Evidence map›Paper›PMID 15965261›Full record

ArticleGenetics2005

A Drosophila model of multiple endocrine neoplasia type 2.

Renee D Read, Paul J Goodfellow, Elaine R Mardis, Nancy Novak, Jon R Armstrong, Ross L Cagan

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02363647 (Personalized Cancer Therapy for Patients With Metastatic Medullary Thyroid or Metastatic Colon Cancer), which is not on this map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
1.0field-weighted citation impact, top 26% 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.

NCT02363647 naterminatednot on this mapstarted 2015, after this paper: background citation

Personalized Cancer Therapy for Patients With Metastatic Medullary Thyroid or Metastatic Colon Cancer

TypeinterventionalSponsorIcahn School of Medicine at Mount SinaiRan2015 to 2022Enrolled10ConditionsMedullary Thyroid Cancer, Colon CancerArmsTumor Genomic Analysis
3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Medical science pulse · 2025
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  3. TransgenicPharmaceuticals (Basel, Switzerland) · 2024
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  5. Human ERG oncoprotein repressesProceedings of the National Academy of Sciences of the United States of America · 2023
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  6. Article
  7. Frontiers in oncology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020
    Review
  14. Article
  15. Article
  16. Prp8 regulates oncogene-induced hyperplastic growth inDevelopment (Cambridge, England) · 2018
    Article
  17. Article
  18. Review
  19. Article
  20. TheDevelopment (Cambridge, England) · 2018
    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 1 institution in 1 country.

Renee D ReadDepartment of Genetics, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Paul J Goodfellow
Elaine R Mardis
Nancy Novak
Jon R Armstrong
Ross L Cagan
Washington University in St. Louis · US

Funding

A DROSOPHILA MODEL FOR MEN2B AND SPORADIC MTCR01CA084309 · NCI · WASHINGTON UNIVERSITY · PI CAGAN, ROSS LEIGH · 2000 to 2009
$2.0M
NCI NIH HHS R01 CA084309NCI NIH HHS R01CA084309
6 · The paper itself

Abstract

Dominant mutations in the Ret receptor tyrosine kinase lead to the familial cancer syndrome multiple endocrine neoplasia type 2 (MEN2). Mammalian tissue culture studies suggest that RetMEN2 mutations significantly alter Ret-signaling properties, but the precise mechanisms by which RetMEN2 promotes tumorigenesis remain poorly understood. To determine the signal transduction pathways required for RetMEN2 activity, we analyzed analogous mutations in the Drosophila Ret ortholog dRet. Overexpressed dRetMEN2 isoforms targeted to the developing retina led to aberrant cell proliferation, inappropriate cell fate specification, and excessive Ras pathway activation. Genetic analysis indicated that dRetMEN2 acts through the Ras-ERK, Src, and Jun kinase pathways. A genetic screen for mutations that dominantly suppress or enhance dRetMEN2 phenotypes identified new genes that are required for the phenotypic outcomes of dRetMEN2 activity. Finally, we identified human orthologs for many of these genes and examined their status in human tumors. Two of these loci showed loss of heterozygosity (LOH) within both sporadic and MEN2-associated pheochromocytomas, suggesting that they may contribute to Ret-dependent oncogenesis.

Indexed as

Disease Models, AnimalAmino Acid SequenceAnimalsDrosophilaHumansJNK Mitogen-Activated Protein KinasesMolecular Sequence DataMultiple Endocrine Neoplasia Type 2aProtein IsoformsProto-Oncogene Proteins c-retProto-Oncogene Proteins pp60(c-src)ras ProteinsRetinaJNK Mitogen-Activated Protein KinasesProtein IsoformsProto-Oncogene Proteins c-retProto-Oncogene Proteins pp60(c-src)ras ProteinsRET protein, human

Identifiers

PMID15965261
PMCPMC1456812
OpenAlexW2121134652

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.