Evidence map›Paper›PMID 18698018›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2008

Clinical-translational approaches to the Nm23-H1 metastasis suppressor.

Patricia S Steeg, Christine E Horak, Kathy D Miller

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. The vital role of ATP citrate lyase in chronic diseases.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  7. Article
  8. Article
  9. The dosage-dependent effect exerted by the NM23-H1/H2 homolog NDK-1 on distal tip cell migration in C. elegans.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  10. NM23/NDPK proteins in transcription regulatory functions and chromatin modulation: emerging trends.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Regulation of the metastasis suppressor Nm23-H1 by tumor viruses.Naunyn-Schmiedeberg's archives of pharmacology · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Patricia S SteegWomen's Cancers Section, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, 37 Convent Drive, Bethesda, MD 20892, USA. steegp@mail.nih.gov
Christine E Horak
Kathy D Miller
Center for Cancer Research · USIndiana University – Purdue University Indianapolis · US

Funding

Molecular Biology of the Metastatic PhenotypeZIASC000892 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI STEEG, PATRICIA SCHRIVER · 2009 to 2023
$8.4M
MOLECULAR BIOLOGY OF THE METASTATIC PHENOTYPEZ01SC000892 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI STEEG, PATRICIA SCHRIVER · 1996 to 2008
$1.3M
Intramural NIH HHS Z01 SC000892
6 · The paper itself

Abstract

Nm23-H1 significantly reduces metastasis without effects on primary tumor size and was the first discovered metastasis suppressor gene. At least three mechanisms are thought to contribute to the metastasis-suppressive effect of Nm23-H1: (a) its histidine kinase activity toward ATP-citrate lyase, aldolase C, and the kinase suppressor of ras, with the last inactivating mitogen-activated protein kinase signaling; (b) binding proteins that titer out "free" Nm23-H1 and inhibit its ability to suppress metastasis; and (c) altered gene expression downstream of Nm23-H1, particularly an inverse association with the lysophosphatidic acid receptor endothelial differentiation gene-28 (EDG2). Most metastasis suppressor genes, including Nm23-H1, affect metastatic colonization, which is the outgrowth of tumor cells in distant locations; therefore, they are of high translational interest. A phase II trial is ongoing to test the hypothesis that a compound, high-dose medroxyprogesterone acetate (MPA), used as an unconventional gluocorticoid, will stimulate breast cancer cells to reexpress Nm23-H1 and limit subsequent metastatic colonization.

Indexed as

AnimalsAntineoplastic AgentsClinical Trials, Phase II as TopicHumansNeoplasm InvasivenessNeoplasmsNM23 Nucleoside Diphosphate KinasesSignal TransductionAntineoplastic AgentsNM23 Nucleoside Diphosphate Kinases

Identifiers

PMID18698018
PMCPMC2730725
OpenAlexW2105175007

What OpenQuestion holds

Textmetadata
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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.