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Lopez-Otin and Daley retract Nature Cell Biology paper

The 2015 Nature Cell Biology paper by the Spanish cancer researcher Carlos Lopez-Otin and his US partner George Q Daley, stem cell titan and dean of Harvard Medical School, is being retracted. First author and Lopez-Otin's student Clara Soria-Valles caused Daley even more trouble: her next groundbreaking paper was meant to be already published, but it is not even submitted and might never be.

Boom, the 2015 Nature Cell Biology paper by the famous, award-winning and now fugitive Spanish cancer and ageing researcher Carlos Lopez-Otin and his US partner George Q Daley, stem cell titan and dean of Harvard Medical School, is retracted. That happens because correct original data was unavailable, prompted by a prolonged debate on PubPeer (which in turn followed my reporting on Lopez-Otin’s data integrity practices), which established that the figures do not match what the authors deposited as supplement.

The paper Soria-Valles et al 2015 established the role of the transcription factor protein NF-kB in cellular senescence and cell reprogramming, while offering a potential cure to child patients suffering from the deadly premature ageing syndrome, such as Néstor–Guillermo or Hutchinson–Gilford progeria. Under this premise, the impactful Nature-themed paper earned Lopez-Otin in 2017 an ERC grant of €2.5 million, for a project named “Deconstructing Ageing: from molecular mechanisms to intervention strategies“. Earlier this year however, Lopez-Otin abandoned his ERC funded lab at University of Oviedo and escaped to Paris, to stay with his Photoshop expert friend Guido Kroemer. If past behaviour is anything to go by, ERC will now probably again play three monkeys and pretend that Lopez-Otin is still in Spain and his grant-deciding Nature Cell Biology paper was never retracted.

Another Soria-Valles et al paper from Daley lab, which proposed a way to produce haematopoietic stem cells via iPS technology and save people with leukaemia, was meant to be already published, but it is not even submitted and might never be. This and the retracted study’s first author Clara Soria-Valles was a former PhD student of Lopez-Otin, funded by EMBO postdoctoral fellowship and delegated to the Harvard labs of Daley and his junior partner Thorsten Schlaeger, to learn cellular reprogramming technique. Daley and Schlaeger are reported to be all but ready to apply the blood cell making technique in the clinic, at Boston Children’s Hospital, but now nobody knows if Soria-Valles’ preclinical data is anywhere near reproducible.

It is indeed difficult to find out what results still might be reliable. Soria-Valles disappeared already in April 2018 on a medical leave, though Daley still pays her (neither Daley nor Harvard normally pays any medical leaves for other sick lab members). Nobody else on that manuscript is available, because the Schlaeger lab people involved also left since. Money to try and reproduce it is not an issue though: the research project was funded from Daley’s biggest grant, the NHLBI Progenitor Cell Translational Consortium (NIH U01), which is worth almost $50 million.

Screenshot_2018-12-05 Blood stem cell breakthrough 'tantalizingly close'
Breakthrough manuscript as yet not even submitted to a journal. Screenshot: UBS

As I was informed, that Soria-Valles paper on haematopoietic reprogramming was meant to be originally submitted to the elite Cell family journal Cell Stem Cell (this is how the circulated draft was labelled in April 2018). Later on, roughly in August 2018, when my article appeared, the chosen target journal was Stem Cell Reports (published by International Society for Stem Cell Research, ISSCR). For someone like Daley this is a huge status reduction of journal venue. The results were presented earlier by Soria-Valles at the ISSCR annual meeting in 2017:

Soria-Valles, Clara 1 , Sugimura, Ryohichi 1 , Kumar Jha, Deepak 1 , Lummertz da Rocha, Edroaldo 1 and Daley, George 2
1 Boston Children’s Hospital, Boston, MA, USA, 2 Stem Cell Program, Boston Children´s Hospital, Boston, MA, USA
The generation of hematopoietic stem cells (HSCs) from human pluripotent stem cells (PSCs) constitutes a valuable tool with promising applications for research and therapy. However, derivation of HSCs with in vivo long-term engraftment and multi-lineage potential remains elusive. We have described a combinatorial approach, based on the directed differentiation of hemogenic endothelium (HE) and transduction with five transcription factors (TF) (RUNX1, ERG, LCOR, HOXA5 and HOXA9) expressed in lentiviral vectors that allowed the conversion of human PSCs into hematopoietic stem
and progenitor cells (HSPCs). The resulted cells exhibited long-term and multi-lineage hematopoietic capabilities when injected into irradiated immune-deficient mice.
Despite this proof of principle, the engineered cells have a limited self-renewal capacity due to the integration of the transgenes and are still molecularly distinct from bona fide HSCs. Thus, in an attempt to achieve bona fide HSCs and make them safer for future therapeutic interventions, we have established integration-free systems that have shown comparable efficiency to the previously developed lentiviral strategy through in vitro and in vivo experiments. Therefore, this new method may overcome some limitations of the lentiviral approach and hold the key for future regenerative medicine advances in blood diseases.

Soria-Valles however was not present at the 2018 ISSCR meeting (a conference which I incidentally wrote about here, in a story about another dishonest stem cell researcher, who was set to be ISSCR 2018 keynote speaker). Nobody knows how much of Soria-Valles’ claim to make haematopoietic stem cells via iPS technology is still valid. Sources were quoted with estimates of too low a yield or even not sure of producing any haematopoietic stem cells at all. Yet just this September 2018, Daley spoke at a lecture at Dana-Farber-Institute of his future Stem Cell Reports paper and even of his plans to apply the method to treat paediatric patients with congenital bone marrow deficiencies, in particular Shwachman Diamond Syndrome and Diamond Blackfan Anemia.

Screenshot_2018-12-05 University of Oviedo - nueva terapia logra reprogramar envejecimiento celular - News
Press release by University of Oviedo. Photo shows Soria-Valles with her fiancée and co-author Fernando Garcia Osorio

But now back to the main subject, the Nature Cell Biology retraction. The journal warned readers on 4 October 2018 with an editorial note that “that the reliability of data presented in this manuscript has been the subject of criticisms“. 4 December 2018 was the deadline imposed by the publisher to submit signatures from co-authors for a retraction. Lopez-Otin’s Oviedo colleague Jose Maria Perez Freije collected the signatures of all authors, including the elusive Soria-Valles, and submitted them to the publisher Nature.

This is the retraction notice:

“We, the authors, are retracting this Article due to issues that have come to our attention regarding data availability, data description and figure assembly. Specifically, original numerical data are not available for the majority of the graphs presented in the paper. Although original data were available for most EMSA and immunoblot experiments, those corresponding to the published EMSA data of Supplementary Fig. 8a, the independent replicate immunoblots of Fig. 8b and Supplementary Fig. 1e, and the independent replicate EMSA data of Supplementary Figs 6e, 8b, 8c and 8d, are unavailable. Mistakes were detected in the presentation of Figs 3c, 4i and Supplementary Figs 6a, 8a, 8d, 9, and in some cases the β-actin immunoblots were erroneously described in the figure legends as loading controls, rather than as sample processing controls that were run on separate gels. Although we, the authors, believe that the key findings of the paper are still valid, given the issues with data availability we have concluded that the most appropriate course of action is to retract the Article. We deeply regret these errors and apologize to the scientific community for any confusion this publication may have caused. All authors agree with the retraction.”

