Evidence map›Paper›PMID 18227349›Full record

ArticleBlood2008

Requirement of c-Myb for p210(BCR/ABL)-dependent transformation of hematopoietic progenitors and leukemogenesis.

Maria Rosa Lidonnici, Francesca Corradini, Todd Waldron, Timothy P Bender, Bruno Calabretta

Abstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Article
  2. Review
  3. Loss of expression of both miR-15/16 loci in CML transition to blast crisis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  4. c-MYB and DMTF1 in Cancer.Cancer investigation · 2019
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Oncotarget · 2017
    Article
  10. Oncotarget · 2017
    Review
  11. Dual Mechanism ofMolecular and cellular biology · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Role of epigenetics in chronic myeloid leukemia.Current hematologic malignancy reports · 2013
    Review
  20. Review
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.

Maria Rosa LidonniciDepartment of Cancer Biology, and Kimmel Cancer Center, Thomas Jefferson University Medical College, Philadelphia, PA 19107, USA.
Francesca Corradini
Todd Waldron
Timothy P Bender
Bruno Calabretta

Funding

CONDITIONAL MUTAGENESIS TO STUDY C MYB FUNCTIONR01CA085842 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BENDER, TIMOTHY P. · 2001 to 2011
$3.2M
TRANSCRIPTION FACTOR REGULATION BY THE BCR/ABL ONCOGENER01CA095111 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CALABRETTA, BRUNO · 2002 to 2012
$2.8M
c-myb in B Cell Development and FunctionR01AI059294 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BENDER, TIMOTHY P. · 2005 to 2009
$1.8M
TRAINING PROGRAMS IN CANCER IMMUNOLOGYT32CA009683 · NCI · THOMAS JEFFERSON UNIVERSITY · PI EISENLOHR, LAURENCE CRANE · 1993 to 2007
$1.5M
NCI NIH HHS CA95111NCI NIH HHS R01 CA085842NCI NIH HHS R01 CA095111NCI NIH HHS T32 CA009683NCI NIH HHS T32-CA09683-14NIAID NIH HHS R01 AI059294
6 · The paper itself

Abstract

The c-Myb gene encodes a transcription factor required for proliferation and survival of normal myeloid progenitors and leukemic blast cells. Targeting of c-Myb by antisense oligodeoxynucleotides has suggested that myeloid leukemia blasts (including chronic myelogenous leukemia [CML]-blast crisis cells) rely on c-Myb expression more than normal progenitors, but a genetic approach to assess the requirement of c-Myb by p210(BCR/ABL)-transformed hematopoietic progenitors has not been taken. We show here that loss of a c-Myb allele had modest effects (20%-28% decrease) on colony formation of nontransduced progenitors, while the effect on p210(BCR/ABL)-expressing Lin(-) Sca-1(+) and Lin(-) Sca-1(+)Kit(+) cells was more pronounced (50%-80% decrease). Using a model of CML-blast crisis, mice (n = 14) injected with p210(BCR/ABL)-transduced p53(-/-)c-Myb(w/w) marrow cells developed leukemia rapidly and had a median survival of 26 days, while only 67% of mice (n = 12) injected with p210(BCR/ABL)-transduced p53(-/-)c-Myb(w/d) marrow cells died of leukemia with a median survival of 96 days. p210(BCR/ABL)-transduced c-Myb(w/w) and c-Myb(w/d) marrow progenitors expressed similar levels of the c-Myb-regulated genes c-Myc and cyclin B1, while those of Bcl-2 were reduced. However, ectopic Bcl-2 expression did not enhance colony formation of p210(BCR/ABL)-transduced c-Myb(w/d) Lin(-)Sca-1(+)Kit(+) cells. Together, these studies support the requirement of c-Myb for p210(BCR/ABL)-dependent leukemogenesis.

Indexed as

Cell Transformation, NeoplasticAnimalsFusion Proteins, bcr-ablHematopoietic Stem CellsHematopoietic Stem Cell TransplantationLeukemiaMiceMice, Inbred C57BLNeoplasms, ExperimentalProto-Oncogene Proteins c-mybTransduction, GeneticFusion Proteins, bcr-ablProto-Oncogene Proteins c-myb

Identifiers

PMID18227349
PMCPMC2343605

What OpenQuestion holds

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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.