Evidence map›Paper›PMID 17671136›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2007

Corruption of the Fas pathway delays the pulmonary clearance of murine osteosarcoma cells, enhances their metastatic potential, and reduces the effect of aerosol gemcitabine.

Nancy Gordon, Nadezhda V Koshkina, Shu-Fang Jia, Chand Khanna, Arnulfo Mendoza, Laura L Worth, Eugenie S Kleinerman

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. CD103Cancers · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Osteosarcoma and Metastasis.Frontiers in oncology · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Natural Killer Cell Immunotherapy for Osteosarcoma.Advances in experimental medicine and biology · 2020
    Review
  15. The Histone Deacetylase Inhibitor Entinostat/Syndax 275 in Osteosarcoma.Advances in experimental medicine and biology · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Nancy GordonChildren's Cancer Hospital, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
Nadezhda V Koshkina
Shu-Fang Jia
Chand Khanna
Arnulfo Mendoza
Laura L Worth
Eugenie S Kleinerman
The University of Texas MD Anderson Cancer Center · USCenter for Cancer Research · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
LIPOSOME THERAPY--A POTENTIAL ADJUVANT FOR OSTEOSARCOMAR01CA042992 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KLEINERMAN, EUGENIE S · 1986 to 2010
$3.3M
Tumor and Metastasis BiologyZ01BC010566 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KHANNA, CHAND · 2005 to 2008
$1.8M
NCI NIH HHS CA16672NCI NIH HHS CA42992NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA042992
6 · The paper itself

Abstract

purposePulmonary metastases continue to be a significant problem in osteosarcoma. Apoptosis dysfunction is known to influence tumor development. Fas (CD95, APO-1)/FasL is one of the most extensively studied apoptotic pathways. Because FasL is constitutively expressed in the lung, cells that express Fas should be eliminated by lung endothelium. Cells with low or no cell surface Fas expression may be able to evade this innate defense mechanism. The purpose of these studies was to evaluate Fas expression in osteosarcoma lung metastases and the effect of gemcitabine on Fas expression and tumor growth. EXPERIMENTAL DESIGN AND

resultsUsing the K7M2 murine osteosarcoma model, Fas expression was quantified using immunohistochemistry. High levels of Fas were present in primary tumors, but no Fas expression was present in actively growing lung metastases. Blocking the Fas pathway using Fas-associated death domain dominant-negative delayed tumor cell clearance from the lung and increased metastatic potential. Treatment of mice with aerosol gemcitabine resulted in increased Fas expression and subsequent tumor regression.

conclusionsWe conclude that corruption of the Fas pathway is critical to the ability of osteosarcoma cells to grow in the lung. Agents such as gemcitabine that up-regulate cell surface Fas expression may therefore be effective in treating osteosarcoma lung metastases. These data also suggest that an additional mechanism by which gemcitabine induces regression of osteosarcoma lung metastases is mediated by enhancing the sensitivity of the tumor cells to the constitutive FasL in the lung.

Indexed as

AerosolsAnimalsApoptosisBlotting, WesternBone NeoplasmsDeoxycytidinefas ReceptorFlow CytometryGemcitabineLung NeoplasmsMiceMice, Inbred BALB COsteosarcomaRNA, MessengerSurvival RateTumor Cells, CulturedAerosolsDeoxycytidinefas ReceptorGemcitabineRNA, Messenger

Identifiers

PMID17671136
PMCPMC4503209
OpenAlexW2082452180

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.