This slide show illustrates the data issues mentioned in the retraction notice. 

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And this slide show illustrates the issues the retraction notice chose not to address at all. 

This slideshow requires JavaScript.

In Daley’s lab, more things do not work as expected. His most famous Nature paper, Park et al 2008 , meant to compete with Shinya Yamanaka for induced pluripotency (iPS) fame and the Nobel Prize, is being plucked apart on PubPeer, accused of not having delivered any pluripotency as such. The exogenously delivered reprogramming transgenes remained namely active, while they were supposed to become silenced as cells’ own pluripotency genes become active. Also, Daley’s method of using Large T Antigen and telomerase TERT in addition to Yamanaka’s four iPS reprogramming factors proved rather counterproductive.

Whom to believe? A retracted Soria-Valles paper? Or Daley’s 2008 Nature paper which desperately wanted to prove better than Yamanaka’s iPS discovery? Source: PubPeer.

For someone like Daley, all of this is not the end of the world. There are always new windows of opportunity. Just as Chinese scientist Jiankui He caused a worldwide scandal with his unethical human experiments with CRISPR-modified babies, Daley (and his Harvard colleague George Church) offered a more enthusiastic view: America cannot afford a CRISPR gap to China. Daley suggested that Harvard should take the lead and apply CRISPR eugenics to ensure the survival of the human race:

“There have even been discussions that we as a species need to maintain the flexibility in the face of future threats to take the control of our own heredity.”

Harvard’s CRISPR experiments on human germ line editing are already starting. An Alzheimer’s associated gene is to be edited in human sperm, while Daley announced big plans to design the children of the future to be resistant to various diseases. Ethics is something this Harvard dean is apparently less interested in.

Harvard recently received a $200 million donation to set up a new institute, the money came from a controversial tycoon Leonard Blavatnik with Russian origins, whose lawyers made The Guardian apologise for erroneously calling him a “Putin pal” and an oligarch. 

It is Daley’s Spanish collaborator, the fugitive Lopez-Otin, who is in deep trouble with that retraction now. Lopez-Otin did manage to bring himself into news recently with his new paper (in a Nature -themed journal!) where his Oviedo lab analysed the genome of Lonesome George, the last member of his giant tortoise species who died in 2012. The press release omitted to say whether he spoke from Oviedo or Paris, Lopez-Otin the turtle geriatrics researcher was quoted with:

“We had previously described nine hallmarks of aging, and after studying 500 genes on the basis of this classification, we found interesting variants potentially affecting six of those hallmarks in giant tortoises, opening new lines for aging research” 

Nature now probably deeply regrets having awarded him with a 2017 Mentoring Award. Maybe they can give next one to Daley? Maybe Daley can get Soria-Valles to CRISPR some of those turtle genes to create a new long-lived human race of Homo harvardiensis crispri?

Update 21.12.2018. My article was apparently well received in Harvard, according to this information I was privy to:

“Daley was complaining intensely at lab meeting in front of entire lab and his junior faculty labs (Trista North and Thorsten Schlaeger) about potential lab members who might have leaked Soria-Valles information to the German blogger. It was intense”

I also learned that the now retracted Soria-Valles Nature Cell Biology 2015 paper was originally submitted to Science, were it was rejected due to some statistics issues.

Update 5.01.19. I was recently alerted by a source:

“George [Daley, -LS] has scared the lab members and provoked Stockholm syndrome among members. The Daley lab is trying to figure out who the leaks are now. Some of the members are trying to crash the German website by sending Hakenkreuz images.”

This was exactly what happened. Commenters used several fake identities to post highly defamatory comments about Daley on my site, equalling his research to Macchiarini’s trachea transplants and, indeed, using Nazi Swastika armband photoshopped on a photo of Daley. Exactly same picture was shared by Daley lab members in preparation of the campaign, it was confirmed to me. I deleted all those comments, but made backup, also of IP addresses.

Specifically, those IP addresses were located in US to Connecticut, 06902 Stamford, and New York State, 10022 New York. My source suggested I contact these Daley lab alumni: In-Hyun Park at Yale, CT, and Kitai Kim at MSKCC in NY, as well as the person allegedly orchestrating the campaign, the current Daley postdoc Deepak Jha. None of them replied, but Jha immediately blocked me on Twitter. This is how some grown men behave to please their mighty (ex-)boss. Maybe they should rather relax and read the book by Daley’s wife, Amy C. Edmondson, “The Fearless Organization: Creating Psychological Safety in the Workplace for Learning, Innovation, and Growth“.

Daley will be opening the Blavantik institute in ceremony on February 5th, at 5:30 PM. Come to talk about plans of CRISPR babies!





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65 comments on “Lopez-Otin and Daley retract Nature Cell Biology paper

  1. Good news!
    It was good that other shameless Nature papers would be also retracted


  2. What will happen to Soria-Valles Stem Cell Reports? Given her Nature Cell Biology retracted, can the author with retraction history submit to other journals and continue research work?


    • Razielclein

      We should wait that cheater learn the lesson, and overall that the science has a powerful weapon to catch them.


  3. Indigofera Tanganyikensis

    Thank you Leonid for your tremendous contribution to science.

    I started the discussion regarding the Nature Cell Biology paper by Soria Valles on PubPeer one year ago after I got inspiration from your article about Lopez-Otin.

    I will continue to fight against the cheaters and will encourage all the vigilant scientist out there to stand up against the producers of fake science. Put pressure on those “scientist” and the journals and research institutes which protect them.


  4. First retraction ever from both Daley and Lopez-Otin.


  5. Another Daley’s most famous Nature paper to claim possible ectogenesis of life was under debate on PubPeer about its reproducibility and image fabrication.

    Derivation of embryonic germ cells and male gametes from embryonic stem cells
    Nature (2004) – 3 Comments
    pubmed: 14668819 doi: 10.1038/nature02247 issn: 1476-4687 issn: 0028-0836 issn: 1476-4679

    Niels Geijsen , Melissa Horoschak , Kitai Kim , Joost Gribnau , Kevin Eggan , George Q. Daley

    “Indeed 10 years later and this method has not been adopted or reproduced. ”

    “The Daley group should have applied their guidelines for establishing provenance of pluripotent states
    ( )
    ( ), on their previous study claiming the generation of functional sperm from mouse ESCs published in Nature 2004, which remains to be reproduced!!!!

    They should have reproduced this controversial study and used “forensic genomics” to establish provenance of in vitro generated haploid male gametes and sperm. Alternatively, publishing “Failure to replicate the STAP cell phenomenon” in 2015, would have made a good occasion to retract Geijsen et al. 2004 paper. ”

    “Image splicing.”


