Evidence map›Paper›PMID 39223295›Full record

ReviewLeukemia2024

Star wars against leukemia: attacking the clones.

Monika M Toma, Tomasz Skorski

Abstract readReview
In one paragraph

Review in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Monika M TomaFels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.ORCID 0000-0001-8414-253X
Tomasz SkorskiFels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA. tskorski@temple.edu.ORCID 0000-0002-3809-4538

Funding

Targeting DNA repair to eradicate TKi-refractory/resistant CML and Ph+ALLR01CA186238 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SKORSKI, TOMASZ · 2014 to 2024
$4.5M
AML mutation-guided drugging of DNA repairR01CA237286 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI MAZIN, ALEXANDER V, SKORSKI, TOMASZ · 2020 to 2024
$2.8M
Divergent Functions of ERK Substrate Binding Domains in Pathogenesis of Myeloproliferative NeoplasmsR01CA283396 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI TOMASZ SKORSKI, DAVID L. WIEST · 2023 to 2026
$2.8M
PolQ as a novel therapeutic target in AMLR01CA244179 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI POMERANTZ, RICHARD T, SKORSKI, TOMASZ · 2020 to 2024
$2.7M
MPN-inducing mutations as biomarkers of synthetic lethalityR01CA247707 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SKORSKI, TOMASZ · 2020 to 2024
$2.1M
Oncogenic tyrosine kinases inhibitors abrogate DNA repair and sensitive leukemias to PARP inhibitorsR01CA244044 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SKORSKI, TOMASZ · 2020 to 2024
$1.9M
Leukemia and Lymphoma Society (Leukemia & Lymphoma Society) TRP-6628-21NCI NIH HHS R01 CA186238NCI NIH HHS R01 CA237286NCI NIH HHS R01 CA244044NCI NIH HHS R01 CA244179NCI NIH HHS R01 CA247707NCI NIH HHS R01 CA283396U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA186238U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA237286U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA244044U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA244179U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA244707U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA247707U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA283396
6 · The paper itself

Abstract

Leukemia, although most likely starts as a monoclonal genetic/epigenetic anomaly, is a polyclonal disease at manifestation. This polyclonal nature results from ongoing evolutionary changes in the genome/epigenome of leukemia cells to promote their survival and proliferation advantages. We discuss here how genetic and/or epigenetic aberrations alter intracellular microenvironment in individual leukemia clones and how extracellular microenvironment selects the best fitted clones. This dynamic polyclonal composition of leukemia makes designing an effective therapy a challenging task especially because individual leukemia clones often display substantial differences in response to treatment. Here, we discuss novel therapeutic approach employing single cell multiomics to identify and eradicate all individual clones in a patient.

Indexed as

LeukemiaEpigenesis, GeneticHumansTumor Microenvironment

Identifiers

PMID39223295
PMCPMC11519008

What OpenQuestion holds

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LicenceCC BY
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.