Evidence map›Paper›PMID 16291810›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Transformation of breast cells by truncated neurokinin-1 receptor is secondary to activation by preprotachykinin-A peptides.

Hiral J Patel, Shakti H Ramkissoon, Prem S Patel, Pranela Rameshwar

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 67 citations in OpenAlex.

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  18. Truncated neurokinin-1 receptor is increased in colonic epithelial cells from patients with colitis-associated cancer.Proceedings of the National Academy of Sciences of the United States of America · 2011
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  19. Article
  20. SR140333 counteracts NK-1 mediated cell proliferation in human breast cancer cell line T47D.Journal of experimental & clinical cancer research : CR · 2010
    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

4 authors at 1 institution in 1 country.

Hiral J PatelDepartment of Medicine and Graduate School of Biomedical Sciences, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.
Shakti H Ramkissoon
Prem S Patel
Pranela Rameshwar
Brookdale University Hospital and Medical Center · US

Funding

BREAST CANCER/BONE MARROW STROMAL INTERACTIONSR01CA089868 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RAMESHWAR, PRANELA · 2000 to 2003
$873k
NCI NIH HHS CA-89868NCI NIH HHS R01 CA089868
6 · The paper itself

Abstract

Breast cancer remains the cancer with the highest mortality among women in the United States. Peptides derived from the oncogenic Tac1 gene (full transcript: betaPPT-A) stimulate the proliferation of breast cancer cells (BCCs) via seven-transmembrane G protein-coupled neurokinin 1 (NK1) and NK2 receptors. The NK1 gene could generate full-length (NK1-FL) and truncated (NK1-Tr) transcripts. NK1-Tr lacks 100 residues in their cytoplasmic end, could couple to G proteins, and shows reduced efficiency with respect to internalization and desensitization. This study reports on a role of NK1-Tr in the transformation of nontumorigenic breast cells, and investigates whether Tac1 expression is linked to the generation of NK1-Tr. Western blots and Northern analyses showed coexpressions of NK1-Tr and NK1-FL in BCCs (cell lines and primary cells from patients with different stages of breast cancer). Stable transfections of betaPPT-A or NK1-Tr expression vectors in nontumorigenic cells showed each induces the expression of the other, consequently resulting in a transformed phenotype. Analyses with microarrays indicate similar patterns of cytokine production by NK1-Tr transfectants and BCCs, but not NK1-FL transfectants. These observations indicate tumor-promoting properties by NK1-Tr, but not NK1-FL. Overall, the oncogenic property of Tac1 in breast cells involves concomitant expression of NK1-Tr and vice versa, consequently leading to the production of cytokines with growth promoting functions.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedBlotting, NorthernBlotting, WesternBreastCell Line, TumorCell Transformation, NeoplasticCloning, MolecularCytokinesDNA PrimersFemaleHumansMicroarray AnalysisMiddle AgedProtein PrecursorsCytokinesDNA PrimerspreprotachykininProtein PrecursorsReceptors, Neurokinin-1Tachykinins

Identifiers

PMID16291810
PMCPMC1297665
OpenAlexW2089155105

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.