogeneous nuclear ribonucleoprotein K (hnRNP K), a multifunctional cellul…
https://twitter.com/poons21?lang=en
https://www.insider.co.uk/special-reports/role-models-mentorship-key-gender-23625916
Role models and mentorship – key to gender equality
Poonam Malik, a Scottish Enterprise board member, says businesses should mark International Women’s Day with new programme for change
Today is International Women’s Day, a United Nations’-supported annual event that both celebrates the achievements of women and serves as a clarion call for gender equality.
We should use this occasion to spotlight all the budding and brilliant women scientists, entrepreneurs, business leaders, innovators, investors and home builders out there, and those fortunate to work and live with them.
McKinsey’s seminal report, Delivering Through Diversity , showed companies in the top-quartile for gender diversity on executive teams were 21% more likely to outperform on profitability and 27% more likely to have superior value creation.
Progress is being made and work has been done on getting women into executive positions at firms. Recent research showed that women now make up more than a third of top jobs at the UK’s 350 largest firms, while the number of women on boards has risen 50% from 682 to 1,026 in five years.
All of these women will be a role model to someone.
However, global milestones such as IWD are vital in reminding the world that despite the progress that has been made, gender parity has still not been achieved.
It’s incumbent on all of us, whether in business, government, academia or the arts, to think every day, not just on IWD, about how our actions help achieve gender equality and better inclusion. And an effective way of doing this is creating role-models.
You can’t be what you can’t see
This one sentence captures the whole essence of the diversity debate.
When I arrived in Scotland from India exactly 22 years ago, I could not see many women of colour in positions of influence in science, business or politics. Reflecting upon my career that developed from not knowing a single person in the UK to today, I’ve been privileged to receive so many incredible opportunities.
These include having mentors who believed in my potential, serving on the board of Scottish Enterprise, becoming a Court Member at the University of Highlands & Islands and joining the GlobalScot diaspora network. In these roles, I’ve made it my mission to highlight the importance of having diverse leaders that the next generation can aspire to.
Role-models and mentorship from senior colleagues cannot be underestimated. Look across the Pond at the positive reaction to Kamala Harris becoming the United States’ first female vice president and the first Asian American and first African American vice president as testament to that.
However, business and academia remain guilty of not having a diverse make-up. Progress in diverse female representation at the highest level remains fragile and slow.
Women and ethnic minorities continue to be under-represented in senior leadership roles and this has a detrimental impact on the chances of women-led businesses becoming successful. Indeed in 2019, less than 3% of all venture capital investment went to women-led companies.
Despite women holding 46% of the UK’s wealth, less than 6% angel investors in Scotland are women: a direct correlation is less than 2% of venture funding going to female-founder companies as the Rose Review established and less than 0.6% to people of colour.
So, how do we get more female and diverse role models in positions of power and influence?
One way is challenging the status quo and not just accepting things as they are. How apt, therefore, the theme of this year’s IWD is Choose to Challenge .
This was one of the subjects discussed at a recent GlobalScot virtual panel discussion I chaired to coincide with IWD 2021.
Our event consisted of leading GlobalScots, all of whom have made a significant impact in their chosen field. The conversation was incredibly powerful, with questions about diversity and the bottom-line, conversations with the right people, the power of networks and the impact of Covid-19 on gender parity all passionately debated.
One thing we all agreed on was the power of GlobalScots to spotlight the incredible, diverse women in Scotland. There’s no shortage of female talent here, all it needs is more exposure, something that our well-connected GlobalScot network can do internationally.
Here in Scotland, we need all our people, organisations and businesses to ensure women leaders are supported and offered the same opportunities as their male peers. There are some fantastic projects that are doing just that.
For example, Scottish Enterprise’s Principally Women programme supports female business leaders to gain the right skills and confidence to reach senior positions, Investing Women focuses on changing the face of angel investing and helping more women realise their growth potential, while Changing The Chemistry, champions increasing and enriching diversity of all kinds sustainably on all types of boards.
As an organisation Scottish Enterprise has also created many employee-affinity groups for its people, including on gender balance. This provides support and new thinking on gender equality issues, particularly on a more equal uptake of family leave.
