Research integrity Research Reproducibility

Pontus Boström: cheater carousel in Sweden

Sweden is a tolerant country, which is a very good thing. Unfortunately, sometimes this Swedish tolerance seems ill-advised. Dishonest scientists caught faking data are happily given another chance and fat funding, like the case of the diabetes researcher Pontus Boström shows.

This scientist was found to have fabricated data during his PhD studies with late Sven‐Olof Olofsson at the University of Gothenburg, and went afterwards to publish a seminal paper in Nature with the biggest godfather of the diabetes research field, Bruce Spiegelman. Also this high-impact study turned out to be irreproducible by other researchers and a likely artefact of erroneous antibody use. Yet due to his impressive publishing record and unwavering support of the mighty Spiegelman, Boström was invited to head a group leader position at several Swedish universities, while he settled on the best offer by the Department of Cell and Molecular Biology at the prestigious Karolinska Institutet (KI) in Stockholm, supported by the elite EU funder ERC.  All despite his previous convictions of research misconduct in Gothenburg and ensuing retractions of two meeting abstracts, which were at all times perfectly known to all parties involved.

UPDATE 7.07.2016: just as my article went online, KI chose to finally reply to my email. Tomas Ahlbeck, KI Press secretary declared:

“About Pontus Boström:

The research group was discontinued during the autumn 2015. Mr Boström is since 31 Dec 2015 not an employee at KI. His postdocs are not at KI anymore, they continue their work at other Universities abroad”.

The ERC press team informs me that Boström’s grant funding was stopped:

“Dr Pontus Boström’s grant agreement (Novel_myokine) was terminated on 31 December 2015”.

Boström was obviously sacked by KI and lost his ERC funding, please take it into account while reading this article.

The 2012 Gothenburg investigation found that Boström manipulated excel sheets for a manuscript, which publication was subsequently prevented. Now, new evidence on PubPeer suggests serious image integrity problems in his publications, including his and Spiegelman’s papers in Nature and Cell. Here are two examples of apparently duplicated western blot bands and image re-use in papers from Olafsson’s Gothenburg lab, which Boström signed as first author in Diabetes, 2010 and Nature Cell Biology 2007, respectively.

Boström’s case has its entertainment value, because it is similar to that of Suchitra Sumitran-Holgersson, but in reverse. Basically, KI and University of Gothenburg traded cheaters. Sumitran-Holgersson was found guilty of deliberate data manipulation while working at the KI and had to retract a paper, yet she was soon acquitted under most bizarre circumstances (see my detailed report here).  As result, she was allowed to retain all her funding and her professorship at the Sahlgrenska University Hospital of the University of Gothenburg. Meanwhile, Sumitran-Holgersson and her colleagues are being investigated for faking ethics approvals in order to perform questionable experiments in regenerative medicine on human patients, at least one of whom has died (details in my follow-up report here).

I obtained key original documents of the Gothenburg investigation. First, I present a note submitted by Boström’s former Gothenburg colleague Jan Borén, chair of the Department of Molecular and Clinical Medicine at the Sahlgrenska University Hospital, to their Vice-Chancellor (original here):

“Professor Sven‐Olof Olofsson, from the Institute of Medicine, died unexpectedly on December 28, 2011, leaving his research group without a principal investigator. To support the research group, the undersigned participated in their group meetings and project meetings. This was an obvious course of action because Sven‐Olof and the undersigned had discussed the projects on a frequent basis.

The research group decided to complete a project that focuses on syntaxin‐5 and its role in fatty acid‐induced insulin resistance, a project that they had worked on for several years. The project had been inactive for about 6 months but there was a manuscript, Decreased syntaxin‐5 in skeletal muscle in type 2 diabetes impairs insulin action on AKT by inhibiting its sorting to the plasma membrane, which had been submitted to the journal Diabetes, and then rejected on 19 July, 2011 (Appendix 1). The research group, together with their collaborator Kurt Højlund at Aarhus University, Denmark, decided to revise the work and submit it to another journal (Appendix 1). We therefore designed different control experiments, but these did not give the expected results. When this situation occurs, there are in principle three different explanations:

