Evidence map›Paper›PMID 17980712›Full record

ReviewBiochimica et biophysica acta2008

FoxO tumor suppressors and BCR-ABL-induced leukemia: a matter of evasion of apoptosis.

Zainab Jagani, Amrik Singh, Roya Khosravi-Far

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
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  9. Article
  10. FoxO proteins in the nervous system.Analytical cellular pathology (Amsterdam) · 2015
    Review
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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

3 authors at 2 institutions in 1 country.

Zainab JaganiDepartment of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Amrik Singh
Roya Khosravi-Far
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

TRAINING PROGRAM IN MOLECULAR HEMATOLOGYT32HL007623 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI HANDIN, ROBERT I · 1985 to 2010
$7.0M
Tumor Selective Apoptosis by TRAILR01HL080192 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2005 to 2010
$3.6M
Novel Strategies for Treatment of Myeloproliferative DisordersR01CA131664 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2008 to 2012
$1.8M
Oncogene-Induced Evasion from ApoptosisR01CA105306 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHOSRAVI-FAR, ROYA · 2005 to 2009
$1.6M
NCI NIH HHS CA105306NCI NIH HHS R01 CA105306NCI NIH HHS R01 CA131664NHLBI NIH HHS 5T32HL007623-22NHLBI NIH HHS HL080192NHLBI NIH HHS R01 HL080192NHLBI NIH HHS T32 HL007623
6 · The paper itself

Abstract

Numerous studies have revealed that the BCR-ABL oncoprotein abnormally engages a multitude of signaling pathways, some of which may be important for its leukemogenic properties. Central to this has been the determination that the tyrosine kinase function of BCR-ABL is mainly responsible for its transforming potential, and can be targeted with small molecule inhibitors, such as imatinib mesylate (Gleevec, STI-571). Despite this apparent success, the development of clinical resistance to imatinib therapy, and the inability of imatinib to eradicate BCR-ABL-positive malignant hematopoietic progenitors demand detailed investigations of additional effector pathways that can be targeted for CML treatment. The promotion of cellular survival via the suppression of apoptotic pathways is a fundamental characteristic of tumor cells that enables resistance to anti-cancer therapies. As substrates of survival kinases such as Akt, the FoxO family of transcription factors, particularly FoxO3a, has emerged as playing an important role in the cell cycle arrest and apoptosis of hematopoietic cells. This review will discuss our current understanding of BCR-ABL signaling with a focus on apoptotic suppressive mechanisms and alternative approaches to CML therapy, as well as the potential for FoxO transcription factors as novel therapeutic targets.

Indexed as

ApoptosisBenzamidesDrug Resistance, NeoplasmForkhead Box Protein O3Forkhead Transcription FactorsFusion Proteins, bcr-ablHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveModels, BiologicalPiperazinesPyrimidinesSignal TransductionBenzamidesForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanFusion Proteins, bcr-ablImatinib MesylatePiperazinesPyrimidines

Identifiers

PMID17980712
PMCPMC2180393
OpenAlexW1968730099

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.