  6. One of the current lab members at Daley’s lab is a postdoctoral fellow named Pavlos Missios. He did his PhD under Karl Lenhard Rudolph who was accused of profound scientific misconduct ( as 8 of Rudolph’s had evidence of data fabrication/manipulation. Pavlos Missios is the primary author of one of those 8 paper which also been criticized on pubpeer (

    Collectively such incidences suggest that Daley is inclined in recruiting such postdocs.


  7. Why this retraction note avoided to address more issues? The notice only addressed superficially. Daley and Lopez-Otin still want to hide some worse detail of this paper?
    “And this slide show illustrates the issues the retraction notice chose not to address at all.”


  8. Unfortunately the truth behind many iconic papers maybe quite sinister and their revelation even a scandal to governments


  9. Comparing with Daley’s talk at DFCI this Sept. 2018, his following NIH talk Nov. 2018 dramatically shrunk Soria-Valles work. He did not repeat his claim that “(Soria-Valles’) haematopoietic stem cells showed similar capacity as cord blood haematopoietic stem cells” that was most outstanding point at DFCI talk.
    56-57: Soria-Valles work in three slides
    57-59: Daley proposed scale-up production strategy to test Soria-Valles haematopoietic stem cells in human patients.


  10. Apparently, the retraction note was written in too mild manner. As you described in the slide show, most of critical points from pubpeer were not chosen to address. These include progeria patients’ sample swapping in figure 6b; aged donors’ sample swapping in figure 7a, contradictory expression of pluripotent genes in adult cells in figures 6g, 7f; and band-donor films used throughout in entire paper.


  11. Pingback: Aperto al dibattito - Ocasapiens - Blog -

  12. “award-winning and now fugitive Spanish cancer and ageing researcher”, now fugitive? Did I miss any fun here?


  13. Soria-Valles’ thesis was based on now retracted Nature Cell Biology paper and another PubPeer alleged Oncogene paper on which they deposited someone else’s irrelevant microarray data from irrelevant tissue as their own breast cancer microarray data.

    The act of defending the Thesis of Dna. Clara Soria Valles, titled “Tissue remodeling and cell reprogramming in cancer and aging” directed by Dr. Carlos Lopez Otin and Dr. Ana Y. Gutierrez Fernandez, will take place on June 12 at 12.00 in the Sala de Grados of the Faculty of Medicine.


    • A PhD thesis in Spain as far as I know is supposed to be an original, unpublished work with the exceptions of certain regions in Spain where they follow the Dutch model where a PhD thesis is a compilation of published papers
      If a PhD student comes from a big lab will be very difficult he/she gets enough attention from their supervisor which maybe just interested in adding more PhD theses to his/her CV as well as nature papers rather than conveniently forming someone to be a competent researcher


      • Razielclein

        Dear Ana, I don’t know if you are Spaniard or Hispanic, but as Spaniard, my thesis is the addition of 3 articles published on international peer-reviewed journals. I think that very probably in big labs and is not the case of the Otin one, the student can cheat easily the PI. Hence, in these cases, the punishment should lie on the student. If Otin is compulsively cheating then is when he should be investigated.

        Does somebody know what will happen to this young first author-researcher?


      • Razielclein,
        Lopez-Otin has 23 of problematic papers with copy-paste of images. The retracted Nature Cell Bio. paper was a flagship of a fleet of their problematic papers.
        Soria-Valles mocked data deposition policy not only for Nature Cell Bio. but also for another npg journal Oncogene. They, instead of their own, linked microarray data of someone else’s lab of totally irrelevant samples.
        I assume all these papers are under investigation.


      • “Does somebody know what will happen to this young first author-researcher?”
        The first author Clara Soria-Valles safely returned back to her home university with fund from Spanish government called Juan de la Cierva-incorporación. The Spanish system encourages cheaters, rather giving them penalty.


  14. The Retraction Watch Database indexed this paper and all authors.


  15. I inquired Oncogene editors to dig into Soria-Valles’ microarray data and original numerical data to make graphs in the article.
    The chief editor Dr. Stebbing said he will deal with this.


  16. Another reader on PubPeer argues back that gel splicing seems nitpicky.

    Derivation of embryonic germ cells and male gametes from embryonic stem cells
    Nature (2004) – 4 Comments
    pubmed: 14668819 doi: 10.1038/nature02247 issn: 1476-4687 issn: 0028-0836 issn: 1476-4679

    Niels Geijsen , Melissa Horoschak , Kitai Kim , Joost Gribnau , Kevin Eggan , George Q. Daley

    “Whether the findings in this paper are truly reproducible is a worrisome question, but it’s hard to see how the splicing in figure 2D is terribly problematic. I would imagine the gel comb has 24 wells and therefore some combining of non-adjacent images would be necessary here, either at the position shown or just before the controls. It’s actually better that the experimenter put some experimental lanes together with the control lanes, rather than probing the controls separately. No, there isn’t a separation between the non-contiguous membranes, but the splice is quite obvious and this is a 2004 paper. Seems nitpicky to me.”


    • If one has so many samples that a second gel is needed, one should also load control samples on both gels. Unless this is a Harvard paper meant for Nature, of course.


  17. Complex history of biorxiv pre-print from Daley. How many reincarnation this pre-print needs to be real print?

    Short hairpin RNAs artifactually impair cell growth and suppress clustered microRNA expression
    bioRxiv (2018) – 7 Comments
    doi: 10.1101/372920

    John Powers author has email , Edroaldo Lummertz Da Rocha , Daniel Pearson , Pavlos Missios , Tarja Yvanka De Soysa , Jessica Barragan , Patrick Cahan author has email , George Daley

    “You can find the original version here. I found the article has two older versions. The mistake of copy-paste and splicing was introduced in the first version (July 20, 2018), stil remained in the second version (July 26, 2018), and finally replaced with new images in the latest version (December 11, 2018). The second version added two missing references to introduce this sentence ” LentiCRISPRv2 was a gift from F. Zhang19,20.”

    Sanjana, N. E., Shalem, O. & Zhang, F. Improved vectors and genome-wide libraries for CRISPR screening. bioRxiv 11, 006726 (2014).
    Shalem, O. et al. Genome-scale CRISPR-Cas9 knockout screening in human cells. Science 343, 84–7 (2014)."