− The control experiments are incorrectly designed or executed

− The interpretation of the original data is incorrect

− The original data are incorrect

We went through these possibilities and excluded the first two. The undersigned therefore asked Linda Andersson [who took the lead of the lab after Olofsson’s death, -LS] in the research group to carefully review the original data. Linda checked the original data and reported to the undersigned on April 24 that the values she found were not consistent with those found in the manuscript (Appendix 2). She then checked additional files and found the same phenomenon, which she reported on April 26 (Appendix 3). The original data were calculated by Pontus Boström who was a PhD student in the research group and defended his thesis on 21 December, 2007. He then continued to work in the research group in parallel with his medical training, until he moved to the US in 2009 to undertake postdoctoral training at the Dana‐Farber Cancer Institute, Harvard Medical School [with Bruce Spiegelman, funded for 2 years by the Swedish Heart-Lung Foundation -LS]. Pontus Boström has been working at the Karolinska Institute in Stockholm since spring 2012.

The undersigned therefore contacted Pontus Boström (Appendices 4‐8) and asked him to explain why:

  1. The raw data have been altered without an explanation of why this has happened.

This is notable since the altered values give significant differences between the groups which were not different in the first analysis

  1. Western gels or qPCR files for the new data are missing
  2. In the altered values, only the digits with the highest value differ (illustrated in the table below). […]

When the undersigned failed to clarify these ambiguities, the Vice‐chancellor of Gothenburg University, Pam Fredman, and the Head of the Institute of Medicine, Hans Carlsten, were informed on August 16, in accordance with the Handling procedure at Gothenburg University for cases of suspected research misconduct. The Vice‐Chancellor, Pam Fredman, then contacted the university lawyer Kristina Ullgren, who on August 30 asked the undersigned to submit this summary.

The undersigned has also informed Sven‐Olof Olofsson’s collaborators and research leaders at other universities. The research group has also checked the raw data for published work, but has not found similar ambiguities”.

I contacted Borén about the background of the Boström misconduct investigation and received this comment:

These issues are difficult but I think it’s critical that we handle them transparent and don’t try to hide scientific misconduct. We must learn from mistakes. I learned this from my former PhD supervisor, late Professor Sven-Olof Olofsson. Science integrity and honesty was critical for him, and I’m glad that the investigation fully cleared him from any suspicions of scientific misconduct.”

In early 2014, Boström was investigated and found guilty of “conscious preparation and presentation of falsified results”, as evidenced by the full report of the investigative  committee and the Vice-Chancellor’s decision which I make available exclusively (both in Swedish). There is also an English-language report of the external investigator Ugo Moens, professor for medical biology at the University of Tromsø in Norway. Moens analysed Boström’s excel files and found out that “it is beyond doubt that primary data have been changed when composing the xls.files”. He also determined that Boström manipulated data to create a significant difference (100% vs 74,5%) between two experimental groups which were actually same (100% vs 98,3%).  The rigged data was then used by Boström to present a phony result in a manuscript subsequently submitted to two journals, as mentioned by Borén above.


These were the translated “Conclusions from the Committee on Academic Misconduct” of the 1.5 year long Boström investigation, official number Dnr D 2012/26 (highlights mine):

“The Committee on Academic Misconduct has taken into account that several people were involved in the research project in question during the time period that the inquiry relates to. The investigation has received answers to questions regarding the extent to which there are modifications to the raw data and to what extent these modified data formed the basis of scientific manuscripts. Against this background, the Committee on Academic Misconduct then assessed to what extent there had been a deliberate alteration of data with the aim of obtaining a favorable outcome to the research project.

The Committee on Academic Misconduct could not come to any conclusion other than that alteration of data has occurred in this case. There is nothing to suggest anything other than that the modified data, through having been changed in a certain way, shows a finding that makes the modified data more scientifically interesting. This finding would not have been shown if the data had not been modified in the way that happened.

The modified data can be traced to Pontus Almer Boström, because they were first found in Pontus Almer Boström’s folder on the Wallenberg Laboratory’s file server and in the form of the diagrams attached to two emails that he sent to Sven-Olof Olofsson.

The claim that the modified data originates from any other person has not been shown to be credible.

