Evidence map›Paper›PMID 23001823›Full record

ArticleJournal of cellular physiology2013

Differential mechanisms of tumor progression in clones from a single heterogeneous human melanoma.

Walburga Croteau, Molly H Jenkins, Siying Ye, David W Mullins, Constance E Brinckerhoff

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. The BRAF(V600E) inhibitor, PLX4032, increases type I collagen synthesis in melanoma cells.Matrix biology : journal of the International Society for Matrix Biology · 2015
    Article
  6. Article
  7. Article
  8. Article
  9. 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

5 authors at 1 institution in 1 country.

Walburga CroteauDepartment of Medicine, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire 03756, USA.
Molly H Jenkins
Siying Ye
David W Mullins
Constance E Brinckerhoff
Dartmouth College · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
Invasive Behavior of Tumor Cells Producing Collagenase-1R01CA077267 · NCI · DARTMOUTH COLLEGE · PI BRINCKERHOFF, CONSTANCE E · 1999 to 2013
$2.6M
REGULATION OF COLLAGENASE GENE EXPRESSIONR37AR026599 · NIAMS · DARTMOUTH COLLEGE · PI BRINCKERHOFF, CONSTANCE E · 1999 to 2006
$1.9M
REGULATION OF METALLOPROTEINASE GENE EXPRESSIONR01AR026599 · NIAMS · DARTMOUTH COLLEGE · PI BRINCKERHOFF, CONSTANCE E · 1986 to 2011
$1.7M
Role of CXCR3 for CD8+ T cells in cancer immunotherapyR01CA134799 · NCI · UNIVERSITY OF VIRGINIA · PI MULLINS, DAVID W. · 2009 to 2013
$1.6M
NCI NIH HHS CA-134799NCI NIH HHS CA-77267NCI NIH HHS P30 CA023108NCI NIH HHS R01 CA077267NCI NIH HHS R01 CA134799NIAMS NIH HHS AR-26599NIAMS NIH HHS R01 AR026599NIAMS NIH HHS R37 AR026599PHS HHS T32-009658
6 · The paper itself

Abstract

We used vertical growth phase (VGP) human VMM5 melanoma cells to ask whether the tumor microenvironment could induce matrix metalloproteinase-1 (MMP-1) in vivo, and whether this induction correlated with metastasis. We isolated two clones from parental VMM5 cells: a low MMP-1 producing clone (C4) and high producing clone (C9). When these clones were injected orthotopically (intradermally) into nude mice, both were equally tumorigenic and produced equivalent and abundant amounts of MMP-1. However, the tumors from the C4 clones displayed different growth kinetics and distinct profiles of gene expression from the C9 population. The C4 tumors, which had low MMP-1 levels in vitro, appeared to rely on growth factors and cytokines in the microenvironment to increase MMP-1 expression in vivo, while MMP-1 levels remained constant in the C9 tumors. C9 cells, but not C4 cells, grew as spheres in culture and expressed higher levels of JARID 1B, a marker associated with melanoma initiating cells. We conclude that VMM5 melanoma cells exhibit striking intra-tumor heterogeneity, and that the tumorigenicity of these clones is driven by different molecular pathways. Our data suggest that there are multiple mechanisms for melanoma progression within a tumor, which may require different therapeutic strategies.

Indexed as

AnimalsClone CellsCytokinesDisease ProgressionFemaleGene ExpressionHumansMatrix Metalloproteinase 1MelanomaMiceMice, NudeNeoplasm MetastasisNeoplastic Stem CellsRNA, MessengerTumor Cells, CulturedTumor MicroenvironmentCytokinesMatrix Metalloproteinase 1RNA, Messenger

Identifiers

PMID23001823
PMCPMC3864099
OpenAlexW2022176861

What OpenQuestion holds

Textmetadata
LicenceTDM
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.