Evidence map›Paper›PMID 12134042›Full record

ArticleJournal of virology2002

Kaposi's sarcoma-associated herpesvirus-induced upregulation of the c-kit proto-oncogene, as identified by gene expression profiling, is essential for the transformation of endothelial cells.

Ashlee V Moses, Michael A Jarvis, Camilo Raggo, Yolanda C Bell, Rebecca Ruhl, B G Mattias Luukkonen, Diana J Griffith, Cecily L Wait, Brian J Druker, Michael C Heinrich and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 150 citations in OpenAlex.

  1. Phase II trial of imatinib in AIDS-associated Kaposi's sarcoma: AIDS Malignancy Consortium Protocol 042.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014
    Trial
  2. Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  3. Infectious etiologies of conjunctival tumors.Expert review of ophthalmology · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. HIV-Associated Cancer Biomarkers: A Requirement for Early Diagnosis.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Mast Cell Activation and KSHV Infection in Kaposi Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  12. Article
  13. Review
  14. Kaposi sarcoma herpesvirus pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

12 authors at 2 institutions in 1 country.

Ashlee V MosesVaccine and Gene Therapy Institute, Portland, Oregon 97201, USA. mosesa@ohsu.edu
Michael A Jarvis
Camilo Raggo
Yolanda C Bell
Rebecca Ruhl
B G Mattias Luukkonen
Diana J Griffith
Cecily L Wait
Brian J Druker
Michael C Heinrich
Jay A Nelson
Klaus Früh
Oregon Health & Science University · USVaccine and Gene Therapy Institute

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI OJEDA, SERGIO R · 1985 to 2011
$140.8M
REPRODUCTIVE STEROIDS AND EXPERIMENTAL STROKEK01RR000163 · NCRR · OREGON HEALTH AND SCIENCE UNIVERSITY · PI MURPHY, STEPHANIE J · 2000 to 2004
$479k
NCRR NIH HHS K01 RR000163NCRR NIH HHS P51 RR000163
6 · The paper itself

Abstract

Kaposi's sarcoma (KS), the most frequent malignancy afflicting AIDS patients, is characterized by spindle cell formation and vascularization. Infection with KS-associated herpesvirus (KSHV) is consistently observed in all forms of KS. Spindle cell formation can be replicated in vitro by infection of dermal microvascular endothelial cells (DMVEC) with KSHV. To study the molecular mechanism of this transformation, we compared RNA expression profiles of KSHV-infected and mock-infected DMVEC. Induction of several proto-oncogenes was observed, particularly the receptor tyrosine kinase c-kit. Consistent with increased c-Kit expression, KHSV-infected DMVEC displayed enhanced proliferation in response to the c-Kit ligand, stem cell factor (SCF). Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation. Importantly, inhibition of c-Kit signal transduction reversed the KSHV-induced morphological transformation of DMVEC. Furthermore, overexpression studies showed that c-Kit was sufficient to induce spindle cell formation. Together, these data demonstrate an essential role for c-Kit in KS tumorigenesis and reveal a target for pharmacological intervention.

Indexed as

Base SequenceBenzamidesCell AdhesionCell DivisionCell LineCell SizeCell Transformation, NeoplasticCell Transformation, ViralDNAEndothelium, VascularGene Expression ProfilingHerpesvirus 8, HumanHumansImatinib MesylateNeovascularization, PathologicPiperazinesBenzamidesDNAImatinib MesylateMAS1 protein, humanPiperazinesProto-Oncogene MasProto-Oncogene Proteins c-kitPyrimidinesStem Cell Factor

Identifiers

PMID12134042
PMCPMC155158
OpenAlexW1968258480

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.