The Committee on Academic Misconduct finds that the data have been modified in a systematic manner, which contradicts Pontus Almer Boström’s statement that he did not knowingly corrupt or modify any data.

The Committee on Academic Misconduct finds that Pontus Almer Boström is guilty of misdemeanor with reference to point 7a) “conscious fabrication, corruption or suppression of basic material” and point 7b) “conscious preparation and presentation of falsified results” and therefore finds reason to believe that scientific misconduct has occurred.

The Committee on Academic Misconduct’s opinion is unanimous”.

Boström had to retract two conference abstracts: Andersson et al, Atherosclerosis 2011 and Højlund et al, Diabetologia 2011. He had to fully admit having faked his data, yet towards RetractionWatch, Bostöm attacked his critics by speaking of “an old conflict”, “a very biased investigation” and “science politics”. He was then supported by his former mentor Spiegelman, who declared to be “confident” in Boström’s work in his lab. But who else is confident in that 2012 Nature paper?

Together with Boström, Spiegelman has discovered a miracle cure for obesity: the elusive hormone Irisin, a soluble version of a cell membrane-bound receptor FNDC5. Irisin is allegedly a produced by exercising muscle and turns white adipose tissue into brown one, which then literally burns energy. Basically, a fantasy come true for the pharma industry: pop an irisin pill and you lose weight and straighten your muscles while watching TV, and  you heat your room on top. Everything was set to tap the huge and bloated obesity market in US:  irisin was patented by Boström and Spiegelman, then licenced to a pharma company and scheduled to go from 2014 on for clinical treatment of obesity and type 2 diabetes. If you have not heard of this miracle cure yet, it is because very soon doubts arose about what these two scientists claimed to have discovered.

The scientific reliability of their Nature paper was soon vigorously debated on PubPeer, but also in research literature. Some immediately questioned the role of FNDC5 in muscle function and exercise (Timmons et al, 2012). Harold Erickson, cell biology professor at Duke University, published in 2013 his detailed criticisms, among which was the lack of validation for the novel irisin antibody which Spiegelman and Boström based their discovery on.  Later on, Erickson teamed up with Steffen Maak, professor at Leibniz Institute for Farm Animal Biology, to show by the simple means of molecular weight analysis by western blot that the irisin antibody was unspecific and the ground-breaking Nature-result most likely an artefact (Albrecht et al 2015). Boström and Spiegelman apparently never bothered about proper antibody specificity controls: their experiments delivered exciting results, and no one questioned what exactly they were detecting.

Despite all counter-evidence against his high-impact discoveries, Spiegelman’s enormous (and as I was told, rather intimidating and oppressive) influence in the diabetes field hardly took a dent. Soon science journalists proclaimed “Irisin Redeemed”, all because the irisin discovery was reproduced, by antibody-independent method of mass spectrometry [update: as Maak comments below, also this paper relied on the faulty antibody]. The unbiased reproducer was actually Spiegelman himself (together with his original irisin-co-discoverer and Harvard department colleague Steven Gygi), but this hardly makes any difference to some scientists, as I learn again and again. The fact that no obesity or diabetes cures (or for that matter, no sufficiently trustworthy follow-up research) came out of irisin, seems hardly relevant. Certainly one can ignore an occasional blot duplication, which a PubPeer user reported for the Boström et al Nature paper now:


Science moves one irreproducible break-through discovery at a time. Prior to their irisin scoop, Boström and Spiegelman found a way to easily train an athlete’s heart by suppressing the function of the protein C/EBPβ. This was published also not somewhere, but in Cell (Boström et al 2010). There were some strange band duplications as well, apparently some of Boström’s western blots from his Diabetes paper with Olafsson found their way in his Cell paper with Spiegelman:


It seems, as long as patients don’t start dying, scientific misconduct is not only tolerated by academic institutions in Sweden (and elsewhere), but actively covered-up, while whistle-blowers are being threatened. It is all for a good cause after all: securing public research funding.

