Evidence map›Paper›PMID 12101257›Full record

ReviewJournal of leukocyte biology2002

Role of CXCL1 in tumorigenesis of melanoma.

Punita Dhawan, Ann Richmond

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

142 citing papers in PubMed, 1 synthesis or guideline pooled it, 308 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Lnk Governs chemokine-directed trafficking of CD8Molecular therapy. Oncology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The role of CXC chemokines and receptors in breast cancer.Clinical and experimental medicine · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. TGFβ1 induces CXCL1 to promote stemness features in lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Article

82 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

2 authors at 1 institution in 1 country.

Punita DhawanDepartment of Veterans Affairs, Nashville, TN 37232, USA.
Ann Richmond
Vanderbilt University · US

Funding

MELANOMA GROWTH STIMULATORY ACTIVITYR01CA034590 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN · 1986 to 2017
$5.2M
Role of NIK Activation in Melanoma ProgressionR01CA098807 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN · 2005 to 2009
$1.3M
REGULATION OF EXPRESSION OF MGSA/GRO GENES IN MELANOMAR01CA056704 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN · 1993 to 2001
$482k
BLRD VA IK6 BX005225NCI NIH HHS R01 CA034590NCI NIH HHS R01 CA056704NCI NIH HHS R01 CA098807
6 · The paper itself

Abstract

The CXC chemokine, CXCL1 (melanoma growth-stimulatory activity/growth-regulated protein alpha), plays a major role in inflammation, angiogenesis, tumorigenesis, and wound healing. Recently, chemokines have been extensively related to cellular transformation, tumor growth, homing, and metastasis. CXCL1 and its mouse homologue MIP-2 have been shown to be involved in the process of tumor formation. When chemokines such as CXCL1 and CXCL8 (IL-8) become disregulated so that they are chronically expressed, tissue damage, angiogenesis, and tumorigenesis can follow. This up-regulation of chemokines has been attributed to constitutive activation of NF-kappaB. The constitutive NF-kappaB activation is an emerging hallmark in various types of tumors including breast, colon, pancreatic, ovarian, as well as melanoma. Previous findings from our laboratory and other laboratories have demonstrated the role of endogenous activation of NF-kappaB in association with enhanced metastatic potential of malignant melanoma cells and suggest that targeting NF-kappaB may have potential therapeutic effects in clinical trials. An important step in this direction would be to delineate the important intracellular pathways and upstream kinases involved in up-regulation of NF-kappaB in melanoma cells. In this review, the signaling pathways involved in the disregulation of NF-kappaB and chemokine expression are discussed.

Indexed as

Intercellular Signaling Peptides and ProteinsAnimalsApoptosisCell Transformation, NeoplasticChemokine CXCL1ChemokinesChemokines, CXCChemotactic FactorsGrowth SubstancesMelanocytesMelanomaMiceModels, ImmunologicalNF-kappa BReceptors, ChemokineSignal TransductionChemokine CXCL1ChemokinesChemokines, CXCChemotactic FactorsCxcl1 protein, mouseGrowth SubstancesIntercellular Signaling Peptides and ProteinsNF-kappa BReceptors, Chemokine

Identifiers

PMID12101257
PMCPMC2668262
OpenAlexW2096216039

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.