Cancer Science, the journal of the Japanese Cancer Association, has retracted a 2012 article by a group of researchers because, well, it wasn’t clear who made up the group in the first place.
The article, “Antitumor activity of human γδ T cells transducted with CD8 and with T-cell receptors of tumor-specific cytotoxic T lymphocytes,” appeared online in July 2012 and was written, ostensibly, by Takeshi Hanagiri, Yoshiki Shigematsu, Koji Kuroda, Tetsuro Baba, Hironobu Shiota, Yoshinobu Ichiki, Yoshika Nagata, Manabu Yasuda, Tomoko So, Mitsuhiro Takenoyama and Fumihiro Tanaka from the Second Department of Surgery at the University of Occupational and Environmental Health, in Kitakyushu.
The abstract states:
The difficulty in the induction and preparation of a large number of autologous tumor-specific cytotoxic T lymphocytes (CTL) from individual patients is one of major problems in their application to adoptive immunotherapy. The present study tried to establish the useful antitumor effectors by using γδ T cells through tumor-specific TCRαβ genes transduction, and evaluated the efficacy of their adoptive transfer in a non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice model. The TCRαβ gene was cloned from the HLA-B15-restricted CTL clone specific of the Kita-Kyushu Lung Cancer antigen-1 (KK-LC-1). The cloned TCRαβ as well as the CD8 gene were transduced into γδ T cells induced from peripheral blood lymphocytes (PBL). Cytotoxic T lymphocyte activity was examined using a standard 4 h 51Cr release assay. Mice with a xenotransplanted tumor were treated with an injection of effector cells. Successful transduction of TCRαβ was confirmed by the staining of KK-LC-1-specific tetramers. The γδ T cells transduced with TCRαβ and CD8 showed CTL activity against the KK-LC-1-positive lung cancer cell line in a HLA B15-restricted manner. Adoptive transfer of the effector cells in a mice model resulted in marked growth suppression of KK-LC-1- and HLA-B15-positive xenotransplanted tumors. Co-transducing TCRαβ and CD8 into γδ T cells yielded the same antigen-specific activity as an original CTL in vitro and in vivo. The TCRαβ gene transduction into γδ T cells is a promising strategy for developing new adoptive immunotherapy. (Cancer Sci, doi: 10.1111/j.1349-7006.2012.02337.x, 2012)
According to the retraction notice:
The above article in Cancer Science (doi: 10.1111/j.1349-7006.2012.02337.x), published online on 6 July 2012 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the authors, the journal Editor in Chief, Yusuke Nakamura, and Wiley Publishing Asia Pty Ltd. The retraction has been agreed due to lack of agreement between the co-authors and an unlisted author whose claim to authorship could not be solved.
Has to be more to this than meets the eye.
Adding an author is a simple correction.
Perhaps, they could not agree on author order. If that’s the case, then the unlisted author must have done quite a bit.
Why wasn’t the author there in the first place?
We all know the “word that must not be spoken.”
This is a clever work-around.
I once have originated and developed over years a major project on my own, but with help of biophysical and immunology collaborators. It took me years to get the immunology collaborator on the project – just to confirm my project would work not only in mouse, but also in human. I was shocked reading the paper without me as last or even co-author. Unfortunately, the journal editors, nor the collaborators wanted to retract the plagiarized paper nor add me as author, originator of the idea, and developper of the proof of concept…
Maybe in the case above, the retraction was the only possible thing they could agree on. It might be best for the science.
This “unlisted” author is key. Why has his/her identity not been revealed? There must certainly be some validity to the claim, otherwise it would not have led to a retraction. Another case of an incomplete, and untransparent, retraction notice. It’s a shame that good scientific work is going to the trash can because people fail to talk to each other.