Evidence map›Paper›PMID 26312204›Full record

ArticleSpringerPlus2015

Analysis of ALK gene in 133 patients with breast cancer revealed polysomy of chromosome 2 and no ALK amplification.

Matthew G Hanna, Vesna Najfeld, Hanna Y Irie, Joseph Tripodi, Anupma Nayak

Open access · diamondAbstract read
In one paragraph

Article in SpringerPlus, 2015. 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
1.0field-weighted citation impact, top 23% 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, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. ALK: a tyrosine kinase target for cancer therapy.Cold Spring Harbor molecular case studies · 2017
    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

5 authors at 1 institution in 1 country.

Matthew G HannaDepartment of Pathology and Laboratory Medicine, The Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, Box 1194, New York, NY 10029 USA.
Vesna NajfeldDepartment of Pathology and Laboratory Medicine, The Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, Box 1194, New York, NY 10029 USA.
Hanna Y IrieDepartment of Oncological Sciences, The Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, New York, NY USA.
Joseph TripodiDepartment of Pathology and Laboratory Medicine, The Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, Box 1194, New York, NY 10029 USA.
Anupma NayakDepartment of Pathology and Laboratory Medicine, The Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, Box 1194, New York, NY 10029 USA.
Icahn School of Medicine at Mount Sinai · US

Funding

Medical Research Council MR/K000608/1
6 · The paper itself

Abstract

ALK has emerged as a novel tumorigenic factor in several epithelial human cancers. Crizotinib, an ALK tyrosine kinase inhibitor, is currently approved to treat lung cancer patients exhibiting ALK gene rearrangements. Our goal was to determine the incidence of ALK aberrations in relation to different breast cancer types. Tissue micro-arrays were constructed of ER+/PR±/HER2- (n = 37), ER-/PR-/HER2+ (n = 15), ER-/PR-/HER2- (n = 61) and ER+/PR+/HER2+ (n = 20) breast cancers; including 13 inflammatory breast carcinomas. FISH was performed using ALK break-apart and chromosome 2 centromere enumeration probes (CEP2). Neither ALK rearrangements nor amplification were identified in the 133 breast cancer cases evaluated. However, copy number gains (CNG) of ALK were identified in 82 of 133 patients (62 %). The CEP2 analysis revealed polysomy of chromosome 2 in all HCNG and LCNG cases, indicating the CNG of ALK are due to polysomy of chromosome 2, rather than true amplification of ALK. To conclude, we observed CNG of ALK secondary to chromosome 2 polysomy in a significant percentage of breast cancer cases, a phenomenon similar to polysomy 17. This study is one of the largest studies to have investigated ALK aberrations in breast cancer and the only study to include all subtypes.

Indexed as

ALKBreast cancerFISHInflammatoryPolysomyTMA

Identifiers

PMID26312204
PMCPMC4544610
OpenAlexW1876667604

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.