Evidence map›Paper›PMID 21960246›Full record

ArticleLeukemia2012

Targeting survivin and p53 in pediatric acute lymphoblastic leukemia.

J W Tyner, A M Jemal, M Thayer, B J Druker, B H Chang

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Survivin splice variants and their diagnostic significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  18. Article
  19. Review
  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

5 authors at 2 institutions in 1 country.

J W TynerDivision of Hematology and Medical Oncology, and OHSU Knight Cancer Institute, OHSU, Portland, OR, USA.
A M Jemal
M Thayer
B J Druker
B H Chang
OHSU Knight Cancer InstituteHoward Hughes Medical Institute · US

Funding

OREGON CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR024140 · NCRR · OREGON HEALTH & SCIENCE UNIVERSITY · PI ORWOLL, ERIC S. · 2006 to 2011
$61.1M
Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
NCI NIH HHS P30 CA069533NCRR NIH HHS UL1 RR024140
6 · The paper itself

Abstract

Despite advances in treatment and outcomes for patients with pediatric acute lymphoblastic leukemia (ALL), there continue to be subsets of patients who are refractory to standard chemotherapy and hematopoietic stem cell transplant. Therefore, novel gene targets for therapy are needed to further advance treatment for this disease. RNA interference technology has identified survivin as a potential therapeutic target. Survivin, a member of the inhibitor of apoptosis (IAP) proteins and chromosome passenger complex, is expressed in hematologic malignancies and overexpressed in relapsed pediatric ALL. Our studies show that survivin is uniformly expressed at high levels in multiple pediatric ALL cell lines. Furthermore, silencing of survivin expression in pediatric ALL cell lines as well as primary leukemic blasts reduces viability of these cells. This includes cell lines derived from patients with relapsed disease featuring cytogenetic anomalies such as t(12;21), Philadelphia chromosome t(9;22), t(1;19) as well as a cell line carrying t(17;19) from a patient with de novo ALL. Furthermore, inhibition of survivin increases p53-dependent apoptosis that can be rescued by inhibition of p53. Finally, a screen of randomly selected primary patient samples confirms that survivin-specific small interfering RNA and survivin-targeted drug, YM155, effectively reduce viability of leukemic blasts.

Indexed as

ApoptosisBenzamidesCell DivisionCell Line, TumorFusion Proteins, bcr-ablG2 PhaseHumansImatinib MesylateInhibitor of Apoptosis ProteinsPiperazinesPrecursor Cell Lymphoblastic Leukemia-LymphomaPyrimidinesSurvivinTumor Suppressor Protein p53BenzamidesBIRC5 protein, humanFusion Proteins, bcr-ablImatinib MesylateInhibitor of Apoptosis ProteinsPiperazinesPyrimidinesSurvivinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID21960246
PMCPMC3364442
OpenAlexW2162157012

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.