Evidence map›Paper›PMID 12881713›Full record

ArticleOncogene2003

Tyrosine kinase oncoprotein, RET/PTC3, induces the secretion of myeloid growth and chemotactic factors.

John P Russell, Shogo Shinohara, Rosa M Melillo, Maria D Castellone, Massimo Santoro, Jay L Rothstein

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

33 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Review
  3. Immune and Inflammatory Cells in Thyroid Cancer Microenvironment.International journal of molecular sciences · 2019
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Urinary neopterin levels in patients with thyroid cancer.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2014
    Article
  10. Interleukins as markers of inflammation in malignant and benign thyroid disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014
    Article
  11. Review
  12. Central role of RET in thyroid cancer.Cold Spring Harbor perspectives in biology · 2013
    Review
  13. Review
  14. Article
  15. Article
  16. Thyroid Cancer: Role of RET and Beyond.European thyroid journal · 2012
    Review
  17. Article
  18. Targeting stroma to treat cancers.Seminars in cancer biology · 2012
    Review
  19. Article
  20. Inflammation in thyroid oncogenesis.American journal of cancer research · 2012
    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

6 authors at 2 institutions in 2 countries.

John P RussellDepartment of Microbiology/Immunology, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Shogo Shinohara
Rosa M Melillo
Maria D Castellone
Massimo Santoro
Jay L Rothstein
Institute for Experimental Endocrinology and Oncology · ITThomas Jefferson University · US

Funding

Structural Analysis of TCL-1 and MTCP-1 ProteinsP01CA076259 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CROCE, CARLO M · 1999 to 2003
$6.1M
TRAINING PROGRAMS IN MOLECULAR GENETICS OF CANCERT32CA009678 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BUCHBERG, ARTHUR M. · 1992 to 2008
$2.3M
NCI NIH HHS CA-76259NCI NIH HHS T32-CA09678
6 · The paper itself

Abstract

Differentiated thyroid carcinomas are the most frequent endocrine neoplasms, but account for few cancer-related deaths. Although the indolent growth of these cancers correlates well with longevity, the biological basis for this good prognosis is not known. In contrast, two of the most frequent autoimmune diseases involve the thyroid suggesting a high propensity for this organ to invoke destructive immunity. Unfortunately, the mechanism linking malignancy and autoimmunity is not clear, although the expression of the oncogenic fusion protein RET/PTC3 (RP3) in both of these disorders may provide a clue. Interestingly, the signaling caused by activated RET kinase involves overlapping pathways and some common to the inflammatory response. Accordingly, we analyzed the function of RP3 and a mutant RP3 molecule to induce proinflammatory pathways in thyroid epithelial cells. Indeed, we find that RP3 alone causes increases in nuclear NF-kappaB activity and secretion of MCP-1 and GM-CSF. Finally, transfer of RP3-expressing thyrocytes into mice in vivo attracted dense macrophage infiltrates, which lead to rapid thyroid cell death. Further, cytokine synthesis and inflammation was largely abrogated by mutation of RP3 Tyr588; an important protein-binding site for downstream signaling. Together, these studies implicate oncogene-induced cytokine-signaling pathways in a new mechanism linking inflammation with cancer.

Indexed as

Transcription FactorsAnimalsCells, CulturedChemokine CCL2Chemotactic FactorsCytokinesFibroblastsGranulocyte-Macrophage Colony-Stimulating FactorInflammationMacrophagesMiceMutationNF-kappa BNuclear Receptor CoactivatorsOncogene ProteinsProtein-Tyrosine KinasesChemokine CCL2Chemotactic FactorsCytokinesGranulocyte-Macrophage Colony-Stimulating FactorNCOA4 protein, humanNF-kappa BNuclear Receptor CoactivatorsOncogene ProteinsProtein-Tyrosine KinasesTranscription Factors

Identifiers

PMID12881713
OpenAlexW1993578875

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.