KI has a fine history of such behaviour, the Paolo Macchiarini scandal had all: dead and abused patients, fake medical records, harassed whistle-blowers, misconduct investigation disregarded and even trashed patient samples (for more, read my original report and this letter by a disappointed investigator Bengt Gerdin to the KI ex-rector Anders Hamsten). All because Swedish government was throwing big money for stem cell research around, and Macchiarini was a genius at catching it.

In Bostöm’s case, nobody died, thus he retains his position at KI. Apparently, KI hopes to cash in on his irisin patents with Spiegelman. Despite (or most likely, because of) his certified data fakery, Boström is also a fine money magnet: he received in an ERC starting grant of €2 Million, valid till end of 2017, to study (despite misconduct and irreproducibility) yes, what else: irisin. Though that probably non-existing hormone does not help at all against obesity or diabetes, it creates lots of cash out of thin air: Boström also pulled a “Collaborative Project Award” with the Mayo Clinic in US.

Then there was an up to SEK 4 Million Ingvar Carlsson Award from the Swedish Foundation for Strategic Research. Only last month, Boström was given another SEK 4 Million (~€420,000) from the Hållsten Research Foundation (where he is a fellow since 2014) to employ some research assistants. One wonders what exactly KI expects these junior scientists to learn under Boström’s tutelage.

Update 9.07.2016. A first hand source (identity known  to me) gave me these details:

“Since the misconduct was only proven for a manuscript that hadn’t been published, Pontus kept his PhD title and his position at KI (under some conditions). During 2015 [his lab members, -LS] were told that Pontus decided to end the group and would leave KI by the end of the year. Not sure if this indeed was his own decision or whether KI wanted to have him go [Boström’s ERC funding was terminated on 31.12.2015, -LS]. Pontus still has an affiliation with KI for 2016 for economical and administrative matters.
Pontus left Academia. He’s an MD, has been working one day a week at a GP practice during his time at KI ( and I assume that he now works there full-time”.

Update 19.07.2016 Boström was funded by ERC for almost 2 years, between the misconduct verdict by University of Gothenburg in early 2014 and its termination in December 2015. ERC has now answered my inquiry about how much he and KI received:

the total ERC Starting Grant funding initially planned for the project ‘Irisin – a novel myokine protective against metabolic disease’ was €1,999,433.00 of which Dr Boström has received € 666,858.46″.

31 comments on “Pontus Boström: cheater carousel in Sweden

  1. Pretty regrettable what happens in Sweden… I am sorry but since some time ago, any time I see a paper from KI or from Sweden in general, I doubt of the information presented there… I could just be data fabrication.

    Also, they have gone to limits nobody else went before, like the Macchiarini case and now that lady that is being: “investigated for faking ethics approvals”… those are not only examples of scientific misbehaviour, they rather look like actions from super agents of criminal international organizations…

    Congratulations Sweden, bit-by-bit you are gaining a reputation of a corrupt nation.

    It is now responsibility of the Swedish government and competent institutions and of the fraction of the scientific community that is NOT corrupt to clean up all the mess and mud that the above-referred “researchers” have caused; they have trashed not only the dignity and reputation of Sweden, but those of the nordic countries historically admired by me and many others for their justice and, ironically, dignity…


  2. Sweden is country where fraud is exposed at least sometimes. That is why you, jjovel, get impression that things are worse in that country. It is actually other way around. Why countries like Italy and Spain never expose fraud in science, do you think because they are clean ? No, just because whistleblowers have zero chance to succeed there so they don’t even try. Not to mention countries like China or Korea. Sweden at least has some official (often declarative) system which might lead to exposure and investigation. Not very good investigation, not always fair or even functioning. But still there is some chance in some places. Research system is ill in general. Thanks to Macchiarini case we know how ill on example of one institution. Thanks to open Swedish system which gives free access to any documents and thanks to some honest journalists. Germany actually also had good chance to expose Macchiarini but did not do it. Julia Tuulik wrote letters to ARTE producers of “Supercell” documentary describing her terrible condition after 30 operations followed transplantation. Producers approved documentary claiming super success and simply disregarded her letters and all strange facts filmed by their own operators. Italy had all possible reasons to expose Macchiarini but failed to make public his CV fraud. Nobody is punished for exagerrations of success, for wild fantasies in press releases and promises of new wonderful “applications” in grant proposals. It is so common now that not even considered as lies. But these are lies and only the top of iceberg of lies which undermine public trust to Science and scientists.

