Evidence map›Paper›PMID 25770293›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

Translational implications of tumor heterogeneity.

Mariam Jamal-Hanjani, Sergio A Quezada, James Larkin, Charles Swanton

Abstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 312 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
312citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

312 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  10. Cross-assay RNA modeling reveals cancer biomarkers.bioRxiv : the preprint server for biology · 2026
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252 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.

Mariam Jamal-HanjaniUCL Cancer Institute, Paul O'Gorman Building, London, United Kingdom. Cancer Research UK London Research institute, London, United Kingdom.
Sergio A QuezadaUCL Cancer Institute, Paul O'Gorman Building, London, United Kingdom.
James LarkinDepartment of Oncology, Royal Marsden NHS Foundation Trust, London, United Kingdom.
Charles SwantonUCL Cancer Institute, Paul O'Gorman Building, London, United Kingdom. Cancer Research UK London Research institute, London, United Kingdom. Charles.Swanton@cancer.org.uk.

Funding

Cancer Research UK 12100Cancer Research UK 17786Cancer Research UK 19310Cancer Research UK A11590Cancer Research UK A17786Cancer Research UK A19310Department of Health
6 · The paper itself

Abstract

Advances in next-generation sequencing and bioinformatics have led to an unprecedented view of the cancer genome and its evolution. Genomic studies have demonstrated the complex and heterogeneous clonal landscape of tumors of different origins and the potential impact of intratumor heterogeneity on treatment response and resistance, cancer progression, and the risk of disease relapse. However, the significance of subclonal mutations, in particular mutations in driver genes, and their evolution through time and their dynamics in response to cancer therapies, is yet to be determined. The necessary tools are now available to prospectively determine whether clonal heterogeneity can be used as a biomarker of clinical outcome and to what extent subclonal somatic alterations might influence clinical outcome. Studies that use longitudinal tissue sampling, integrating both genomic and clinical data, have the potential to reveal the subclonal composition and track the evolution of tumors to address these questions and to begin to define the breadth of genetic diversity in different tumor types and its relevance to patient outcome. Such studies may provide further evidence for drug-resistance mechanisms informing combinatorial, adaptive, and tumor immune therapies placed within the context of tumor evolution.

Indexed as

Genetic HeterogeneityAntigens, NeoplasmDrug Resistance, NeoplasmGenes, NeoplasmGenome, HumanHigh-Throughput Nucleotide SequencingHumansNeoplasmsTreatment FailureAntigens, Neoplasm

Identifiers

PMID25770293
PMCPMC4374162

What OpenQuestion holds

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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.