  18. Soria-Valles’ NCB paper (2015) was retracted and finally removed from Lopez-Otin lab website.

    Selected publications from our lab
    Ferrando, A. A. and Lopez-Otin, C. Clonal evolution in leukemia. Nature Med, 23, 1135-1145 (2017). PubMed
    de la Rosa, J., Weber, J., Friedrich, M. J., Li, Y., Rad, L., Ponstingl, H., Liang, Q., de Quiros, S. B., Noorani, I., Metzakopian, E., Strong, A., Li, M. A., Astudillo, A., Fernandez-Garcia, M. T., Fernandez-Garcia, M. S., Hoffman, G. J., Fuente, R., Vassiliou, G. S., Rad, R., Lopez-Otin, C., Bradley, A. and Cadinanos, J. A single-copy Sleeping Beauty transposon mutagenesis screen identifies new PTEN-cooperating tumor suppressor genes. Nature Genet, 49, 730-741 (2017). PubMed
    Lopez-Otin, C., Galluzzi, L., Freije, J. M., Madeo, F. and Kroemer, G. Metabolic Control of Longevity. Cell, 166, 802-21 (2016). PubMed
    Osorio, F. G., Soria-Valles, C., Santiago-Fernandez, O., Bernal, T., Mittelbrunn, M., Colado, E., Rodriguez, F., Bonzon-Kulichenko, E., Vazquez, J., Porta-de-la-Riva, M., Ceron, J., Fueyo, A., Li, J., Green, A. R., Freije, J. M. and Lopez-Otin, C. Loss of the proteostasis factor AIRAPL causes myeloid transformation by deregulating IGF-1 signaling. Nature Med, 22, 91-6 (2016). PubMed
    Puente, X. S., et al. Non-coding recurrent mutations in chronic lymphocytic leukaemia. Nature, 526, 519-24 (2015). PubMed
    Quiros, P. M., Langer, T. and Lopez-Otin, C. New roles for mitochondrial proteases in health, ageing and disease. Nature Rev Mol Cell Biol, 16, 345-59 (2015). PubMed
    Robles-Espinoza, C. D.,et al. POT1 loss-of-function variants predispose to familial melanoma. Nature Genet, 46, 478-81 (2014). PubMed

    Loi, M., Cenni, V., Duchi, S., Squarzoni, S., Lopez-Otin, C., Foisner, R., Lattanzi, G. and Capanni, C. Barrier-to-autointegration factor (BAF) involvement in prelamin A-related chromatin organization changes. Oncotarget, 7, 15662-77 (2016). PubMed
    Alioto, T. S., et al. A comprehensive assessment of somatic mutation detection in cancer using whole-genome sequencing. Nature Commun, 6, 10001 (2015). PubMed
    Puente, X. S., et al. Non-coding recurrent mutations in chronic lymphocytic leukaemia. Nature, 526, 519-24 (2015). PubMed
    Xargay-Torrent, S., Lopez-Guerra, M., Rosich, L., Montraveta, A., Roldan, J., Rodriguez, V., Villamor, N., Aymerich, M., Lagisetti, C., Webb, T. R., Lopez-Otin, C., Campo, E. and Colomer, D. The splicing modulator sudemycin induces a specific antitumor response and cooperates with ibrutinib in chronic lymphocytic leukemia. Oncotarget, 6, 22734-49 (2015). PubMed
    Gutierrez-Fernandez, A., Soria-Valles, C., Osorio, F. G., Gutierrez-Abril, J., Garabaya, C., Aguirre, A., Fueyo, A., Fernandez-Garcia, M. S., Puente, X. S. and Lopez-Otin, C. Loss of MT1-MMP causes cell senescence and nuclear defects which can be reversed by retinoic acid. EMBO J, 34, 1875-88 (2015). PubMed
    Rodriguez, D., Bretones, G., Quesada, V., Villamor, N., Arango, J. R., Lopez-Guillermo, A., Ramsay, A. J., Baumann, T., Quiros, P. M., Navarro, A., Royo, C., Martin-Subero, J. I., Campo, E. and Lopez-Otin, C. Mutations in CHD2 cause defective association with active chromatin in chronic lymphocytic leukemia. Blood, 126, 195-202 (2015). PubMed
    Quiros, P. M., Langer, T. and Lopez-Otin, C. New roles for mitochondrial proteases in health, ageing and disease. Nature Rev Mol Cell Biol, 16, 345-59 (2015). PubMed
    Cal, S. and Lopez-Otin, C. ADAMTS proteases and cancer. Matrix Biol, 44-46C, 77-85 (2015). PubMed
    Cabrera, S., Maciel, M., Herrera, I., Nava, T., Vergara, F., Gaxiola, M., Lopez-Otin, C., Selman, M. and Pardo, A. Essential role for the ATG4B protease and autophagy in bleomycin-induced pulmonary fibrosis. Autophagy, 11, 670-84 (2015). PubMed
    Aguilera, O., Gonzalez-Sancho, J. M., Zazo, S., Rincon, R., Fernandez, A. F., Tapia, O., Canals, F., Morte, B., Calvanese, V., Orgaz, J. L., Niell, N., Aguilar, S., Freije, J. M., Grana, O., Pisano, D. G., Borrero, A., Martinez-Useros, J., Jimenez, B., Fraga, M. F., Garcia-Foncillas, J., Lopez-Otin, C., Lafarga, M., Rojo, F. and Munoz, A. Nuclear DICKKOPF-1 as a biomarker of chemoresistance and poor clinical outcome in colorectal cancer. Oncotarget, 6, 5903-17 (2015). PubMed
    Wallace, D. F., Secondes, E. S., Rishi, G., Ostini, L., McDonald, C. J., Lane, S. W., Vu, T., Hooper, J. D., Velasco, G., Ramsay, A. J., Lopez-Otin, C. and Subramaniam, V. N. A critical role for murine transferrin receptor 2 in erythropoiesis during iron restriction. Br J Haematol, 168, 891-901 (2015). PubMed
    Rodriguez, D., Bretones, G., Arango, J. R., Valdespino, V., Campo, E., Quesada, V. and Lopez-Otin, C. Molecular pathogenesis of CLL and its evolution. Int J Hematol, 101, 219-28 (2015). PubMed
    Bassaganyas, L., Bea, S., Escaramis, G., Tornador, C., Salaverria, I., Zapata, L., Drechsel, O., Ferreira, P. G., Rodriguez-Santiago, B., Tubio, J. M., Navarro, A., Martin-Garcia, D., Lopez, C., Martinez-Trillos, A., Lopez-Guillermo, A., Gut, M., Ossowski, S., Lopez-Otin, C., Campo, E. and Estivill, X. Sporadic and reversible chromothripsis in chronic lymphocytic leukemia revealed by longitudinal genomic analysis. Leukemia, 29, 758 (2015). PubMed
    Queiros, A. C., Villamor, N., Clot, G., Martinez-Trillos, A., Kulis, M., Navarro, A., Penas, E. M., Jayne, S., Majid, A., Richter, J., Bergmann, A. K., Kolarova, J., Royo, C., Russinol, N., Castellano, G., Pinyol, M., Bea, S., Salaverria, I., Lopez-Guerra, M., Colomer, D., Aymerich, M., Rozman, M., Delgado, J., Gine, E., Gonzalez-Diaz, M., Puente, X. S., Siebert, R., Dyer, M. J., Lopez-Otin, C., Rozman, C., Campo, E., Lopez-Guillermo, A. and Martin-Subero, J. I. A B-cell epigenetic signature defines three biologic subgroups of chronic lymphocytic leukemia with clinical impact. Leukemia, 29, 598-605 (2015). PubMed
    Keane, M., Semeiks, J., Webb, A. E., Li, Y. I., Quesada, V., Craig, T., Madsen, L. B., van Dam, S., Brawand, D., Marques, P. I., Michalak, P., Kang, L., Bhak, J., Yim, H. S., Grishin, N. V., Nielsen, N. H., Heide-Jorgensen, M. P., Oziolor, E. M., Matson, C. W., Church, G. M., Stuart, G. W., Patton, J. C., George, J. C., Suydam, R., Larsen, K., Lopez-Otin, C., O’Connell, M. J., Bickham, J. W., Thomsen, B. and de Magalhaes, J. P. Insights into the evolution of longevity from the bowhead whale genome. Cell Rep, 10, 112-22 (2015). PubMed
    Caravia, X. M. and Lopez-Otin, C. Regulatory Roles of miRNAs in Aging. Adv Exp Med Biol, 887, 213-30 (2015). PubMed
    Soria-Valles, C., Osorio, F. G. and Lopez-Otin, C. Reprogramming aging through DOT1L inhibition. Cell Cycle, 14, 3345-6 (2015). PubMed
    Galluzzi, L., et al. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015. Cell Death Differ, 22, 58-73 (2015). PubMed
    Fernandez, A. F. and Lopez-Otin, C. The functional and pathologic relevance of autophagy proteases. J Clin Invest, 125, 33-41 (2015). PubMed
    Lopez-Guerra, M., Xargay-Torrent, S., Rosich, L., Montraveta, A., Roldan, J., Matas-Cespedes, A., Villamor, N., Aymerich, M., Lopez-Otin, C., Perez-Galan, P., Roue, G., Campo, E. and Colomer, D. The gamma-secretase inhibitor PF-03084014 combined with fludarabine antagonizes migration, invasion and angiogenesis in NOTCH1-mutated CLL cells. Leukemia, 29, 96-106 (2015). PubMed

