Evidence map›Paper›PMID 19643988›Full record

ArticleBlood2009

Mer receptor tyrosine kinase is a novel therapeutic target in pediatric B-cell acute lymphoblastic leukemia.

Rachel M A Linger, Deborah DeRyckere, Luis Brandão, Kelly K Sawczyn, Kristen M Jacobsen, Xiayuan Liang, Amy K Keating, Douglas K Graham

RetractedOpen access · bronzeAbstract readRetracted Publication
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. It has been retracted, and should not be counted. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. EXT1, Regulated by MiR-665, Promotes Cell Apoptosis via ERK1/2 Signaling Pathway in Acute Lymphoblastic Leukemia.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  3. Article
  4. TAM receptor tyrosine kinase function and the immunopathology of liver disease.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Rachel M A LingerDepartment of Pediatrics, Section of Hematology, Oncology, and Bone Marrow Transplantation, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA.
Deborah DeRyckere
Luis Brandão
Kelly K Sawczyn
Kristen M Jacobsen
Xiayuan Liang
Amy K Keating
Douglas K Graham
University of Colorado Denver · US

Funding

COG FOREIGN ACCRUALU10CA098543 · NCI · NATIONAL CHILDHOOD CANCER FOUNDATION · PI ADAMSON, PETER C. · 2003 to 2013
$335.5M
Support for Human Specimen Banking in NCI-Supported Cancer Clinical TrialsU24CA114766 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI RAMIREZ MILAN, NILSA DEL CARMEN · 2005 to 2014
$14.5M
MerTK contribution to leukemogenesis and validation as a therapeutic targetF32HL096416 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BRANDAO, LUIS N · 2009 to 2011
$168k
NCI NIH HHS CA114766NCI NIH HHS CA98543NCI NIH HHS U10 CA098543NCI NIH HHS U24 CA114766NHLBI NIH HHS F32 HL096416NHLBI NIH HHS F32HL096416
6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) is currently treated with an intense regimen of chemotherapy yielding cure rates near 80%. However, additional changes using available drugs are unlikely to provide significant improvement in survival. New therapies are warranted given the risk of severe therapy-associated toxicities including infertility, organ damage, and secondary malignancy. Here, we report ectopic expression of the receptor tyrosine kinase Mer in pediatric B-cell ALL. Inhibition of Mer prevented Erk 1/2 activation, increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting apoptosis, and delayed disease onset in a mouse model of leukemia. In addition, we discovered cross-talk between the Mer and mammalian target of rapamycin (mTOR) signaling pathways. Our results identify Mer as a novel therapeutic target in ALL and suggest that inhibitors of Mer will interact synergistically with currently used therapies. This strategy may allow for dose reduction resulting in decreased toxicity and increased survival rates. Mer is aberrantly expressed in numerous other malignancies suggesting that this approach may have broad applications.

Indexed as

Drug Delivery SystemsAnimalsAntineoplastic AgentsCell SurvivalChildc-Mer Tyrosine KinaseGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansMiceMice, Inbred NODMice, SCIDPrecursor B-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRNA, Small InterferingAntineoplastic Agentsc-Mer Tyrosine KinaseMERTK protein, humanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRNA, Small Interfering

Identifiers

PMID19643988
PMCPMC2927045
OpenAlexW2032295860

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.