Investigation raises questions about top cancer researcher’s work

A prominent pancreatic cancer researcher has lost a meeting abstract and corrected a Nature paper following an institutional investigation.

Queen Mary University of London determined that, in an abstract by Thorsten Hagemann, “elements of the study summarised by this abstract are not reliable.” Hagemann has recently issued a correction to a 2014 Nature paper he co-authored, which also cited the Queen Mary University of London (QMUL) investigation, noting there was “reason to question the provenance of the data.”

Hagemann is currently the medical director of Immodulon Therapeutics, and has long been recognized for his work in the field, including a three-year grant of £180,000 from the Pancreatic Cancer Research Fund in 2013.

Here’s the retraction notice from the The Journal of Pathology, regarding an abstract from the 7th Joint Meeting of the British Division of the International Academy of Pathology and the Pathological Society of Great Britain & Ireland:

‘Utilising Pre-clinical Models to Refine Immune Modulation in Pancreatic Cancer’ by Thorsten Hagemann

The above abstract, published online on 13 September 2013 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between Queen Mary University of London, the journal Editor-in-Chief, Prof. C. Simon Herrington, and John Wiley & Sons Limited. Following a formal investigation, the author’s institution has concluded that elements of the study summarised by this abstract are not reliable.

The abstract is yet to be cited, according to Thomson Reuters Web of Science.

A spokesperson from QMUL sent us this statement:

Following a rigorous investigation by QMUL, QMUL found reason to question the provenance of the data for the abstract ‘Utilising Pre-clinical Models to Refine Immune Modulation in Pancreatic Cancer’ published in The Journal of Pathology, 2013; 231, S1: 9. doi: 10.1002/path.4254. The investigation found no evidence of institutional or systemic failings and confirmed that the issue related to a single individual who has since left the employment of QMUL.

Simon Herrington, editor-in-chief of The Journal of Pathology based at the University of Edinburgh in Scotland, added:

Since the request to retract this abstract was made by the employing institution, the journal did not seek agreement from the author.

In 2016, Hagemann issued a corrigendum to a 2014 Nature letter on which he is listed as the fourth author. It reads:

Queen Mary University London notified Nature and University College London that there is reason to question the provenance of the data for Fig. 5b, d, e of this Letter (Fig. 5a, c data are unaffected). Ongoing studies are investigating the reported effect of p110δ inhibition in the pancreatic cancer mouse model. We therefore wish to withdraw these figure panels and associated text from the published paper. This does not affect the overall conclusion of the manuscript or any of the other experiments performed for this study as they repeat effects shown using other model systems in the paper (see Supplementary Information for raw data of experiments). We apologise for the inconvenience that this may have caused.

“Inactivation of PI(3)K p110δ breaks regulatory T-cell-mediated immune tolerance to cancer” has been cited 50 times since 2014.

One of Hagemann’s 2008 papers in the Journal of Experimental Medicine has been cited 327 times.

We’ve reached out to the press team at Immodulon, but weren’t able to get in touch with Hagemann directly.

Here’s the text from the now-retracted abstract:

Recent developments of novel targeted and combined therapies have improved survival for patients with solid tumours. However, therapy failure, drug resistance and subsequently disease progression still occurs invariably in the vast majority of solid cancers and eventually leads to patient death. As a consequence, 2 year survival rate for advanced pancreatic cancer is still dismal 1%. Pancreatic ductal adenocarcinoma is naturally resistant to current chemo- and radiation-therapy. Therefore there is an urgent need for the improvement of current therapy. Immunotherapy recently gained significant momentum with new therapeutic options at the horizon. There is a growing awareness that immunosuppression by infiltrating immune cells in the tumour microenvironment plays an important role in the resistance of tumours to endogenous anti-tumour immune responses as well as against a variety of therapeutic interventions. Thus efforts towards improving the clinical efficacy of PDAC therapy should involve strategies to neutralise or overcome immune suppression. However the immune suppressive microenvironment of pancreatic cancer has not yet been systematically characterised. However, human and mouse immunity demonstrate significant differences and studies are needed to define patient immunity in detail to develop and improve immune therapies. Our work aims to define the immunity in pancreatic cancer patients in a spatio-temporal manner and to redefine therapeutic points of intervention.

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