    Liked by 1 person

    • Angry, I have never said that Sweden is worse than other countries Sir…but if you compare yourself with the worse, then there is not much hope. I am very aware of Chinese scientific misbehaviour, for instance, and Indian’s too… They are even famous for not releasing the data after publishing, which is mandatory in my area of ‘omics… I consider that also a form of misconduct…

      I also agree that scientific misconduct happens everywhere… but this post is about scientific corruption in Sweden and therefore my comment is pertinent… The fact that happens everywhere does not justify it in any country…

      On the other hand, there are cases of misconduct scandals in Spain that have been exposed in these pages (remember Susana Gonzales), and in Germany too (remember the ophthalmologist)… Also Macchiriani’s barbarities took place when he was an employee of KI therefore it is their main responsibility… (btw, they acted responsibly at the end, in my opinion)… Yes the Italian and German could have acted more belligerently than they did, but apparently everybody is scared of scandals, not realizing that at the end, scandals are only worse for those that do not act…


  3. Kfir Lapid

    As bad as scientific misconduct is, politics in science is even worse. You mentioned Bruce Spiegelmann as an example for an intimidating scientist. Funding is granted to those who have power and good connections. If they perform bad science, nobody will say a word. On the other hand, good scientists that have promising results, but no elbows, will be left behind. Even mocked, if they don’t follow the so called field leaders.

    Liked by 2 people

  4. Ana Pedro

    Pontus Bostrom makes me remember very much Hector Peinado’s case which I commented one or two before. Several papers with Hector Peinado as first author or co-author are all being investigated in PubPeer:

    in all of the papers where he appears as first author, all of them have problems with the WB manipulation among other issues as you can see by accessing PubPeer comments (link above).

    Moreover, at least Costa-Silva et al., 2015 has IF images issues, Costa-Silva et al, 2015 and Hoshino et al, 2015 have also problems with lack of control experiments, data reproducibility (n) and experimentation design and interpretation.

    Given this I also would ask for the raw data files in special those related to proteomics data of Hector Peinado’s manuscripts commented on PubPeer (please, see link above)


    • Ana Pedro

      I submitted the comment above to the NPG editor F. Cesari.


    • Moreover, the conclusions of my brief analysis of my raw mass spectrometry data comparing with the following manuscripts:
      1. Costa-Silva et al. 2015. Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver. Nat Cell Biol. 2015 Jun;17(6):816-26
      2. Hoshino et al., 2015. Tumour exosome integrins determine organotropic metastasis. Nature. 2015 Nov 19;527(7578):329-35.
      3. Peinado et al., 2015. Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET. Nat Med. 2012 Jun;18(6):883-91
      – Indeed, MIF is present in the exosomes of several human pancreatic cancer cell lines but not in the exosomes derived from PANC1 cells. MIF is also present in the exosomes derived from normal mouse pancreas exosomes and also I cannot found MIF in plasma derived from pancreatic tumor-bearing mouse or control mouse. Finally, MIF is not highly expressed in PDAC exosomes (MIF has a similar expression in normal mouse pancreas exosomes)
      – I didn’t find any integrins in exosomes derived from plasma samples of mammary tumour-bearing MMTV-PyMT at the PMN and MN levels. Also, neither I didn’t find any integrins or the pattern of integrins I found is not consistent with Hoshino et al., 2015 in the exosomes derived from the plasma samples of breast cancer patients with liver and/or bone and/or skin and/or lung and/or brain metastases
      – By analyzing hepatocyte growth factor receptor (met) in exosomes derived from melanoma F1 (parental, poorly metastatic), F0 (poorly metastatic variant) and F10 (highly aggressive variant) cell lines by quantitative mass spectrometry: F0 exosomes have more or equal amounts of met when compared with F10 exosomes, although F1 exosomes indeed have no met or have vestigial met. Moreover, 5B2 brain tropic melanoma exosomes have no met and exosomes derived both from control and metastatic patient melanoma patients LF show no met.


