Evidence map›Paper›PMID 24002944›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2013

Has discovery-based cancer research been a bust?

R J Epstein

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

1 author.

R J EpsteinDepartment of Oncology, Clinical Cancer Informatics & Research Centre, The Kinghorn Cancer Centre, Sydney, Australia, repstein@stvincents.com.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The completion of the human genome sequence sparked optimism about prospects for new anticancer drug development, but clinical progress over the last decade has proven slower than expected. Here it is proposed that unrealistically high expectations of first-generation discovery-based diagnostics have contributed to this problem. Hypothesis-based single-molecule tests (e.g., mutation screening of KRAS, EGFR, BRAF or KIT genes) continue to change clinical practice incrementally, whereas first-generation multiplex assays--such as gene expression profiling and proteomics--have identified few high-impact therapeutic targets despite numerous correlations with prognosis. To move forward, second-generation multiplex diagnostics should be based not on statistical patterns/associations alone, but on clinically interpretable ('high-signal-to-noise') data such as change-of-function mutations, gene amplifications, recurrent chromosomal anomalies, and abnormal phosphorylation profiles of ERK or mTOR signaling cascades.

Indexed as

Biomedical ResearchBiomarkers, TumorHumansMutationNeoplasmsPredictive Value of TestsBiomarkers, Tumor

Identifiers

What OpenQuestion holds

Textmetadata
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.