Evidence map›Paper›PMID 33773846›Full record

ReviewBlood reviews2021

Chronic Myeloid Leukemia: Modern therapies, current challenges and future directions.

Afaf E G Osman, Michael W Deininger

Open access · greenAbstract readReview
In one paragraph

Review in Blood reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 1 pooled it
19.0field-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.

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

117 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

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  17. Uncovering cancer dependencies in peptide-interacting protein pockets.bioRxiv : the preprint server for biology · 2026
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57 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

2 authors at 1 institution in 1 country.

Afaf E G OsmanDivision of Hematology & Hematologic Malignancies, Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA. Electronic address: afaf.osman@hci.utah.edu.
Michael W DeiningerDivision of Hematology & Hematologic Malignancies, Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA.
University of Utah · US

Funding

Targeting the Metabolic Regulator SIRT5 in Acute Myeloid LeukemiaR01CA254354 · NCI · VERSITI WISCONSIN, INC. · PI DEININGER, MICHAEL W. · 2020 to 2024
$2.9M
Mechanisms of resistance to ponatinib therapy in chronic myeloid leukemiaR01CA178397 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W., O'HARE, THOMAS J. · 2014 to 2018
$2.6M
Strategies to target BCR-ABL1 compound mutants in CML and Ph+ ALLR01CA257602 · NCI · VERSITI WISCONSIN, INC. · PI DEININGER, MICHAEL W. · 2021 to 2025
$1.8M
NCI NIH HHS R01 CA178397NCI NIH HHS R01 CA254354NCI NIH HHS R01 CA257602
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by a reciprocal translocation [t(9;22)(q34;q11.2)] that leads to the fusion of ABL1 gene sequences (9q34) downstream of BCR gene sequences (22q11) and is cytogenetically visible as Philadelphia chromosome (Ph). The resulting BCR/ABL1 chimeric protein is a constitutively active tyrosine kinase that activates multiple signaling pathways, which collectively lead to malignant transformation. During the early (chronic) phase of CML (CP-CML), the myeloid cell compartment is expanded, but differentiation is maintained. Without effective therapy, CP-CML invariably progresses to blast phase (BP-CML), an acute leukemia of myeloid or lymphoid phenotype. The development of BCR-AB1 tyrosine kinase inhibitors (TKIs) revolutionized the treatment of CML and ignited the start of a new era in oncology. With three generations of BCR/ABL1 TKIs approved today, the majority of CML patients enjoy long term remissions and near normal life expectancy. However, only a minority of patients maintain remission after TKI discontinuation, a status termed treatment free remission (TFR). Unfortunately, 5-10% of patients fail TKIs due to resistance and are at risk of progression to BP-CML, which is curable only with hematopoietic stem cell transplantation. Overcoming TKI resistance, improving the prognosis of BP-CML and improving the rates of TFR are areas of active research in CML.

Indexed as

AnimalsAntineoplastic AgentsDisease ManagementDisease Models, AnimalHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveModels, MolecularProtein Kinase InhibitorsAntineoplastic AgentsProtein Kinase InhibitorsBCR/ABL1Chronic myeloid leukemiaPhiladelphia chromosomeTreatment free remissionTyrosine kinase inhibitor

Identifiers

PMID33773846
PMCPMC8563059
OpenAlexW3137154050

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.