Evidence map›Paper›PMID 23634980›Full record

ArticleBreast cancer research : BCR2013

Activating mutations and senescence secretome: new insights into HER2 activation, drug sensitivity and metastatic progression.

Swarnali Acharyya

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 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
0.2field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  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 at 1 institution in 1 country.

Swarnali Acharyya
Memorial Sloan Kettering Cancer Center · US

Funding

Defining mechanisms of cancer chemoresistance and metastasisK99CA172697 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI ACHARYYA, SWARNALI · 2013 to 2013
$159k
NCI NIH HHS K99 CA172697-01
6 · The paper itself

Abstract

HER2 amplification and overexpression is observed in approximately 20% of breast cancers and is strongly associated with poor prognosis and therapeutic responsiveness to HER2 targeted agents. A recent study by Bose and colleagues suggests that another subset of breast cancer patients without HER2 amplification but with activating HER2 mutation might also benefit from existing HER2-targeted agents and the authors functionally characterize these somatic mutations in experimental models. In a second study on HER2-driven breast cancer, Angelini and colleagues investigate how the constitutively active, truncated carboxy-terminal fragment of HER2, p95HER2, promotes metastatic progression through non-cellautonomous secretion of factors from senescent cells. These new findings advance our understanding of HER2 biology in the context of HER2 activation as well as offer new insights into our understanding of drug sensitivity and metastatic progression.

Indexed as

Cell CommunicationAnimalsBreast NeoplasmsCellular SenescenceDisease ProgressionDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesFemaleHumansMutationERBB2 protein, humanErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID23634980
PMCPMC3672670
OpenAlexW2097141003

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.