Evidence map›Paper›PMID 16946306›Full record

ArticleBlood2006

Continuous in vivo infusion of interferon-gamma (IFN-gamma) enhances engraftment of syngeneic wild-type cells in Fanca-/- and Fancg-/- mice.

Yue Si, Samantha Ciccone, Feng-Chun Yang, Jin Yuan, Daisy Zeng, Shi Chen, Henri J van de Vrugt, John Critser, Fre Arwert, Laura S Haneline and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Loss of the homologous recombination geneProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. TNF-α signaling in Fanconi anemia.Blood cells, molecules & diseases · 2014
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Mouse models of Fanconi anemia.Mutation research · 2009
    Review
  18. Fanconi anemia.Hematology/oncology clinics of North America · 2009
    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

11 authors at 2 institutions in 2 countries.

Yue SiDepartment of Microbiology and Immunology, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, USA.
Samantha Ciccone
Feng-Chun Yang
Jin Yuan
Daisy Zeng
Shi Chen
Henri J van de Vrugt
John Critser
Fre Arwert
Laura S Haneline
D Wade Clapp
Amsterdam UMC Location VUmc · NLUniversity of Missouri–St. Louis · US

Funding

VectorP01HL053586 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI CLAPP, DAVID W · 1995 to 2009
$16.0M
NHLBI NIH HHS P01 HL053586NHLBI NIH HHS P01HL053586
6 · The paper itself

Abstract

Fanconi anemia (FA) is a heterogeneous genetic disorder characterized by bone marrow (BM) failure and cancer susceptibility. Identification of the cDNAs of FA complementation types allows the potential of using gene transfer technology to introduce functional cDNAs as transgenes into autologous stem cells and provide a cure for the BM failure in FA patients. However, strategies to enhance the mobilization, transduction, and engraftment of exogenous stem cells are required to optimize efficacy prior to widespread clinical use. Hypersensitivity of Fancc-/- cells to interferon-gamma (IFN-gamma), a nongenotoxic immune-regulatory cytokine, enhances engraftment of syngeneic wild-type (WT) cells in Fancc-/- mice. However, whether this phenotype is of broad relevance in other FA complementation groups is unresolved. Here we show that primitive and mature myeloid progenitors in Fanca-/- and Fancg-/- mice are hypersensitive to IFN-gamma and that in vivo infusion of IFN-gamma at clinically relevant concentrations was sufficient to allow consistent long-term engraftment of isogenic WT repopulating stem cells. Given that FANCA, FANCC, and FANCG complementation groups account for more than 90% of all FA patients, these data provide evidence that IFN-gamma conditioning may be a useful nongenotoxic strategy for myelopreparation in FA patients.

Indexed as

Genetic TherapyAnimalsAntiviral AgentsFanconi AnemiaFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group G ProteinGraft Enhancement, ImmunologicGraft SurvivalHematopoietic Stem Cell MobilizationHumansInterferon-gammaMiceMice, KnockoutMyeloid Progenitor CellsTransduction, GeneticTransplantation, AutologousAntiviral AgentsFanca protein, mouseFancg protein, mouseFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group G ProteinInterferon-gamma

Identifiers

PMID16946306
PMCPMC1895443
OpenAlexW2055348053

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.