These programmes are placing Scotland on the right path. But with the challenges of Covid-19, more can be done to ensure gender parity. We should harness the potential of women to be agents of positive societal change for Scotland and beyond, who will help play a key role in the global economic recovery.
All of us should commit to:
Enhancing mentoring and training opportunities for women business founders
Making available investment for female businesses to recover better and faster
Providing platform opportunities to young, diverse people of colour and BAME women to make their work visible and their voices more prominent, and
Advocating for a sustainable future of work policy environment and flexible, open and transparent funding for business ‘Fempreneurs’
So, as we mark International Women’s Day, let’s ensure our efforts extend beyond one day a year.
Let’s help build a pipeline of diverse talent from the grassroots levels for succession planning of tomorrow’s leaders. Let’s collaborate, promote and celebrate our female colleagues. And let’s ensure they are the role models for future generations.
Dr Poonam Malik, MBA PhD FRSB
“And let’s ensure they are the role models for future generations.”
Except herself.
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Yet more problematic data Nucleic Acids Res. 2004; 32(18): 5553–5569.
Figure 8B. Much more similar than expected.
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Nucleic Acids Res. 2004; 32(18): 5553–5569.
https://pubpeer.com/publications/BCE5F8FADDAE33607C9EC30F00AE3D#6
John Barklie Clements has passed, but could Poonam Malik post the original blots here?
https://www.deepdyve.com/lp/springer-journals/in-memoriam-john-barklie-clements-1946-2005-Fr9K4Q1SOc
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https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkac574/6619470
Retraction of ‘Protein kinase CK2 phosphorylation regulates the interaction of Kaposi’s sarcoma-associated herpesvirus regulatory protein ORF57 with its multifunctional partner hnRNP K’
Nucleic Acids Research, gkac574, https://doi.org/10.1093/nar/gkac574
Published: 04 July 2022
Following allegations of image manipulation in Figures 1A, 6C, 8B, 8C, and 8E in 2021, the journal conducted a brief investigation, referred the matter to the authors’ institution, and published an Expression of Concern. In May 2022, the institutional panel investigating the allegations concluded the figures are not authentic and the scientific integrity of the article is compromised, and they recommended retracting the article. Their report includes: ‘On the balance of probabilities, the Panel believe that these data as presented in the publication have been inappropriately manipulated. As such, the data and its interpretation are misleading and unreliable.’ The Editors of the journal are, therefore, now retracting this article.
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The University of Glasgow beat the University of Cambridge to retract a problematic hnRNP K paper.
The University of Cambridge is vastly more wealthy than the University of Glasgow.
Is the University of Cambridge going to plead poverty for not correcting the scientific record?
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Figure 2A.
Much more similar after 180 degree rotation and slight horizontal and horizontal re-sizing than expected.
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https://www.insider.co.uk/special-reports/role-models-mentorship-key-gender-23625916
Is very much like the clap-trap that Jane M Valentine spouts.
https://www.kcl.ac.uk/people/jane-valentine
Biography
Jane is a Senior Lecturer in Medical Education and Co-Director of King’s Extended Medical Degree Programme (EMDP). She is also Admissions Tutor for the EMDP, Chair of the MBBS Prizes Panel and an MBBS Senior Tutor. Jane is a keen advocate for diversity, equity and inclusion (DEI) within medical education. She has authored blogs, contributed to Parliamentary discussions and advised Government on social mobility, widening participation (WP) and access to the professions. Her academic interests are in curriculum development, teaching innovation – particularly the use of non-traditional teaching methods and environments – and DEI/WP-focused research.
Author of
ttps://www.insider.co.uk/special-reports/role-models-mentorship-key-gender-23625916
has:
Nucleic Acids Res. 2004; 32(18): 5553–5569.
Published online 2004 Oct 14. doi: 10.1093/nar/gkh876
PMCID: PMC524287
PMID: 15486205
Protein kinase CK2 phosphorylation regulates the interaction of Kaposi’s sarcoma-associated herpesvirus regulatory protein ORF57 with its multifunctional partner hnRNP K
Poonam Malik and J. Barklie Clements*
Author information
Division of Virology, Institute of Biomedical and Life Sciences, University of Glasgow, Church Street, Glasgow, G11
5JR, Scotland, UK
*To whom correspondence should be addressed. Tel: +44 141 330 4027; Fax: +44 141 337 2236; Email: b.clements@vir.gla.ac.uk.