    In contrast, Daley lab website still displays this paper in Publication section.


  19. Does anyone know there are any progeria patients and researchers associations in europe, Spain, US etc? They need to be alerted that Harvard, International society of stem cell research and uniovi produced a big fake hope using public fund of EMBO.


  20. Progeria Research Foundation has been operating clinical trials to progeria kids since 2007 at Boston Children’s Hospital, where Soria-Valles’ progeria study took place at the Daley lab located there. The study was published in Nature Cell Biology and retracted by now.

    The clinical trial is based on 2003 discovery of progeria gene lamin A in HGPS progeria by Francis Collins, NIH director. Soria-Valles’ retracted study proposed a method to rejuvenate HGPS patients cells, where they swapped samples to make up the claim.

    “Twenty-eight (28) children from sixteen countries participated, ages 3 to 15 years. Children returned to Children’s Hospital Boston every four months, for testing and to receive new drug supply, and stayed in Boston for 4-8 days each visit. While at home, their doctors kept a close watch over the children and submitted periodic health reports to the Boston research team. For the duration of the trial, an average of 2 children per week traveled to Boston to participate.”


  21. Here are Supporting Organizations for progeria according to NORD website.
    Ironically, Progeria Research Foundation (PRF) who runs clinical trials for progeria kids is based on Daley’s home ground Boston Children’s Hospital. There Soria-Valles and Daley worked for both retracted progeria paper and haematopoietic reprogramming to treat paediatric patients with Shwachman Diamond Syndrome (SDS) and Diamond Blackfan Anemia (DBA). For both diseases, Daley has been publishing intensively for years.

    Genetic and Rare Diseases (GARD) Information Center
    PO Box 8126
    Gaithersburg, MD 20898-8126
    Phone: (301) 251-4925
    Toll-free: (888) 205-2311

    Progeria Research Foundation, Inc.
    P.O. Box 3453
    Peabody, MA 01961-3453 USA
    Phone: (978) 535-2594


  22. At NIH this November 2018, Daley shared his roadmap to inject Soria-Valles stem cells to pediatric patients.

    And graphs show that Soria-Valles stem cells successfully engrafted in mice for long-term.


    • Daley was promoting pipeline of Clara Soria-Valles to patients. Question is if he KNEW about Soria-Valles problems, yet still wanted to apply her research to children patients.

      Very concerning if true.


  23. The co-first author of retracted NCB paper, Fernando G. Osorio has just published a quick paper in Cell Reports with his current host lab Fernando Camargo (Boston Children’s Hospital) and Ruben van Boxtel (Princess Maxima Center).
    Somatic Mutations Reveal Lineage Relationships and Age-Related Mutagenesis in Human Hematopoiesis
    Fernando G. Osorio, Axel Rosendahl Huber, Rurika Oka, Ignacio Varela, Fernando D. Camargo, Ruben van Boxtel
    Publication History
    Published: November 27, 2018
    Accepted: October 31, 2018
    Received in revised form: October 10, 2018
    Received: June 14, 2018

    Nicely free from any immunoblot!
    See his former research at Lopez-Otin lab.


  24. Soria-Valles retraction notice is saying that they did not have original numerical data for majority of graphs. So the graphs made from scratch? And there were lots of image problems. These are terrible fraud, cannot say honest mistakes at all. And they got fund because of this fraud paper. How much fund do they have to return to funding bodies?


  25. The funding source and amount of money related with Soria-Valles’ retracted NCB paper and haematopoietic stem cell paper she had done at Daley lab;
    – NIH U01 grant to Daley
    $1,044,680 as of the fiscal year 2016

    EMBO long-term fellowship to Soria-Valles
    $45,133/first year + $49,646/second year
    ERC grant to Lopez-Otin
    €2,500,000. Through 2017-2022


    • That is why I keep insisting if we all have to pay taxes and support this people minimally a list of all the expenses that were covered by these grants including raw data from the research that was conducted with conclusions should be available to public


  26. This means George Daley was presenting Soria-Valles’ work at NIH who is funding the project, him knowing that the work of Soria-Valles had been under investigation and been alerted by Nature Cell Biology. Knowingly presenting data which may not be right (or not exist) at the own funding body?


  27. More comment on Daley’s Nature paper about deriveration of human iPS cells. The paper lacks a significant evidence to validate pluripotency of their cells. Pluripotent reporter data is missing, while J. Thomson lab has the data. They used the same reporter line originally from Thomson..

