Overexpression of the c-MET/HGF receptor in human thyroid carcinomas derived from the follicular epithelium.

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

24 citing papers in PubMed, 64 citations in OpenAlex.

1. Identification of serum biomarker panel to differentiate malignant from benign thyroid nodules using multiplex bead assay.Journal of the Egyptian National Cancer Institute · 2020
   Article
2. MET targeting: time for a rematch.Oncogene · 2020
   Review
3. Medullary Thyroid Cancer: Clinical Characteristics and New Insights into Therapeutic Strategies Targeting Tyrosine Kinases.Molecular diagnosis & therapy · 2017
   Review
4. Acquired resistance to BRAF inhibition induces epithelial-to-mesenchymal transition in BRAF (V600E) mutant thyroid cancer by c-Met-mediated AKT activation.Oncotarget · 2017
   Article
5. Hepatocyte Growth Factor/C-Met Axis in Thyroid Cancer: From Diagnostic Biomarker to Therapeutic Target.Biomarker insights · 2017
   Review
6. Progress in oncolytic virotherapy for the treatment of thyroid malignant neoplasm.Journal of experimental & clinical cancer research : CR · 2014
   Review
7. Off-target effects of c-MET inhibitors on thyroid cancer cells.Molecular cancer therapeutics · 2014
   Article
8. Signaling pathways as specific pharmacologic targets for neuroendocrine tumor therapy: RET, PI3K, MEK, growth factors, and Notch.Neuroendocrinology · 2013
   Review
9. Silencing of c-Met by RNA interference inhibits the survival, proliferation, and invasion of nasopharyngeal carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
   Article
10. c-MET as a potential therapeutic target and biomarker in cancer.Therapeutic advances in medical oncology · 2011
    Article
11. An overview of the c-MET signaling pathway.Therapeutic advances in medical oncology · 2011
    Article
12. The PI3K-Akt-mTOR pathway in initiation and progression of thyroid tumors.Molecular and cellular endocrinology · 2010
    Review
13. The Met oncogene and basal-like breast cancer: another culprit to watch out for?Breast cancer research : BCR · 2010
    Review
14. What is New on Thyroid Cancer Biomarkers.Biomarker insights · 2008
    Article
15. Functions of cyclin D1 as an oncogene and regulation of cyclin D1 expression.Cancer science · 2007
    Review
16. Molecular pathobiology of thyroid neoplasms.Endocrine pathology · 2002
    Review
17. Tyrosine kinase inhibitor STI571 enhances thyroid cancer cell motile response to Hepatocyte Growth Factor.Oncogene · 2001
    Article
18. Cross-talk between the proto-oncogenes Met and Ron.Oncogene · 2000
    Article
19. Hepatocyte growth factor/scatter factor-induced intracellular signalling.International journal of experimental pathology · 2000
    Review
20. Non-autocrine, constitutive activation of Met in human anaplastic thyroid carcinoma cells in culture.British journal of cancer · 1999
    Article

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

Authors and funding

10 authors at 2 institutions in 2 countries.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

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