Evidence map›Paper›PMID 24349632›Full record

ReviewGenes & cancer2013

Role of p38 MAP Kinase Signal Transduction in Solid Tumors.

Hari K Koul, Mantu Pal, Sweaty Koul

Open access · bronzeAbstract readReview
In one paragraph

Review in Genes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
260citing papers in PubMed, 3 pooled it
16.6field-weighted citation impact, top 1% 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

260 citing papers in PubMed, 3 syntheses or guidelines pooled it, 484 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
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  20. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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200 more citing papers are in PubMed but not listed here.

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.

Hari K KoulDepartment of Biochemistry & Molecular Biology, LSU Health Sciences Center, Shreveport, LA, USA ; Feist-Weiller Cancer Center, Shreveport, LA, USA ; Veterans Administration Medical Center, Shreveport, LA, USA.
Mantu PalDepartment of Biochemistry & Molecular Biology, LSU Health Sciences Center, Shreveport, LA, USA ; Veterans Administration Medical Center, Shreveport, LA, USA.
Sweaty KoulFeist-Weiller Cancer Center, Shreveport, LA, USA ; Department of Urology, LSU Health Sciences Center, Shreveport, LA, USA.
United States Department of Veterans Affairs · USLouisiana State University Health Sciences Center Shreveport · US

Funding

Urolithiasis: Oxalate Interactions with the Renal CellsR01DK054084 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI KOUL, HARI K · 1997 to 2011
$3.2M
Tetrandrine for the treatment of Prostate CancerR01CA161880 · NCI · UNIVERSITY OF COLORADO DENVER · PI KOUL, HARI K · 2011 to 2015
$1.5M
Prostate Cancer: Targeting Androgen Receptor Signaling by TetrandrineI01BX001258 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI KOUL, HARI K · 2011 to 2014
–
BLRD VA I01 BX001258NCI NIH HHS R01 CA161880NIDDK NIH HHS R01 DK054084
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPKs) mediate a wide variety of cellular behaviors in response to extracellular stimuli. One of the main subgroups, the p38 MAP kinases, has been implicated in a wide range of complex biologic processes, such as cell proliferation, cell differentiation, cell death, cell migration, and invasion. Dysregulation of p38 MAPK levels in patients are associated with advanced stages and short survival in cancer patients (e.g., prostate, breast, bladder, liver, and lung cancer). p38 MAPK plays a dual role as a regulator of cell death, and it can either mediate cell survival or cell death depending not only on the type of stimulus but also in a cell type specific manner. In addition to modulating cell survival, an essential role of p38 MAPK in modulation of cell migration and invasion offers a distinct opportunity to target this pathway with respect to tumor metastasis. The specific function of p38 MAPK appears to depend not only on the cell type but also on the stimuli and/or the isoform that is activated. p38 MAPK signaling pathway is activated in response to diverse stimuli and mediates its function by components downstream of p38. Extrapolation of the knowledge gained from laboratory findings is essential to address the clinical significance of p38 MAPK signaling pathways. The goal of this review is to provide an overview on recent progress made in defining the functions of p38 MAPK pathways with respect to solid tumor biology and generate testable hypothesis with respect to the role of p38 MAPK as an attractive target for intervention of solid tumors.

Indexed as

mitogen-activated protein kinase (MAPK)p38 signaling pathwaysolid tumors

Identifiers

PMID24349632
PMCPMC3863344
OpenAlexW2164575467

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.