    Reprogramming of human somatic cells to pluripotency with defined factors
    Nature (2008) – 12 Comments
    pubmed: 18157115 doi: 10.1038/nature06534 issn: 1476-4687 issn: 0028-0836

    In-Hyun Park author has email , Rui Zhao , Jason A. West , Akiko Yabuuchi , Hongguang Huo , Tan A. Ince , Paul H. Lerou author has email , M. William Lensch author has email , George Q. Dale

    “I am curious why this paper did not show GFP data from reprogrammed H1-OGN cells? The line is made from Zwaka and Thomson and can report reprogramming by reactivation of GFP. The most convincing evidence at the time. Indeed both Daley and Thomson papers used the line. You can see GFP reactivation in Thomson 2007 Science, but not in this paper. ”


  28. I am just hoping all the postdocs from these labs don’t be afraid and start telling the truth, how they are under pressure to get certain results, how they are frightened with visa and other issues


  29. Hey Ana Pedro, could you give us more details on your experience as a postdoc in the USA and what happened to you?


    • Hi Sirgraphs,

      You can find a summary of what happened to me in the email bellow (a response to the email Lyden and Cardoso sent Dr. Inglis from BioRxiv) also published in this blog in comments. I recently wrote an email to Cornell RARC Department and I am waiting for their response

      Kind regards,

      Ana Pedro

      Rod Tucker,
      Ronny Schmidt

      Dear Dr Inglis

      The data published pertains to my post doc work at WCMC and Champalimaud Foundation. These data obtained before Ayuko et al 2015 was published clearly contradicts what was published in this manuscript stating that integrins determine cancer metastasis sites. I remember very well I had a meeting as well much time before Hoshino et al was published with Dr Lyden, Dr Hoshino and Dr Bruno Costa Silva and we clearly saw that sample CF33 didn’t have any integrins and the integrins content of CF27 sample was not consistent with Hoshino et al, 2015
      Moreover, given that I mentioned the origin of the samples and the founders and all the intelectual work was performed by myself including project writing (I can proof it and I can mention including that Dr Cardoso and Dr. Lyden did not wrote a line of the project that was approved for funding by FCT), sample processing and analysis I believe I am on the right of publushing these data
      Indeed I believe that instead the manuscript Hoshino et al 2015 should be removed by Nature as it is clearly cheated. Also I can proof there were mouse work irregularities corresponding to the period of time when Hoshino et al 2015 was published
      You can consult the the hotmail address, password:recl@m@cao for details about mouse work issues and project authorship
      Given that Nature or WCMC did not undertook any measure given the mentioned misconduct allegations, instead Dr Inglis, I ask you what I can do in order to get justice and being able to publish my hard work which is a true, transparent work
      I also give permission to Leonid Schneider to publish this email in his site
      I also ask Dr Cardoso and Dr Lyden for some reasonability
      I thank you so much your help regarding the issues I raised above

      Looking forward to hearing from you
      Kind regards
      Ana Pedro


  30. Here are all four slides related with Daley’s data and roadmap to transplant Soria-Valles’ stem cells into pediatric patients at NIH talk this Nov. 1, 2018.
    How to make Soria-Valles’ stem cells

    Long-term engraftment of Soria-Valles’ stem cells in mice

    FACS plots and DNA analysis of Soria-Valles’ stem cells

    Roadmap to transplant Soria-Valles’ stem cells into kids

    Link to NIH videocast of Daley, Nov. 2018


  31. I will be presenting the preliminary data from my “problematic” bioRXIv pre-print at the Frontiers Stem Cell 2019 meeting in the end of April in New York and I will add some independent preliminary data from Lyden lab regarding flow cytometry analysis of circulating HSCs and MDSCs in control and early and metastatic breast cancer patients. It is obvious for me that exosome integrins do not play a fundamental role in metastases and also by analysing the mentioned flow data (unfortunately I do not have the original flow cytometry files, I wrote down the flow results and returned the CDs containing the original data) if it seems obvious that MDSCs play a role in metastasis, this data does not clearly demonstrate that HSCs are involved in metastasis…if this is true we should see more HSCs in those early breast cancer patients who will develop metastases? And also in metastatic breast cancer patients? For sure MDSCs are derived from HSCs…so further experiments are needed
    Discussions are open


  32. “in some cases the β-actin immunoblots were erroneously described in the figure legends as loading controls, rather than as sample processing controls that were run on separate gels”
    Simply precious. Might as well have just used the blots on the manufacturer’s websites.
    Just once I would like to see a journal say this paper was retracted because the authors ignored our instructions for data presentation and faked most of the results. And for heaven’s sake, don’t let them get away with “we, the authors, believe that the key findings of the paper are still valid” when the whole thing is a sham.


  33. PubPeer readers are pointing out that Daley’s observation of telomere elongation in iPS cells may be due to artifact from vector system they chose. The other team Artandi at Stanford used the correct vectors and reported opposing results to Daley.

    Telomere elongation in induced pluripotent stem cells from dyskeratosis congenita patients
    Nature (2010) – 4 Comments
    pubmed: 20164838 doi: 10.1038/nature08792 issn: 1476-4687 issn: 0028-0836

    Suneet Agarwal , Yuin-Han Loh , Erin M. McLoughlin , Junjiu Huang , In-Hyun Park , Justine D. Miller , Hongguang Huo , Maja Okuka , Rosana Maria Dos Reis , Sabine Loewer , Huck-Hui Ng , David L. Keefe , Frederick D. Goldman , Aloysius J. Klingelhutz , Lin Liu , George Q. Daley

    “The contradiction may come from vector method each paper used. Daley team used pMIG retroviral vectors which are tough to be silenced, and prevent complete reprogramming. And causing more artificial results from remaining transgenes. The issues of artificial observation using pMIG vector system are discussed here
    Artandi team used pMX retroviral vectors which can be silenced, leading to complete reprogramming. This vector system was also used by Yamanaka team (Takahashi, Cell, 2007). Artandi’s obsservation of telomere shortening in dyskeratosis iPS cells is plausible.”


  34. Park (Nature 2008) Daley’s first claim of human reprogramming study, is argued intensely on PubPeer.
    The paper did not report crucial data that they should have, and probably negative. The validity of their claim is vague now.

    Reprogramming of human somatic cells to pluripotency with defined factors
    Nature (2008) – 15 Comments
    pubmed: 18157115 doi: 10.1038/nature06534 issn: 1476-4687 issn: 0028-0836

    In-Hyun Park , Rui Zhao , Jason A. West , Akiko Yabuuchi , Hongguang Huo , Tan A. Ince , Paul H. Lerou , M. William Lensch , George Q. Daley

    “In addition, OCT4-neo (geneticin/G418 resistance) was practiced by Thomson to prove acquisition of pluripotency, while not by Daley. Both teams used the same cell line.
    Yu et al. (Thomson) “In this cell line, the expression of neomycin phosphotransferase, which makes cells resistant to geneticin, is driven by an endogenous OCT4 promoter, a gene that is highly expressed in pluripotent cells but not in differentiated cells. Thus, reprogramming events reactivating the OCT4 promoter can be recovered by geneticin selection….. These geneticin-resistant colonies expressed typical human ES cell–specific cell surface markers (fig. S2B) and formed teratomas when injected into immunocompromised severe combined immunodeficient–beige mice ”
    Park et al. (Daley) “Selection with G418 was not required to identify cells with ES-cell-like colony morphology””

    “Actually large T tends to be integrated in DNA during reprogramming. Johns Hopkins group reported that all five clones contained large T DNA in the genomic DNA.
    It is difficult to assume that large T transgene was absent in all the Daley lines. “When we analyzed the presence of the T transgene, we found that all five expanded clones contained the T DNA in the genomic DNA, as in the IL group with the same T vector. Similarly, all seven clones obtained by the NIL OSTM transduction (described above) also contained the T DNA. Considering that the integration rate of NIL vectors is supposed to be 104‐fold lower, these data strongly suggested that sustained presence of T is likely critical to the enhanced reprogramming of human fibroblasts under the conditions we used. ”
    According to Park et al., “the human ES-cell-like colonies that we ultimately isolated failed to show integration or expression of hTERT and SV40 large T (data not shown).””

