ArticleJAK-STAT2013
CCL2 at the crossroad of cancer metastasis.
Article in JAK-STAT, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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.
Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Chemokine ligand 2: beyond chemotaxis-a multifaceted role in tumor progression.Frontiers in immunology · 2025Review
- CCL2 secreted from cancer-associated mesothelial cells promotes peritoneal metastasis of ovarian cancer cells through the P38-MAPK pathway.Clinical & experimental metastasis · 2020Article
- More Than Just Attractive: How CCL2 Influences Myeloid Cell Behavior Beyond Chemotaxis.Frontiers in immunology · 2019Review
- Modulation of double-stranded RNA pattern recognition receptor signaling in ovarian cancer cells promotes inflammatory queues.Oncotarget · 2018Article
- Breast cancer: coordinated regulation of CCL2 secretion by intracellular glycosaminoglycans and chemokine motifs.Neoplasia (New York, N.Y.) · 2014Article
- Beyond the androgen receptor: new approaches to treating metastatic prostate cancer. Report of the 2013 Prouts Neck Prostate Cancer Meeting.The Prostate · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary tumors can affect organ functions, either mechanically when they grow to a considerable size or via production of hormones. However, mortality of cancer patients is in most cases due to formation of secondary growths.(1) (,) (2) Consequently, various drugs are currently employed in clinical trials to impair specific steps of cancer metastasis such as mesenchymal or amoeboid cell migration, intravasation and/or colonization.(2) From the clinical point of view, targeting late metastatic processes such as extravasation or colonization might be required for cancer patients that bear already dormant micrometastases in their capillaries which have left behind earlier metastatic steps. Development of such drugs needs characterization of molecular targets implicated in distinct steps of cancer metastasis.
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Identifiers
What OpenQuestion holds
Registered trials
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.