      • In relation to my complaint to NPG about the 3 papers mentioned above, Dr. Barbara Marte (Nature Senior Editor) commented me that I would need to present independent data showing that you cannot reproduce core parts of the Hoshino et al. 2015 paper. Indeed, my raw proteomics data shows that neither the data from the 3 papers mentioned above neither the data from Melo et al. 2015. Glypican-1 identifies cancer exosomes and detects early pancreatic cancer. Nature. 2015 Jul 9;523(7559):177-82 is reproducible. Concerning the Melo case, please see my comments in:
        The paper Peinado et al, 2012 was selected for the reproducibility project and I am excited to know the results of this study.
        These facts are very worrying as the majority of the publications are not reproducible. Besides the reproducibility project how can we find a solution to this problem?


      • Additional PPPR for:

        Peinado et al., 2012. Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET. Nat Med. 2012 Jun;18(6):883-91
        Mass spec data incongruence:
        LF exosomes from melanoma patients with liver and brain metastases show no VLA-4 (α4β1 integrin).
        IF images/other:
        Figure 2b: The left panels don’t have DAPI. In the 3 images, we cannot see well cell morphology (black and white DAPI images would be nice). No control images.
        Figure 3c: No DAPI, cannot see cell morphology. Are BM-control and BM-educated different? Or it is just a question of bright, contrast, levels, etc. adjustments? May would be worth if authors could provide original images.
        Figure 3d: No DAPI. The image on the right seems to have a bigger magnification. Originals?
        Figure 5g: No DAPI in all. Primary tumor ShScramble may be equal to primary tumor ShRab27a. It is just a question of bright, contrast, levels, etc. adjustments? Originals?
        Figure 5e: it might be manipulated. Originals?
        Costa-Silva et al. 2015. Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver. Nat Cell Biol. 2015 Jun;17(6):816-26
        IF images:
        See also comments in PubPeer about IF images. In general, the quality of the images is poor, cell morphology is not really evident. Therefore, the images shown are not convincing.
        3a. The images don’t match the graphs
        3b. We cannot see real differences in GFP-labeled cells in CTL or exo. This might be more a question of the pictures selected and of playing with bright, contrast, levels, etc. It would be worth to see the originals.
        α-SMA may not be different between Exo and in exo+A83-01.
        5a. There is something strange with the last 2 figures in the bottom right.
        5d. the middle figure in the first row seems to be an artifact; the 2 figures on the right in the middle row might not correspond; in term of F4/80 cells the differences don’t seem so evident between CTL, DTR- and DTR+.
        6a.the last 2 figures in the 3rd column do not correspond; the last 2 figures in the 5th column do not correspond.
        7a. the last 2 images of the 3rd and 4th columns do not correspond. Indeed, it is strange why so many times the merge figures are not shown. Also, the amount of α-SMA seems similar in late PanIn and in PC. The amount of FN seems similar in late PanIn and in PC as well. Finally, the number of F4/80 cells seems similar in CTL, early PanIn, late PanIn and PC.
        Supplemental figure 3. The 2 images on the right middle row are not the same, the green channel picture looks very strange.

        3.Hoshino et al., 2015. Tumour exosome integrins determine organotropic metastasis. Nature. 2015 Nov 19;527(7578):329-35.
        Mass spec data incongruence:
        I didn’t find any integrins in exosomes derived from plasma samples of mammary tumour-bearing MMTV-PyMT at the PMN and MN levels. Also, neither I didn’t find any integrins or the pattern of integrins I found is not consistent with Hoshino et al., 2015 in the exosomes derived from the plasma samples of breast cancer patients with liver and/or bone and/or skin and/or lung and/or brain metastases.
        Moreover, while EVs derived from benign S1-3D cell culture have many integrins, EVs from the malignant T4-3D cells do not have any integrin. Curiously, in the EVs from T4-PD cells, treated with an Erk inhibitor to revert the phenotype of the malignant T4 cell line, integrins re-appear.
        Paper figures:
        4a. Only 2 breast cancer patients with lung metastasis is ridiculous! One of the bone metastasis patients has similar values of β4. This is not at all reproducible, we would need data from at least around 100 patients in each group to start.
        8a. Mass spec data indicates there is no exosomes markers and no integrins in the plasma of mice with PYMT tumors both a PMN and MN.