    “Rudolf Jaenisch said that partially reprogrammed cells have retrovirus transgene on, lack of Oct4 reporter (Daley iPS cells). Fully reprogrammed cells have retrovirus silenced and Oct4 reporter (Yamanaka iPS cells, Thomson iPS cells). Therefore, Park et al. did not fully reprogrammed human cells. ”


  35. PubPeer comments on Soria-Valles’ Oncogene article. The link to their microarray data set is dead, or the authors did not upload the data set.

    The anti-metastatic activity of collagenase-2 in breast cancer cells is mediated by a signaling pathway involving decorin and miR-21
    Oncogene (2014) – 3 Comments
    pubmed: 23851508 doi: 10.1038/onc.2013.267 issn: 1476-5594 issn: 0950-9232

    C Soria-Valles , A Gutiérrez-Fernández , M Guiu , B Mari , A Fueyo , R R Gomis , C López-Otín

    “Here is the link to accession number put on the paper. Actually, this is 2007 data of Kevin Lebrigand lab in France, the samples were of human lung cancer. Does not match with breast cancer cell line microarray conducted for this paper at 2014.

    “Reading the text more carefully one finds that the microarray data “…are available on (follow the link to ‘microRNA’…”.
    This link seems to be dead (the same link is listed in GEO with GPL4718) – you should ask the authors to provide raw data or a working link.
    The link you report refers to the “…platform referenced in GEO accession numbers GPL4718…”.
    It is therefore a GEO platform ID and not a GEO data set ID and describes the type of microarray used. There are two data series in GEO using this platform, neither of which is associated with this publication.
    So: dead link to data set – ask authors. Nothing else to complain about here, apart maybe from the fact that authors did not upload the raw data to GEO, too – the journal should have insisted in case that it is required by data availability policy.”


    • Ana Pedro

      A message for the new year: Any researcher should be allowed to publish a paper without presenting the original data including clinical trial and animal trials protocols and the use of photoshop should be forbidden, WBs should be automated


  36. Let’s not raise the technical bar so high that the cheating megalabs get a further advantage. It is also important to distinguish legitimate scientific discussion of work such as other Daley lab outputs from detection of sloppiness and fraud as occurred in this paper. Not knowing something at the time that has come out later is not a retractable offense. Also worth noting is how prominent authors and major institutions like Harvard can assert their “five hundred pound gorilla” status. This turkey was in the literature for over 3 and a half years. It lumbered along with a mass of PubPeer baggage for over a year and dragged along an official cloud of suspicion from Nature for several months. That inertia indicates powerful backing, as does the mealy-mouthed retraction notice. Last but not least, we should consider the inconsistencies in how institutions and granting agencies deal with such matters. Anversa was canned and his papers were marked for bulk retraction because his institution eventually came to the conclusion that he had fabricated an entire field of research. There is no sign of similar investigations of the major players in this paper, who appear to have been up to similar shenanigans.


  37. Ana Pedro

    The point is these problems are global problems. What measures can the scientific community take to:

    The establishment of cheating megalabs or even cheating worldwide nets of labs?
    Inconsistencies how institutions, journals and granting agencies deal with these problems?


  38. Part of the solution is due diligence. If a funding agency finds out that a research group fraudulently obtained and/or used grant funding, they should cut off the offending researchers and host institutions while pursuing legal means to recover the money and punish those responsible. If research is funded by others, then research fraud is an intentional tort, and a misdemeanor or felony depending on the amounts involved. Yet in most tales of fraudulent research we find the punishments are so mild, avoidable and delayed that they offer no real deterrent, especially for those who gain the most from cheating. The top dogs get wrist slaps in the form of a temporary bans or supervision, and the worst culprits shuffle off to another plum post with minor inconvenience leaving a trail of wrecked lives behind. How else can we expect high-stakes gamblers to behave if we let them play for free?


    • Ana Pedro

      The main problem is that the so called top-dogs are intimately connected with/ get protected by governments and politicians worldwide…so to solve these problems we would need to start by changing science funding and publication policies worldwide

      With this goal a science petition should be organised worldwide and signatures from scientists worldwide should be obtained and this petition should be handed in at United Nations


  39. PubPeer comment on Soria-Valles’ Protocol Exchange. The validity of the protocol is being argued.

    Somatic cell reprogramming using NF-κB inhibitory strategies
    Protocol Exchange (2015) – 7 Comments
    doi: 10.1038/protex.2015.057 issn: 2043-0116

    Clara Soria-Valles , Fernando Osorio , José Freije , Carlos López-Otín

    “The most crucial technical advance in this protocol is that one can achieve visible TRA1-60+ iPSC colonies in 1 weeks of induction, which is still elusive to others in the field. Please refer figure 3e from the original article for this protocol.”


  40. Soria-Valles has been selected for Juan de la Cierva-incorporación to bring her money to uniovi. 35,000 euro for 2019, and 29,000 euro for 2020. Information is as of nomination date at Sept. 28, 2018. Application number, IJCI-2017-31455, UNIVERSIDAD DE OVIED.


  41. For the nomination of 2017 Juan de la Cierva-incorporación organized by Spanish ministry, Soria-Valles has been selected to be top ranked among 63 of Biomedicina candidates. 27 candidates were selected, and rest of 36 failed. Total 64,000 euros will be spent on Soria-Valles’ research back in uniovi from 2019.


  42. PubPeer arguments over Daley’s 2008 Nature paper still continue.

    Reprogramming of human somatic cells to pluripotency with defined factors
    Nature (2008) – 17 Comments
    pubmed: 18157115 doi: 10.1038/nature06534 issn: 1476-4687 issn: 0028-0836

    In-Hyun Park author has email , Rui Zhao , Jason A. West , Akiko Yabuuchi , Hongguang Huo , Tan A. Ince , Paul H. Lerou author has email , M. William Lensch author has email , George Q. Daley

    “The reprogramming knowledge and technology in 2008 was not as advanced as it is now. This paper is what it is for that time.

    However, what you need to know dear reader, is that almost the entire discussion above is from one single troll, recently also using cross-site posting tactics. I’ve been waiting to see if anyone would notice. And now they have! But, as has happened before, the wrong person has very regrettably been identified on teh intarwebs.

    Well done, very clever!

    And who fed this gullible tweeter with false information? Let’s just say that the correct troll is the one trying to defend bogus Mbd3-/- reprogramming. Perhaps Professor Daley is being trolled because he knows too much?”

    “Actually, the Jaenisch paper was published in 2008. Therefore, even by 2008 standards, the Park iPS cells are partially reprogrammed.”


  43. PubPeer reader found image duplication in Deepak Jha’s publication.
    Pictures were copied and pasted over Figures 1 and 2. They were supposed to be differentially treated samples.

