Evidence map›Paper›PMID 26119941›Full record

ReviewOncogene2016

Evaluation of targeted therapies in advanced breast cancer: the need for large-scale molecular screening and transformative clinical trial designs.

Z Fadoukhair, D Zardavas, M A Chad, T Goulioti, P Aftimos, M Piccart

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Transposon insertional mutagenesis in mice identifies human breast cancer susceptibility genes and signatures for stratification.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
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

6 authors.

Z FadoukhairDepartment of Medical Oncology, National Institute of Oncology, Rabat, Morocco.
D ZardavasBreast International Group (BIG, aisbl), Brussels, Belgium.
M A ChadDepartment of Medicine, Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.
T GouliotiBreast International Group (BIG, aisbl), Brussels, Belgium.
P AftimosDepartment of Medicine, Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.
M PiccartDepartment of Medicine, Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) has been classified into four intrinsic subtypes through seminal studies employing gene expression profiling analysis of primary tumours, namely the luminal A and B subtypes, the human epidermal growth factor receptor 2-like subtype and the basal-like subtype. More recently, the emergence of high-throughput genomic sequencing techniques, such as next-generation or massive parallel sequencing has expanded our understanding of the complex genomic landscapes of BC, with marked intertumour heterogeneity seen among different patients. In addition, increasing evidence indicates intratumour heterogeneity, with molecular differences observed within one patient, both spatially and longitudinally. These phenomena have an impact on the clinical development of molecularly targeted agents, with the classical paradigm of population-based clinical trials being no longer efficient. In the era of genomically driven oncology, three complementary tools can accelerate the clinical development of targeted agents for advanced BC as follows: (i) the implementation of molecular profiling of metastatic tumour lesions, as exemplified by the AURORA (Aiming to Understand the Molecular Aberrations in Metastatic Breast Cancer) programme; (ii) serial assessments of circulating tumour DNA, allowing a more thorough molecular interrogation of metastatic tumour burden; and (iii) new innovative clinical trial designs able to address the challenges of the increasing molecular fragmentation of BC.

Indexed as

High-Throughput Nucleotide SequencingMicroarray AnalysisBreast NeoplasmsErb-b2 Receptor Tyrosine KinasesFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyNeoplasm StagingERBB2 protein, humanErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID26119941

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.