        In all the 3 papers there is a reproducibility issue. Finally, mouse data maybe very different from human data. For these studies to be feasible, accurate and reproducible we would need to use large cohorts of patients’ samples. In some cases, the data of only 2 patients is shown.


  5. The Press secretary at the Karolinska Institute states that “The research group was discontinued during the autumn 2015. Mr Bostrom is since 31 Dec 2015 not an employee at KI”. However, according to Pubmed, Pontus Bostrom is still affiliated with the Karolinska Institute. On his latest publication (Nat Commun. 2016; 7: 11314) which was submitted on 2016 Jan 11 and accepted on 2016 Mar 11, Bostrom’s affiliation is Department of Cell and Molecular Biology, Stockholm SE-171 77, Sweden. In addition, according to the KI homepage, Pontus Bostrom has an active e-mail account at the Karolinska Institute, and his status is “anknyten” (=affiliated).

    Liked by 1 person

  6. does he still get to keep that Ph.D. degree?


  7. The post contains a small inaccuracy regarding the irisin story. The Spiegelman and Gygi labs provided a mass spectrometry analysis where irisin was detected and quantified in human plasma at 3.03-4.79 ng/ml (Jedrychowski et al. 2015). In a comment on PubPeer Dr. Spiegelman (or someone using his name) proclaimed: “I hope and trust that this paper will answer (without any antibodies) all questions concerning the existence, structure and regulation of human irisin.” This was cited in the current post. However, they used an antibody in their study (Adipogen IN102 = A-25B-0027) to localize an irisin band after deglycosylation. This was the basis to cut out the region from the gel where they detected irisin. Interestingly, this antibody (most likely from the same lot) was shown before to be the one with the heaviest unspecific staining (Albrecht et al. 2015). The presentation of the western blot in the Jedrychowski paper (controls were from a different gel) was subject to heavy criticism at PubPeer. Moreover, it was widely ignored, that the results of the Jedrychowski study completely discounted the original study of Boström et al. (2012), i.e. Jedrychowski et al. (2015) “confirmed” a discovery which was not made before.


  8. Pingback: Does ERC help cheaters pay protection money? – For Better Science

  9. The original comment by Hedvig Zackrisson from August 19th was removed upon her own request. This is her explanatory message by email:

    ”I personally asked Leonid Schneider to remove my comment because I understand now that it was highly irrelevant on his page. Lots of water has passed under the bridges so he may actually be a different man now.”


  10. Pingback: Can lawyers influence misconduct investigation? Case of Tina Wenz – For Better Science

  11. Retraction for Borström’s paper from his PhD period:
    “Statement of Retraction. The SNARE Protein SNAP23 and the SNARE-Interacting Protein Munc18c in Human Skeletal Muscle Are Implicated in Insulin Resistance/Type 2 Diabetes. Diabetes 2010;59:1870–1878. DOI: 10.2337/db09-1503. PMID: 20460426
    Pontus Boström, Linda Andersson, Birgitte Vind, Liliana Håversen, Mikael Rutberg, Ylva Wickström, Erik Larsson, Per-Anders Jansson, Maria K. Svensson, Richard Brånemark, Charlotte Ling, Henning Beck-Nielsen, Jan Borén, Kurt Højlund, and Sven-Olof Olofsson
    DOI: 10.2337/db17-rt05a
    The following statement was submitted by Jan Borén of the University of Gothenburg
    (Gothenburg, Sweden) on behalf of the coauthors listed below and has been
    reviewed and approved for publication by the American Diabetes Association’s Panel
    on Ethical Scientific Programs:
    This study represents a major effort from several laboratories and considerable
    resources over several years. While we remain confident that the majority of the
    results presented are correct, we are concerned by ambiguities identified in this
    article in light of the fact that the first author, Pontus Almer Boström, who left
    the University of Gothenburg in 2009, has been found guilty of scientific misconduct
    by the Vice-Chancellor of the University of Gothenburg. Science must
    be credible. In this context, we would like to thank “Peer 1” from the PubPeer
    .com discussion for this article (
    for detecting the ambiguities and bringing them to our attention.
    We have no evidence of scientific misconduct in this study, but because the
    corresponding author, Sven-Olof Olofsson, sadly passed away in 2011 and
    none of the coauthors have continued working in this field, we are unable to
    repeat the experiments performed in the study to clarify the identified ambiguities.
    Furthermore, we have been unable to contact Pontus Almer Boström to
    discuss these ambiguities. Therefore, the coauthors listed below have decided
    that the most reasonable course of action is to retract the article.
    Linda Andersson Birgitte Vind Liliana Håversen Mikael Rutberg
    Ylva Wickström Erik Larsson Per-Anders Jansson Maria K. Svensson
    Richard Brånemark Charlotte Ling Henning Beck-Nielsen Jan Borén
    Kurt Højlund”

