Evidence map›Paper›PMID 25881064›Full record

ArticlePloS one2015

Accumulation of an endogenous tryptophan-derived metabolite in colorectal and breast cancers.

Paolo Puccetti, Francesca Fallarino, Antoine Italiano, Isabelle Soubeyran, Gaetan MacGrogan, Marc Debled, Valerie Velasco, Dominique Bodet, Sandrine Eimer, Marc Veldhoen and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.

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  18. Gut microbiome: decision-makers in the microenvironment of colorectal cancer.Frontiers in cellular and infection microbiology · 2023
    Review
  19. Obesity as a Risk Factor for Breast Cancer-The Role of miRNA.International journal of molecular sciences · 2022
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 6 countries.

Paolo PuccettiDepartment of Experimental Medicine, University of Perugia, Perugia, Italy.
Francesca FallarinoDepartment of Experimental Medicine, University of Perugia, Perugia, Italy.
Antoine ItalianoDepartment of Medical Oncology, Institut Bergonié, Bordeaux, France.
Isabelle SoubeyranDepartment of Medical Oncology, Institut Bergonié, Bordeaux, France.
Gaetan MacGroganDepartment of Medical Oncology, Institut Bergonié, Bordeaux, France.
Marc DebledDepartment of Medical Oncology, Institut Bergonié, Bordeaux, France.
Valerie VelascoDepartment of Medical Oncology, Institut Bergonié, Bordeaux, France.
Dominique BodetImmuSmol, Pessac, France.
Sandrine EimerHistology and Molecular Pathology of Tumors Laboratory EA 2406, University Bordeaux Segalen, Bordeaux, France.
Marc VeldhoenLaboratory for Lymphocyte Signalling and Development, The Babraham Institute, Cambridge, United Kingdom.
Georges C PrendergastLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United states of America.
Michael PlattenCCU Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany; Department of Neurooncology, University Hospital, Heidelberg, Germany.
Alban BessedeImmuSmol, Pessac, France.
Gilles J GuilleminMacquarie University, Faculty of Medicine, Neuroinflammation group, Sydney, New South Wales, Australia; Applied Neurosciences Program, Peter Duncan Neurosciences Research Unit, St Vincent's Centre for Applied Medical Research, Darlinghurst, New South Wales, Australia.
Institut Bergonié · FRUniversity of Perugia · ITBabraham Institute · GBHeidelberg University · DELankenau Institute for Medical Research · USMacquarie University · AUUniversité de Bordeaux · FR

Funding

Biotechnology and Biological Sciences Research Council BB/E021638/1Biotechnology and Biological Sciences Research Council BBS/E/B/000C0409
6 · The paper itself

Abstract

Tumor immune escape mechanisms are being regarded as suitable targets for tumor therapy. Among these, tryptophan catabolism plays a central role in creating an immunosuppressive environment, leading to tolerance to potentially immunogenic tumor antigens. Tryptophan catabolism is initiated by either indoleamine 2,3-dioxygenase (IDO-1/-2) or tryptophan 2,3-dioxygenase 2 (TDO2), resulting in biostatic tryptophan starvation and l-kynurenine production, which participates in shaping the dynamic relationship of the host's immune system with tumor cells. Current immunotherapy strategies include blockade of IDO-1/-2 or TDO2, to restore efficient antitumor responses. Patients who might benefit from this approach are currently identified based on expression analyses of IDO-1/-2 or TDO2 in tumor tissue and/or enzymatic activity assessed by kynurenine/tryptophan ratios in the serum. We developed a monoclonal antibody targeting l-kynurenine as an in situ biomarker of IDO-1/-2 or TDO2 activity. Using Tissue Micro Array technology and immunostaining, colorectal and breast cancer patients were phenotyped based on l-kynurenine production. In colorectal cancer l-kynurenine was not unequivocally associated with IDO-1 expression, suggesting that the mere expression of tryptophan catabolic enzymes is not sufficiently informative for optimal immunotherapy.

Indexed as

Breast NeoplasmsColorectal NeoplasmsHumansTryptophanTryptophan

Identifiers

PMID25881064
PMCPMC4400104
OpenAlexW2015343055

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.