    An RNA polymerase II-coupled function for histone H3K36 methylation in checkpoint activation and DSB repair
    Nature Communications (2014) – 2 Comments
    pubmed: 24910128 doi: 10.1038/ncomms4965 issn: 2041-1723

    Deepak Kumar Jha , Brian D. Strahl

    Figure 1

    Figure 2


  44. Gel splicing in Daley and Baltimore’s old article. PubPeer readers are arguing that it was acceptable practice 30 years ago.

    Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein
    Proceedings of the National Academy of Sciences (1988) – 6 Comments
    pubmed: 3143116 issn: 0027-8424

    G Q Daley , D Baltimore


  45. University of Oviedo had awarded Soria-Valles “Premios Extraordinarios de Doctorado” for her outstanding Thesis study at Lopez-Otin lab based on her now retracted Nature Cell Biology.

    Premios Extraordinarios de Doctorado

    Por otra parte, el Consejo de Gobierno ha aprobado la propuesta de Premios Extraordinarios de Doctorado para las tesis leídas en esta Universidad en el curso académico 2014-2015, abarcando dicho curso el periodo comprendido entre el 1 de septiembre de 2014 y el 31 de agosto del 2015. Estos premios se entregarán de forma solemne el próximo día 27 de enero en el acto conmemorativo de la festividad de Santo Tomás de Aquino. La relación de las candidaturas galardonadas es la siguiente:


    Burón Fernández, Patricia
    García Inclán, María Cristina
    Méndez López, Marta
    Rodrígue Carrio, Javier
    Rodríguez García, Aida
    Sampedro Piquero, Patricia
    Soria Valles, Clara
    Weidberg López, Sara Eva


  46. Daley’s alumnus Kitai Kim published a mega-correction at Nature Cell Biology.
    They had reused bars and figure panels.
    Reminds now-retracted Soria-Valles’ case in the same journal. The only difference is that they own up before PubPeer detection.

    Author Correction: ZSCAN10 expression corrects the genomic instability of iPSCs from aged donors

    Maria Skamagki, Cristina Correia, Percy Yeung, Timour Baslan, Samuel Beck, Cheng Zhang, Christian A. Ross, Lam Dang, Zhong Liu, Simona Giunta, Tzu-Pei Chang, Joye Wang, Aparna Ananthanarayanan, Martina Bohndorf, Benedikt Bosbach, James Adjaye, Hironori Funabiki, Jonghwan Kim, Scott Lowe, James J. Collins, Chi-Wei Lu, Hu Li, Rui Zhao & Kitai Kim 

    Nature Cell Biology (2019) |

    Correction to: Nature Cell Biology, published online 28 August 2017.

    In the version of this Article originally published, Supplementary Fig. 6j showed incorrect values for the LS and AG4 glutathione samples, and Fig. 5c and Supplementary Fig. 6j did not include all n = 6 samples for the hESC, Y-hiPSC and AG4-ZSCAN10 groups as was stated in the legend. In addition, the bars for hESC, Y-hiPSC, AG4-ZCNAN10, AG4 and LS in Supplementary Fig. 6i and j have been reproduced from Fig. 5b and c, respectively. Figure 6e was also reproduced in the lower panel of Supplementary Fig. 6h, to enable direct comparison of the data, however this was not explained in the original figure legends. The correct versions of these figures and their legends are shown below, and Supplementary Table 5 has been updated with the source data for all numerical data in the manuscript.
    Corrected Fig . 6 legend:

    Impaired DNA damage response in human A-hiPSCs caused by deregulation of ZSCAN10 and GSS and recovered by ZSCAN10 expression. a, Excessive oxidation capacity with elevated glutathione in A-hiPSCs, and recovery by ZSCAN10 expression. The total glutathione level was measured to determine the maximum oxidation capacity. Excessive oxidation capacity of glutathione in A-hiPSCs is normalized to the level of hESCs and Y- hiPSCs by transient expression of ZSCAN10. Glutathione analysis was conducted with the glutathione fluorometric assay. Mean ± s.d. is plotted for three biological replicates with two independent clones (n = 6) in each sample group from each condition. Statistical significance was determined by two-sided t-test. b, ROS scavenging activity of hESCs, Y-hiPSCs, A-hiPSCs and A-hiPSCs–ZSCAN10. A cellular ROS assay kit (DCFDA assay) was used to measure H2O2 scavenging activity. A-hiPSCs show strong H2O2 scavenging activity, with a reduced response against treatment with TBHP (tert-butyl hydrogen peroxide; stable chemical form of H2O2, 3 h); the response is recovered by ZSCAN10 expression. Mean ± s.d. is plotted for four biological replicates in each sample group from each condition (n = 4). Statistical significance was determined by two-sided t-test. c, Immunoblot of pATM showing recovery of the DNA damage response after phleomycin treatment in three independent clones of A-hiPSCs with shRNA-mediated knockdown of GSS. d, Immunoblot of pATM showing that lentiviral expression of GSS cDNA impairs the DNA damage response in three independent clones of Y-hiPSCs after phleomycin treatment. e–g, Copy-number profiling analysis of human iPSCs43. Schematic diagrams represent seven rearranged A-hiPSCs, four non-rearranged A-hiPSCs and five non-rearranged A-hiPSCs– ZSCAN10 in the genetically controlled setting of A-hiPSCs. Ten non-rearranged Y-hiPSCs, which were generated from a different tissue donor, were also included. A-hiPSCs (n = 11 (7/11), P = 0.64), (These data are also presented in Supplementary Fig. 6h), A-hiPSCs–ZSCAN10 (n = 5 (0/5), P* = 6.3 × 10−3) and Y-hiPSCs (n = 10 (0/10), P* < 4 × 10−5). The number in parentheses represents detected rearrangements and P and P* are the observed and estimated likelihoods of detecting no rearrangements in the absence of lineage effects using a binomial distribution, respectively50. Unprocessed original scans of blots are shown in Supplementary Fig. 7.


  47. The latest Nature Communication paper from Daley group has been argued over image duplication and weird uniformity in data points.
    The first author Yermalovich received F99/K00 NIH’s career transition award for this project. Funded
    33,026 USD as of 2016. The support continues for 6 years.

    Lin28 and let-7 regulate the timing of cessation of murine nephrogenesis
    Nature Communications (2019) – 2 Comments
    pubmed: 30635573 doi: 10.1038/s41467-018-08127-4 issn: 2041-1723

    Alena V. Yermalovich , Jihan K. Osborne , Patricia Sousa , Areum Han , Melissa A. Kinney , Michael J. Chen , Daisy A. Robinton , Helen Montie , Dan S. Pearson , Sean B. Wilson , Alexander N. Combes author has email , Melissa H. Little author has email , George Q. Daley

    Image duplication.

    “Unexpected uniformity in Serum creatinine level in fig. 3g. The data points are shown as in lattice points. The data points came from 14 independent animals, not mere technical replicates. I initially thought it would represent the feature of this assay. But the other data points of serum creatinine level at fig. 5k did not follow the the same rule… ”


  48. It is interesting to see Lopez-Otin had actually associated his News&Views with this mega-corrected Kitai Kim’s article. Marveling lineage of Soria-Valles’ now-retracted paper.


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