Problematic data figure 6C. Much more similar than expected.
Problematic data figure 8B. Much more similar than expected.
Problematic data figures 8C and 8E. Much more similar than expected.
Jane M Valentine
has:
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
Figure 2A.
Much more similar after 180 degree rotation and slight horizontal and horizontal re-sizing than expected.
Figure 2A.
Much more similar after 180 degree rotation and slight horizontal and horizontal re-sizing than expected.
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Nearly 2 years now. Soon be Easter again.
S.P. Jackson (University of Cambridge) must be happy that he has been let off the hook and can breathe a sigh of relief.
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Data Figure 8C Nucleic Acids Res. 2004; 32(18): 5553–5569 much more similar and different to data in J Virol. 2003 Apr; 77(7): 4315–4325 than expected.
FYI:
J Virol . 2003 Apr;77(7):4315-25. doi: 10.1128/jvi.77.7.4315-4325.2003.
CK2 Protein Kinase Is Stimulated and Redistributed by Functional Herpes Simplex Virus ICP27 Protein
Maria D. Koffa,1,† Joy Kean,1 George Zachos,2 Stephen A. Rice,3 and J. Barklie Clements1,*
Author information
Institute of Virology, University of Glasgow, Glasgow G11 5JR,1 Beatson Laboratories, University of Glasgow,
Glasgow G61 1QH, Scotland, United Kingdom,2 Department of Microbiology, University of Minnesota Medical
School, Minneapolis, Minnesota 554553
*Corresponding author. Mailing address: Institute of Virology, University of Glasgow, Church St., Glasgow, G11 5JR Scotland, United Kingdom. Phone: 44-141-330-4027. Fax: 44-141-337-2236. E-mail: ku.ca.alg.riv@stnemelc.b.
†Present address: Gene Expression Programme, European Molecular Biology Laboratory, D-69117 Heidelberg, Germany.
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J Virol. 2001 Mar; 75(6): 2710–2728 continued.
Figures 6E and 6F. Much more similar and different than expected.
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J Virol. 2001 Mar; 75(6): 2710–2728.
doi: 10.1128/JVI.75.6.2710-2728.2001
PMCID: PMC115896
PMID: 11222695
Herpes Simplex Virus Type 1 Blocks the Apoptotic Host Cell Defense Mechanisms That Target Bcl-2 and Manipulates Activation of p38 Mitogen-Activated Protein Kinase To Improve Viral Replication
George Zachos,1,2,† Margy Koffa,1 Chris M. Preston,3 J. Barklie Clements,1 and Joe Conner2,*
Author information
Institute of Virology, University of Glasgow,1 and MRC Virology Unit, Institute of Virology,3 Glasgow G11 5JR, and
School of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow G4 0BA,2 United Kingdom
*Corresponding author. Mailing address: School of Biological and Biomedical Sciences, Glasgow Caledonian
University, Cowcaddens Rd., Glasgow G4 0BA, United Kingdom. Phone: (44 141) 331 3219. Fax: (44 141) 331
3208. E-mail: J.Conner@gcal.ac.uk
†Present address: CRC Beatson Institute for Cancer Research, Glasgow G61 1BD, United Kingdom.
Problematic data. Much more similar than expected.
Figures 1B and 1C.
Figures 2A and 2C.
Figure 4.
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J Virol. 2001 Mar; 75(6): 2710–2728 continued.
Figure 3B. Much more similar and different than expected.
Figure 2A. Much more similar and different than expected.
Figure 1D. Much more similar than expected.
Figure 2. Much more similar and different.
