Evidence map›Paper›PMID 27857979›Full record

ArticleMolecular & cellular oncology2016

Normoxic or hypoxic adaptation in response to antiangiogenic therapy: Clinical implications.

M Quintela-Fandino

Open access · bronzeAbstract read
In one paragraph

Article in Molecular & cellular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

1 author at 1 institution in 1 country.

M Quintela-FandinoBreast Cancer Clinical Research Unit, CNIO - Spanish National Cancer Research Center , Madrid, Spain.
Spanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In a recent article in Cell Reports, we described a novel mechanism for acquired resistance against new small-molecule antiangiogenic tyrosine-kinase inhibitors (TKIs). Vascular normalization-inducing TKIs block glycolysis and trigger a nutritional stress response in the tumor compartment that induces a (targetable) switch to mitochondrial metabolism. We discuss the implications for clinical/translational studies and suggest areas for future research.

Indexed as

Antiangiogenicsbreast cancerME-344metabolic synthetic lethalitynintedanibphenforminresistance

Identifiers

PMID27857979
PMCPMC5068174
OpenAlexW2523007780

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.