Evidence map›Paper›PMID 20592475›Full record

ReviewThe Journal of clinical investigation2010

Chronic myeloid leukemia: mechanisms of blastic transformation.

Danilo Perrotti, Catriona Jamieson, John Goldman, Tomasz Skorski

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03117816 (Efficacy and Safety of Pegylated Proline Interferon Alpha 2b), which is not on this map. Cited by 194 papers.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed
18.4field-weighted citation impact, top 1% 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.

NCT03117816 phase3completednot on this mapstarted 2017, after this paper: background citation

Efficacy and Safety of Pegylated Proline Interferon Alpha 2b (AOP2014) in Maintaining Deep Molecular Remissions in Patients With Chronic Myeloid Leukemia (CML) Who Discontinue ABL-Kinase Inhibitor Therapy - a Randomized Phase III, Multicenter Trial With Post-study Follow-up

TypeinterventionalSponsorPhilipps University MarburgRan2017 to 2022Enrolled214ConditionsChronic Myeloid Leukemia in RemissionArmsAOP2014 / Pegylated-Proline-interferon alpha-2b, Surveillance
3 · Its place in the literature

Who cites it

194 citing papers in PubMed, 391 citations in OpenAlex.

  1. Trial
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  6. Chronic Myeloid Leukemia and the T315IInternational journal of molecular sciences · 2025
    Review
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  13. Review
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134 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

4 authors at 3 institutions in 2 countries.

Danilo PerrottiDepartment of Molecular Virology, Immunology and Medical Genetics and Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 41230, USA. danilo.perrotti@osumc.edu
Catriona Jamieson
John Goldman
Tomasz Skorski
Hammersmith Hospital · GBTemple University · USThe Ohio State University · US

Funding

Role of RNA-Binding Proteins in BCR/ABL LeukemogenesisR01CA095512 · NCI · OHIO STATE UNIVERSITY · PI PERROTTI, DANILO · 2003 to 2012
$2.2M
Genomic instability causes imatinib resistance in CMLR01CA123014 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SKORSKI, TOMASZ · 2008 to 2012
$2.0M
Genome instability in leukemia stem cellR21CA133646 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SKORSKI, TOMASZ · 2009 to 2010
$363k
NCI NIH HHS CA095512NCI NIH HHS CA123014NCI NIH HHS CA133646NCI NIH HHS R01 CA095512NCI NIH HHS R01 CA123014NCI NIH HHS R21 CA133646
6 · The paper itself

Abstract

The BCR-ABL1 oncoprotein transforms pluripotent HSCs and initiates chronic myeloid leukemia (CML). Patients with early phase (also known as chronic phase [CP]) disease usually respond to treatment with ABL tyrosine kinase inhibitors (TKIs), although some patients who respond initially later become resistant. In most patients, TKIs reduce the leukemia cell load substantially, but the cells from which the leukemia cells are derived during CP (so-called leukemia stem cells [LSCs]) are intrinsically insensitive to TKIs and survive long term. LSCs or their progeny can acquire additional genetic and/or epigenetic changes that cause the leukemia to transform from CP to a more advanced phase, which has been subclassified as either accelerated phase or blastic phase disease. The latter responds poorly to treatment and is usually fatal. Here, we discuss what is known about the molecular mechanisms leading to blastic transformation of CML and propose some novel therapeutic approaches.

Indexed as

AnimalsHematopoietic Stem Cell TransplantationHumansLeukemiaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLymphocyte ActivationMiceProtein Kinase InhibitorsProtein Kinase Inhibitors

Identifiers

PMID20592475
PMCPMC2898591
OpenAlexW2054086725

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.