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From the published record I understand that John Barklie Celements “passed” in 2005.
https://pubpeer.com/publications/BCE5F8FADDAE33607C9EC30F00AE3D#6
https://www.deepdyve.com/lp/springer-journals/in-memoriam-john-barklie-clements-1946-2005-Fr9K4Q1SOc
The two highly problematic papers, the first in 2001 (J Virol. 2001 Mar; 75(6): 2710–2728) and the second in 2004 (Nucleic Acids Res. 2004 Oct 14;32(18):5553-69), make me think of two articles, which have appeared on this site:-
https://forbetterscience.com/2017/11/27/how-irun-cohen-and-weizmann-institute-almost-cured-diabetes/
” while Ofer Lider, associate professor of Immunology at Weizmann, was dying from leukaemia, his dedicated colleagues were apparently secretly stuffing manipulated data into his publications. ”
“What was done to the scientific and human legacy of the immunologist Ofer Lider, is the basically academic equivalent of urinating of someone’s literal grave.”
and
https://forbetterscience.com/2018/07/04/another-dead-scientist-framed-with-manipulated-data/
“On 7 April 2010 the Spanish diabetes researcher Margarita Lorenzo, Professor of Biochemistry at the Complutense University in Madrid, died of metastatic melanoma, aged only 51. Two months after her death, Lorenzo’s colleagues submitted a paper to the journal Diabetes (published by American Diabetes Association), which was accepted for publication 4 weeks later.”
“While she was dying of cancer, her colleagues advanced their careers using her reputation, using their own disreputable Photoshop skills.”
It seems that John Barklie Clements was highly regarded in his field, yet a highly problematic paper (where he was senior author, there being only 2 authors) was published the year before he died, and another highly problematic paper was published (where he is penultimate author) was published 4 years before he died.
I do wonder if the 2 articles which have appeared on this site offer “mechanistic insight” into the 2 problematic John Barklie Clements papers. History tells what has happened. Just as there is “unity of biology” there is “unity of human behaviour”.
The extant authors could help disprove this hypothesis:
The data in J Virol. 2001 Mar; 75(6): 2710–2728 and Nucleic Acids Res. 2004 Oct 14;32(18):5553-69 individually are uncommonly similar
FYI:-
First highly problematic paper.
J Virol. 2001 Mar; 75(6): 2710–2728.
doi: 10.1128/JVI.75.6.2710-2728.2001
PMCID: PMC115896
PMID: 11222695
Herpes Simplex Virus Type 1 Blocks the Apoptotic Host Cell Defense Mechanisms That Target Bcl-2 and Manipulates Activation of p38 Mitogen-Activated Protein Kinase To Improve Viral Replication
George Zachos,1,2,† Margy Koffa,1 Chris M. Preston,3 J. Barklie Clements,1 and Joe Conner2,*
Author information
Institute of Virology, University of Glasgow,1 and MRC Virology Unit, Institute of Virology,3 Glasgow G11 5JR, and
School of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow G4 0BA,2 United Kingdom
*Corresponding author. Mailing address: School of Biological and Biomedical Sciences, Glasgow Caledonian
University, Cowcaddens Rd., Glasgow G4 0BA, United Kingdom. Phone: (44 141) 331 3219. Fax: (44 141) 331
3208. E-mail: J.Conner@gcal.ac.uk
†Present address: CRC Beatson Institute for Cancer Research, Glasgow G61 1BD, United Kingdom.
Pubpper record for this paper: https://pubpeer.com/publications/C8355EB31AA9094B285775C81813E5
Second highly problematic paper.
Nucleic Acids Res. 2004 Oct 14;32(18):5553-69. doi: 10.1093/nar/gkh876. Print 2004.
Protein kinase CK2 phosphorylation regulates the interaction of Kaposi’s sarcoma-associated herpesvirus regulatory protein ORF57 with its multifunctional partner hnRNP K
Poonam Malik 1, J Barklie Clements
Affiliation
1Division of Virology, Institute of Biomedical and Life Sciences, University of Glasgow, Church Street, Glasgow, G11 5JR, Scotland, UK.
PMID: 15486205 PMCID: PMC524287 DOI: 10.1093/nar/gkh876
Pubpper record for this paper: https://pubpeer.com/publications/BCE5F8FADDAE33607C9EC30F00AE3D
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J Biol Chem. 2003 May 2;278(18):15973-82. doi: 10.1074/jbc.M212306200. Epub 2003 Feb 20.
