Evidence map›Paper›PMID 11560954›Full record

ArticleThe Journal of clinical investigation2001

Therapeutic targeting of the MEK/MAPK signal transduction module in acute myeloid leukemia.

M Milella, S M Kornblau, Z Estrov, B Z Carter, H Lapillonne, D Harris, M Konopleva, S Zhao, E Estey, M Andreeff

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 310 citations in OpenAlex.

  1. Trial
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  4. Phase II study of the oral MEK inhibitor selumetinib in advanced acute myelogenous leukemia: a University of Chicago phase II consortium trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Trial
  5. Trial
  6. Trial
  7. Review
  8. Article
  9. Article
  10. High TCTA expression is an adverse prognostic biomarker in acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Anti-leukemic principle(s) fromCytotechnology · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. U0126: Not only a MAPK kinase inhibitor.Frontiers in pharmacology · 2022
    Review
  20. Article

79 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

M MilellaDepartment of Blood and Marrow Transplantation, Section of Molecular Hematology and Therapy, The University of Texas, M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
S M Kornblau
Z Estrov
B Z Carter
H Lapillonne
D Harris
M Konopleva
S Zhao
E Estey
M Andreeff
The University of Texas at Austin · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THALL, PETER F · 1990 to 2014
$41.8M
THE THERAPY OF AMLP01CA055164 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMAS, MATTIE J · 1992 to 2011
$25.3M
NCI NIH HHS CA-16672NCI NIH HHS P01 CA049639NCI NIH HHS P01 CA055164NCI NIH HHS P01 CA-49639NCI NIH HHS P01 CA-55164NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

The mitogen-activated protein kinase (MAPK) pathway regulates growth and survival of many cell types, and its constitutive activation has been implicated in the pathogenesis of a variety of malignancies. In this study we demonstrate that small-molecule MEK inhibitors (PD98059 and PD184352) profoundly impair cell growth and survival of acute myeloid leukemia (AML) cell lines and primary samples with constitutive MAPK activation. These agents abrogate the clonogenicity of leukemic cells but have minimal effects on normal hematopoietic progenitors. MEK blockade also results in sensitization to spontaneous and drug-induced apoptosis. At a molecular level, these effects correlate with modulation of the expression of cyclin-dependent kinase inhibitors (p27(Kip1) and p21(Waf1/CIP1)) and antiapoptotic proteins of the inhibitor of apoptosis proteins (IAP) and Bcl-2 families. Interruption of constitutive MEK/MAPK signaling therefore represents a promising therapeutic strategy in AML.

Indexed as

Tumor Suppressor ProteinsApoptosisBenzamidesCell CycleCell Cycle ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsCytarabineEnzyme InhibitorsFlavonoidsHumansLeukemia, Myeloid, AcuteMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinases2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamideBenzamidesCDKN1A protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsCytarabineEnzyme InhibitorsFlavonoidsMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesProteinsProto-Oncogene Proteins c-bcl-2Tumor Suppressor ProteinsXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID11560954
PMCPMC200930
OpenAlexW2122051507

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.