Evidence map›Paper›PMID 19759355›Full record

ArticleBlood2009

Stage-specific Arf tumor suppression in Notch1-induced T-cell acute lymphoblastic leukemia.

Emmanuel J Volanakis, Richard T Williams, Charles J Sherr

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Peripheral tolerance can be modified by altering KLF2-regulated Treg migration.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Tissue-specific p19Arf regulation dictates the response to oncogenic K-ras.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

3 authors at 1 institution in 1 country.

Emmanuel J VolanakisDepartment of Oncology, St Jude Children's Research Hospital, Memphis, TN 38105, USA.
Richard T Williams
Charles J Sherr
Howard Hughes Medical Institute · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
LABORATORY TRAINING FOR CLINICAL ONCOLOGISTST32CA070089 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI DOWNING, JAMES R · 1996 to 2011
$3.7M
Howard Hughes Medical InstituteNCI NIH HHS CA070089NCI NIH HHS CA-21765NCI NIH HHS P30 CA021765NCI NIH HHS T32 CA070089
6 · The paper itself

Abstract

Frequent hallmarks of T-cell acute lymphoblastic leukemia (T-ALL) include aberrant NOTCH signaling and deletion of the CDKN2A locus, which contains 2 closely linked tumor suppressor genes (INK4A and ARF). When bone marrow cells or thymocytes transduced with a vector encoding the constitutively activated intracellular domain of Notch1 (ICN1) are expanded ex vivo under conditions that support T-cell development, cultured progenitors rapidly induce CD4+/CD8+ T-ALLs after infusion into healthy syngeneic mice. Under these conditions, enforced ICN1 expression also drives formation of T-ALLs in unconditioned CD-1 nude mice, bypassing any requirements for thymic maturation. Retention of Arf had relatively modest activity in suppressing the formation of T-ALLs arising from bone marrow-derived ICN1+ progenitors in which the locus is epigenetically silenced, and all resulting Arf (+/+) tumors failed to express the p19(Arf) protein. In striking contrast, retention of Arf in thymocyte-derived ICN1+ donor cells significantly delayed disease onset and suppressed the penetrance of T-ALL. Use of cultured thymocyte-derived donor cells expressing a functionally null Arf-GFP knock-in allele confirmed that ICN1 signaling can induce Arf expression in vivo. Arf activation by ICN1 in T cells thereby provides stage-specific tumor suppression but also a strong selective pressure for deletion of the locus in T-ALL.

Indexed as

Adoptive TransferAnimalsBlotting, SouthernBlotting, WesternCell DifferentiationCyclin-Dependent Kinase Inhibitor p16Disease Models, AnimalHumansMiceMice, KnockoutPrecursor T-Cell Lymphoblastic Leukemia-LymphomaReceptor, Notch1Reverse Transcriptase Polymerase Chain ReactionT-LymphocytesTransduction, GeneticTransfectionCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16NOTCH1 protein, humanReceptor, Notch1

Identifiers

PMID19759355
PMCPMC2777126
OpenAlexW2117932045

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.