Evidence for a mechanism of recombination during reverse transcription dependent on the structure of the acceptor RNA
Abdeladim Moumen 1, Lucette Polomack, Torsten Unge, Michel Véron, Henri Buc, Matteo Negroni
Affiliation
1
Unité de Regulation Enzymatique des Activités Cellulaires, CNRS-FRE 2364, Département de Biologie Structurale et Chimie and CNRS-URA 1960, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris cedex 15, France.
PMID: 12595540 DOI: 10.1074/jbc.M212306200
Problematic data figure 4. Much more similar than expected.
Figure 4Primer extension assays. Denaturing polyacrylamide gel analysis of primer extension products. A, synthesis of DNA was initiated specifically on the dG1Eb RNA in the absence (1–4) or in the presence of an equimolar amount of either aG1Eb (5–8) or aE2 templates (9–12) as acceptor RNA. B, DNA synthesis was primed on dE2 in the absence (1–5) or the presence of either aG1Eb (6–10) or aE2 (11–15). The reactions were terminated at different incubation times: 1, 3, 10, and 30 min (A) and 1, 3, 5, 10, and 30 min (B). The position of the pause site on the sequence corresponding to SL is shown ingray. The drawings at the bottom schematically indicate which donor and acceptor RNA templates were employed in the assays shown above, using the same representation as in Fig. 3.
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Galina Selivanova on PubPeer.
https://pubpeer.com/publications/F5D947C61E8B23CCD1EB716E4A1059#13
” We decided to perform a new experiment for the Figure 4D in my lab in Stockholm (the previous experiment has been performed in S Jackson’s lab in Cambridge). We performed Nutlin treatment of HCT116 cells with MDM2 depleted or not by two different siRNAs and performed immunoblotting for p53 and p21. Please see below the new western blot clearly showing that p21 is induced upon Nutlin treatment with or without MDM2 knockdown.”
The three panels can never show the same gel, for each lane, the band shapes and width do not match. It is two or maybe three separate gels, the p21 gel is definitely a separate one. This suggests either that a) Prof Selivanova engages in questionable research practices or b) she has absolutely no clue how to do simple experiments properly. In either case, I am not sure what use any of her research is.
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“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”
AstraZeneca lapped it all up. What a laugh!
https://www.astrazeneca.com/our-company/our-people/mark-o-connor.html
“I head up the DNA Damage Response (DDR) biology area within AstraZeneca’s IMED Biotech Unit and am the science lead for the company’s broader DDR franchise.”
“In 1999, I returned to the UK to take up a position as one of the three science team leaders at KuDOS, a spin-out biotech company based on the work of Professor Steve Jackson at Cambridge University.”
“As well as being a named inventor on multiple patents, I have a strong publication record, many of which have come through close external collaborations, that include peer reviewed publications in Cell, Cancer Cell, Cancer Discovery, Molecular Cell, Nature Cell Biology, Journal of Clinical Oncology and the New England Journal of Medicine.”
Speaks volumes about peer review.
“Featured publications
hnRNP K: an HDM2 target
hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage. Moumen A1, Masterson P, O’Connor MJ, Jackson SP. Cell 2005 16: 123(6):1065-78.”
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Mol Cancer Ther. 2017 Apr;16(4):566-577. doi: 10.1158/1535-7163.MCT-16-0378. Epub 2017 Jan 30.
AZD6738, A Novel Oral Inhibitor of ATR, Induces Synthetic Lethality with ATM Deficiency in Gastric Cancer Cells
Ahrum Min 1 2, Seock-Ah Im 3 2 4, Hyemin Jang 1, Seongyeong Kim 1, Miso Lee 1, Debora Keunyoung Kim 5, Yaewon Yang 1 4, Hee-Jun Kim 1 6, Kyung-Hun Lee 1 2 4, Jin Won Kim 1 7, Tae-Yong Kim 1 2 4, Do-Youn Oh 1 2 4, Jeff Brown 8, Alan Lau 9, Mark J O’Connor 9, Yung-Jue Bang 1 2 4
Affiliations
1Cancer Research Institute, Seoul National University, Seoul, Korea.
2Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
3Cancer Research Institute, Seoul National University, Seoul, Korea. moisa@snu.ac.kr.
4Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
5Rice University, Houston, Texas.
6Department of Internal Medicine, Chung Ang University College of Medicine, Seoul, Korea.
7Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
8AstraZeneca R&D Boston, Waltham, Massachusetts.
9AstraZeneca UK Ltd., Macclesfield, Cheshire, United Kingdom.
PMID: 28138034 DOI: 10.1158/1535-7163.MCT-16-0378
Figure 5A. Much more similar than expected.
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Apologies I made a terrible mistake.
Figure 5A refers to this paper and involves many more people:
Problematic data figure 5A. Much more similar than expected.
See: https://imgur.com/91xe4No
Breast Cancer Res. 2015 Mar 7;17:33. doi: 10.1186/s13058-015-0534-y.
Histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), enhances anti-tumor effects of the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib in triple-negative breast cancer cells
Ahrum Min 1 2, Seock-Ah Im 3 4 5, Debora Keunyoung Kim 6, Sang-Hyun Song 7, Hee-Jun Kim 8 9, Kyung-Hun Lee 10 11 12, Tae-Yong Kim 13 14 15, Sae-Won Han 16 17 18, Do-Youn Oh 19 20 21, Tae-You Kim 22 23 24, Mark J O’Connor 25, Yung-Jue Bang 26 27 28
Affiliations collapse
Affiliations
1Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. mar6716@snu.ac.kr.
2Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. mar6716@snu.ac.kr.
3Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. moisa@snu.ac.kr.
4Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. moisa@snu.ac.kr.
5Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. moisa@snu.ac.kr.
6Seoul International School, Seongnam, 461-830, Korea. deborak.98@gmail.com.
7Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. song1030@snu.ac.kr.
8Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. heejun.dino11@gmail.com.
9Department of Internal Medicine, Chung Ang University College of Medicine, Seoul, 156-755, Korea. heejun.dino11@gmail.com.
10Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. drleekh@gmail.com.
11Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. drleekh@gmail.com.
12Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. drleekh@gmail.com.
13Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. ktyongmd@gmail.com.
14Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. ktyongmd@gmail.com.
15Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. ktyongmd@gmail.com.
16Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. saewon1@snu.ac.kr.
17Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. saewon1@snu.ac.kr.
18Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. saewon1@snu.ac.kr.
19Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. ohdoyoun@snu.ac.kr.
20Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. ohdoyoun@snu.ac.kr.
21Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. ohdoyoun@snu.ac.kr.
22Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. kimty@snu.ac.kr.
23Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. kimty@snu.ac.kr.
24Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. kimty@snu.ac.kr.
25AstraZeneca UK Ltd, Macclesfield, Cheshire, SK10 2NA, UK. mark.j.occonnor@astrazeneca.com.
26Cancer Research Institute, Seoul National University College of Medicine, Seoul, 110-799, Korea. bangyj@snu.ac.kr.
27Department of Internal Medicine, Seoul National University College of Medicine, Seoul, 110-799, Korea. bangyj@snu.ac.kr.
28Biomedical Research Institute, Seoul National University Hospital, Seoul, 110-799, Korea. bangyj@snu.ac.kr.
PMID: 25888415 PMCID: PMC4425881 DOI: 10.1186/s13058-015-0534-y
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https://retractionwatch.com/2023/05/09/retractions-should-not-take-longer-than-two-months-says-uk-parliament-committee/#more-127086
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Breast Cancer Res. 2015 Mar 7;17:33. doi: 10.1186/s13058-015-0534-y.
Figure 5A. Much more similar than expected.
Figure 4A. Much more similar than expected.
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Nat Commun. 2017; 8: 1392.
Published online 2017 Nov 9. doi: 10.1038/s41467-017-01401-x
PMCID: PMC5680267
PMID: 29123096
ATR kinase inhibition induces unscheduled origin firing through a Cdc7-dependent association between GINS and And-1
Tatiana Moiseeva,1 Brian Hood,2 Sandy Schamus,1 Mark J. O’Connor,3 Thomas P. Conrads,2 and Christopher J. Bakkenistcorresponding author1,4
Author information
1Department of Radiation Oncology, University of Pittsburgh School of Medicine, Hillman Cancer Center, Research Pavilion, Suite 2.6, 5117 Centre Avenue, Pittsburgh, PA 15213-1863 USA
2Inova Schar Cancer Institute, Inova Center for Personalized Health, Annandale, VA 22003 USA
3DNA Damage Response Biology, Innovative Medicines and Early Clinical Development, Little Chesterford, Saffron Walden, CB10 1XL, UK
4Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15261 USA
Christopher J. Bakkenist, Email: bakkenistcj@upmc.edu
corresponding author
Figure 1d. Much more similar than expected.
