Evidence map›Paper›PMID 28256574›Full record

ReviewNature reviews. Cancer2017

Tissue-specific tumorigenesis: context matters.

Günter Schneider, Marc Schmidt-Supprian, Roland Rad, Dieter Saur

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 3 pooled it
11.5field-weighted citation impact, top 1% 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

194 citing papers in PubMed, 3 syntheses or guidelines pooled it, 314 citations in OpenAlex.

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  18. Concept of neuroendocrine neoplasms of all organs with a focus on grading, subtyping.Virchows Archiv : an international journal of pathology · 2026
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134 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Günter SchneiderDepartment of Medicine II (Gastroenterology and GI Oncology), Klinikum rechts der Isar, Technische Universität München, School of Medicine, Ismaningerstr. 22, 81675 München, Germany; and at the German Cancer Research Center (DKFZ) and the German Cancer Consortium (DKTK), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Marc Schmidt-SupprianDepartment of Medicine III (Haematology and Oncology), Klinikum rechts der Isar, Technische Universität München, School of Medicine, Ismaningerstr. 22, 81675 München, Germany; and at the DKFZ and the DKTK, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Roland RadDepartment of Medicine II (Gastroenterology and GI Oncology), Klinikum rechts der Isar, Technische Universität München, School of Medicine, Ismaningerstr. 22, 81675 München, Germany; and at the German Cancer Research Center (DKFZ) and the German Cancer Consortium (DKTK), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Dieter SaurUniversity Hospital Klinikum rechts der Isar, Technische Universität München, School of Medicine, Ismaningerstr. 22, 81675 München, Germany; and at the Division of Translational Cancer Research, DKFZ and DKTK, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Technical University of Munich · DEKlinikum rechts der Isar · DE

Funding

European Research Council 648521
6 · The paper itself

Abstract

How can we treat cancer more effectively? Traditionally, tumours from the same anatomical site are treated as one tumour entity. This concept has been challenged by recent breakthroughs in cancer genomics and translational research that have enabled molecular tumour profiling. The identification and validation of cancer drivers that are shared between different tumour types, spurred the new paradigm to target driver pathways across anatomical sites by off-label drug use, or within so-called basket or umbrella trials which are designed to test whether molecular alterations in one tumour entity can be extrapolated to all others. However, recent clinical and preclinical studies suggest that there are tissue- and cell type-specific differences in tumorigenesis and the organization of oncogenic signalling pathways. In this Opinion article, we focus on the molecular, cellular, systemic and environmental determinants of organ-specific tumorigenesis and the mechanisms of context-specific oncogenic signalling outputs. Investigation, recognition and in-depth biological understanding of these differences will be vital for the design of next-generation clinical trials and the implementation of molecularly guided cancer therapies in the future.

Indexed as

CarcinogenesisOrgan SpecificityCell TransdifferentiationCell Transformation, NeoplasticDNA DamageEpistasis, GeneticHumansMicrobiotaNeoplasmsProto-Oncogene Proteins p21(ras)Signal TransductionTumor MicroenvironmentKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID28256574
PMCPMC5823237
OpenAlexW2591757282

What OpenQuestion holds

Textmetadata
LicenceTDM
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.