    Click to access db17-rt05a.full.pdf


    • With this I questioned myself if the next generations of supposedly successful scientists will still be the ones who have to publish in high impact journals, cheating data and publishing pseudo-miracles.


  12. Cell. 1999 Jul 9;98(1):115-24.
    Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1.
    Wu Z1, Puigserver P, Andersson U, Zhang C, Adelmant G, Mootha V, Troy A, Cinti S, Lowell B, Scarpulla RC, Spiegelman BM.
    Author information
    Dana-Farber Cancer Institute, and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

    Figure 3A.


  13. Mol Cell. 1999 Feb;3(2):151-8.
    Cross-regulation of C/EBP alpha and PPAR gamma controls the transcriptional pathway of adipogenesis and insulin sensitivity.
    Wu Z1, Rosen ED, Brun R, Hauser S, Adelmant G, Troy AE, McKeon C, Darlington GJ, Spiegelman BM.
    Author information
    Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

    Figure 3.

    Figure 4c.

    Figures 2 and 3.


  14. Endocrinology. 2011 Aug;152(8):2996-3004. doi: 10.1210/en.2011-0281. Epub 2011 Jun 28.
    6 comments on PubPeer (by: Peer 1, Unregistered Submission, Peer 3)

    Integrated regulation of hepatic metabolism by fibroblast growth factor 21 (FGF21) in vivo.
    Fisher FM1, Estall JL, Adams AC, Antonellis PJ, Bina HA, Flier JS, Kharitonenkov A, Spiegelman BM, Maratos-Flier E.
    Author information
    Division of Endocrinology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.

    Figure 2C.


  15. Mol Cell. 2001 Nov;8(5):971-82.
    Cytokine stimulation of energy expenditure through p38 MAP kinase activation of PPARgamma coactivator-Puigserver P1, Rhee J, Lin J, Wu Z, Yoon JC, Zhang CY, Krauss S, Mootha VK, Lowell BB, Spiegelman BM.
    Author information
    Dana-Farber Cancer Institute, Department of Cell Biology, Boston, MA 02115, USA.

    Figure 6B.

    Figure 3B.


  16. J Biol Chem. 2000 Jun 16;275(24):18527-33.
    Degradation of the peroxisome proliferator-activated receptor gamma is linked to ligand-dependent activation.
    Hauser S1, Adelmant G, Sarraf P, Wright HM, Mueller E, Spiegelman BM.
    Author information
    Dana-Farber Cancer Institute, Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

    Figure 2A. Only 3 lanes, why differentially splice?


  17. Genes Dev. 2002 Jan 1;16(1):22-6.
    C/EBPalpha induces adipogenesis through PPARgamma: a unified pathway.
    Rosen ED1, Hsu CH, Wang X, Sakai S, Freeman MW, Gonzalez FJ, Spiegelman BM.
    Author information
    Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

    One theory is that it is more of a collage than you think, i.e. all spliced together, but that is not obvious.

    Figure 4B.


  18. Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12017-22. Epub 2007 Jul 3.
    AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1alpha.
    Jäger S1, Handschin C, St-Pierre J, Spiegelman BM.
    Author information
    Dana-Farber Cancer Institute, Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

    Figure 1A.


  19. This is amazing! This shows that exercising is essential for a good life!


  20. Pingback: mTOR: conclusions not affected? – For Better Science

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