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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
Mark J O’Connor is penultimate author here:
PubPeer – Androgen Receptor Inhibitor Enhances the Antitumor Effect of…
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Another Mark J O’Connor, England, problematic publication. Still no correction.
https://pubpeer.com/publications/70794BC33BF7457D7520183185C18B
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Retraction, but Moumen declined to sign the retraction notice.
https://www.cell.com/cell/fulltext/S0092-8674(24)01156-5
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Stephen Jackson has got the green light from the University of Cambridge.
3 retractions and you are in!
Loud and clear message. No ambiguity.
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Festivities which delay retractíons in England.
“We can’t possibly do anything because it’s
the Easter holidays, the summer holidays, the Christmas holidays (2021),
the Easter holidays, the summer holidays, the Christmas holidays (2022),
the Easter holidays, the summer holidays, the Christmas holidays (2023),
the Easter holidays, the summer holidays, (2024).”
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Many of the comments, mirrored in the retraction notice by the authors, appeared at Pubpeer in March 2021.
Another way of looking at the time it took to retract the paper is in comparison with the World Wars. Not as long as World War Two, but approaching the duration of World War One, and it’s only one paper.
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Cambridge researcher pulls Cell paper five years after Nature, Science retractions – Retraction Watch
” Images in some of Moumen’s other papers have been flagged on PubPeer, as reported by For Better Science in 2021. “
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Huh.
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Cambridge researcher pulls Cell paper five years after Nature, Science retractions – Retraction Watch
“The University of Cambridge, with Professor Jackson’s full cooperation, investigated this matter and concluded that these figures are not reliable. The University found no evidence of wrongdoing by Professor Jackson.“
We have it in writing. University of Cambridge gives Stephen Jackson the green light!
He is still at the University, and there was no wrongdoing! What more evidence do you want, except the data?
What we learn is that 4 retractions are O.K. with the University of Cambridge.
3 previous retractions together with the recent retraction from Cell make 4 retractions. It goes with the territory, blame the underlings, modern leadership! The dogs may bark but the caravan goes on! An embodiment of it.
Retraction Watch Database
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27 March 2025 Expression of Concern
https://www.tandfonline.com/doi/full/10.1080/15384101.2025.2463772
Expression of Concern
We, the Publisher and Editor of Cell Cycle, are issuing an Expression of Concern for the following article:
Moumen, A., Magill, C., Dry, K., and Jackson, S. P. ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage. Cell Cycle. 2013;12(4): 698–704. DOI: 10.4161/cc.23592
Following publication of this article, concerns about the integrity of Figures 1A, and 3B in the article were brought to the Publisher’s and Editor’s attention. As part of the investigation, the authors were contacted for any information that would help confirm the validity of Figures 1A and 3B. Whilst the authors were cooperative, given the length of time elapsed since publication, the authors were unable to fully address the concerns as they were unable to provide the original Western blot data, including the molecular weight markers.
Therefore, we are unable to address the concerns regarding Figures 1A and 3B; however, the Editor confirms that the concerns raised about Figure 1A and 3B do not affect the overall validity or integrity of the reported findings. We advise readers to interpret the information presented in Figure 1A and 3B with due caution.
The authors have been notified about this Expression of Concern. Should further information come to light, the journal will reassess any concern raised.
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Steve Jackson saved his fake paper.
White man’s burden.
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“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“
Surely there is enough problematic data in this paper for it to be retracted now?
Fresh problematic data comes to light.
See comments #21 and beyond. For the Cell stable of journals owned by the mega-profitable Elsevier, there is never enough problematic data.
PubPeer – MDM2-dependent downregulation of p21 and hnRNP K provides a…
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