Evidence map›Paper›PMID 17490616›Full record

ArticleBiochemical and biophysical research communications2007

Anaplastic lymphoma kinase is expressed in different subtypes of human breast cancer.

Pablo Perez-Pinera, Y Chang, A Astudillo, J Mortimer, T F Deuel

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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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 3 institutions in 2 countries.

Pablo Perez-PineraThe Scripps Research Institute, La Jolla, CA 92037, USA.
Y Chang
A Astudillo
J Mortimer
T F Deuel
Scripps Research Institute · USHospital Universitario Central de Asturias · ESUniversity of California San Diego · US

Funding

SUPPLEMENT TO INVESTIGATIVE HEMATOLOGYT32DK007022 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI SOLOMON, DANIEL RENEE · 1986 to 2009
$2.3M
PLEIOTROPHIN-- AN ANGIOGENIC SWITCH IN TUMOR PROGRESSIONR01CA084400 · NCI · SCRIPPS RESEARCH INSTITUTE · PI DEUEL, THOMAS F · 2000 to 2004
$2.2M
NCI NIH HHS CA88440NCI NIH HHS R01 CA084400NIDDK NIH HHS 2 T32 DK007022-26NIDDK NIH HHS T32 DK007022
6 · The paper itself

Abstract

Pleiotrophin (PTN, Ptn) is an 18kDa cytokine expressed in human breast cancers. Since inappropriate expression of Ptn stimulates progression of breast cancer in transgenic mice and a dominant negative PTN reverses the transformed phenotype of human breast cancer cells that inappropriately express Ptn, it is suggested that constitutive PTN signaling in breast cancer cells that inappropriately express Ptn activates pathways that promote a more aggressive breast cancer phenotype. Pleiotrophin signals by inactivating its receptor, the receptor protein tyrosine phosphatase (RPTP)beta/zeta, and, recently, PTN was found to activate anaplastic lymphoma kinase (ALK) through the PTN/RPTPbeta/zeta signaling pathway in PTN-stimulated cells, not through a direct interaction of PTN with ALK and thus not through the PTN-enforced dimerization of ALK. Since full-length ALK is activated in different malignant cancers and activated ALK is a potent oncogenic protein, we examined human breast cancers to test the possibility that ALK may be expressed in breast cancers and potentially activated through the PTN/RPTPbeta/zeta signaling pathway; we now demonstrate that ALK is strongly expressed in different histological subtypes of human breast cancer; furthermore, ALK is expressed in both nuclei and cytoplasm and, in the ;;dotted" pattern characteristic of ALK fusion proteins in anaplastic large cell lymphoma. This study thus supports the possibility that activated ALK may be important in human breast cancers and potentially activated either through the PTN/RPTPbeta/zeta signaling pathway, or, alternatively, as an activated fusion protein to stimulate progression of breast cancer in humans.

Indexed as

Anaplastic Lymphoma KinaseBreast NeoplasmsCarrier ProteinsCytokinesGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansProtein-Tyrosine KinasesProtein Tyrosine PhosphatasesReceptor-Like Protein Tyrosine Phosphatases, Class 5Receptor Protein-Tyrosine KinasesTissue DistributionTumor Cells, CulturedALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseCarrier ProteinsCytokinespleiotrophinProtein-Tyrosine KinasesProtein Tyrosine PhosphatasesPTPRZ1 protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 5Receptor Protein-Tyrosine Kinases

Identifiers

PMID17490616
PMCPMC1945107
OpenAlexW2081690557

What OpenQuestion holds

Textmetadata
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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.