Evidence map›Paper›PMID 22764095›Full record

ArticleAmerican journal of hematology2012

Role of c-Myb in the survival of pre B-cell acute lymphoblastic leukemia and leukemogenesis.

Purvaba J Sarvaiya, Jason R Schwartz, Claudia P Hernandez, Paulo C Rodriguez, Wayne V Vedeckis

Abstract read
In one paragraph

Article in American journal of hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. HemaSphere · 2024
    Article
  4. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  5. MicroRNAs in Leukemias: A Clinically Annotated Compendium.International journal of molecular sciences · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Dual Mechanism ofMolecular and cellular biology · 2017
    Article
  12. Overexpression of c-Myb is associated with suppression of distant metastases in colorectal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  13. 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 1 institution in 1 country.

Purvaba J SarvaiyaDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Jason R Schwartz
Claudia P Hernandez
Paulo C Rodriguez
Wayne V Vedeckis
Louisiana State University Health Sciences Center New Orleans · US

Funding

TUMOR MICROENVIRONMENT AND B CELL LYMPHOMASP20RR021970 · NCRR · LSU HEALTH SCIENCES CENTER · PI THOMPSON, HILARY W · 2005 to 2011
$14.1M
Mentoring Translational Researchers in LouisianaP20GM103501 · NIGMS · LSU HEALTH SCIENCES CENTER · PI OCHOA, AUGUSTO C. · 2012 to 2014
$6.3M
Glucocorticoid Receptor Regulation in LeukemiaR01CA116042 · NCI · LSU HEALTH SCIENCES CENTER · PI VEDECKIS, WAYNE V. · 2007 to 2011
$1.2M
Notch-1 in T Cells: a central mediator of tumor induced anergyR21CA162133 · NCI · LSU HEALTH SCIENCES CENTER · PI RODRIGUEZ, PAULO CESAR · 2012 to 2013
$330k
NCI NIH HHS CA116042NCI NIH HHS R01 CA116042NCI NIH HHS R21 CA162133NCRR NIH HHS 2P20RR021970-06NCRR NIH HHS P20 RR021970NIGMS NIH HHS P20 GM103501
6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) is the most common cancer in children. The current treatment protocol for ALL involves an intense chemotherapy regimen yielding cure rates of nearly 80%. However, new therapies need to be designed not only to increase the survival rate but also to combat the risk of severe therapy associated toxicities including secondary malignancies, growth problems, organ damage, and infertility. The c-Myb proto-oncogene is highly expressed in immature hematopoietic cells. In this study, we demonstrate that loss of c-Myb itself decreased the viability of these leukemic cells. Additionally, the inhibition of c-Myb caused a decrease in cell proliferation, significantly increased the number of cells in G(0) /G(1) phase of the cell cycle, increased the sensitivity of pre-B-ALL cells to cytotoxic agents in vitro, and significantly delayed disease onset in a mouse model of leukemia. Furthermore, we demonstrate that Bcl-2 is a target of c-Myb in pre-B-ALL cells. Our results identify c-Myb as a potential therapeutic target in pre-B-ALL and suggest that suppression of c-Myb levels or activity, in combination with currently used therapies and/or dose reduction, may lead to a decrease in toxicity and an increase in patient survival rates. Because c-Myb is aberrantly expressed in several other malignancies, targeting c-Myb will have broad clinical applications.

Indexed as

AnimalsApoptosisCell Line, TumorCell Transformation, NeoplasticDNA ReplicationDoxycyclineFemaleGene Knockdown TechniquesGenes, mybGenetic TherapyGenetic VectorsHumansLentivirusMiceMice, Inbred NODMice, SCIDDoxycyclineMAS1 protein, humanNeoplasm ProteinsProto-Oncogene MasProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mybRNA, Small Interfering

Identifiers

PMID22764095
PMCPMC3578739
OpenAlexW2044980865

What OpenQuestion holds

Textmetadata
LicenceTDM
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.