Evidence map›Paper›PMID 33322769›Full record

ReviewCancers2020

Acute Myeloid Leukemia Stem Cells: The Challenges of Phenotypic Heterogeneity.

Marlon Arnone, Martina Konantz, Pauline Hanns, Anna M Paczulla Stanger, Sarah Bertels, Parimala Sonika Godavarthy, Maximilian Christopeit, Claudia Lengerke

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
7.8field-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

39 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  19. Development and validation of an LC-MS/MS method for ruxolitinib quantification: advancing personalized therapy in hematologic malignancies.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Article
  20. Review
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

8 authors at 1 institution in 1 country.

Marlon ArnoneDepartment of Biomedicine, University of Basel and University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland.
Martina KonantzDepartment of Biomedicine, University of Basel and University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland.ORCID 0000-0002-4319-3119
Pauline HannsDepartment of Biomedicine, University of Basel and University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland.
Anna M Paczulla StangerInternal Medicine II, Hematology, Oncology, Clinical Immunology and Rheumatology, Department for Internal Medicine, University Hospital Tübingen, Otfried-Müller-Str. 10, 72076 Tübingen, Germany.
Sarah BertelsInternal Medicine II, Hematology, Oncology, Clinical Immunology and Rheumatology, Department for Internal Medicine, University Hospital Tübingen, Otfried-Müller-Str. 10, 72076 Tübingen, Germany.
Parimala Sonika GodavarthyInternal Medicine II, Hematology, Oncology, Clinical Immunology and Rheumatology, Department for Internal Medicine, University Hospital Tübingen, Otfried-Müller-Str. 10, 72076 Tübingen, Germany.
Maximilian ChristopeitInternal Medicine II, Hematology, Oncology, Clinical Immunology and Rheumatology, Department for Internal Medicine, University Hospital Tübingen, Otfried-Müller-Str. 10, 72076 Tübingen, Germany.ORCID 0000-0003-4627-0412
Claudia LengerkeDepartment of Biomedicine, University of Basel and University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland.ORCID 0000-0001-5442-2805
University of Basel · CH

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030_179239
6 · The paper itself

Abstract

Patients suffering from acute myeloid leukemia (AML) show highly heterogeneous clinical outcomes. Next to variabilities in patient-specific parameters influencing treatment decisions and outcome, this is due to differences in AML biology. In fact, different genetic drivers may transform variable cells of origin and co-exist with additional genetic lesions (e.g., as observed in clonal hematopoiesis) in a variety of leukemic (sub)clones. Moreover, AML cells are hierarchically organized and contain subpopulations of more immature cells called leukemic stem cells (LSC), which on the cellular level constitute the driver of the disease and may evolve during therapy. This genetic and hierarchical complexity results in a pronounced phenotypic variability, which is observed among AML cells of different patients as well as among the leukemic blasts of individual patients, at diagnosis and during the course of the disease. Here, we review the current knowledge on the heterogeneous landscape of AML surface markers with particular focus on those identifying LSC, and discuss why identification and targeting of this important cellular subpopulation in AML remains challenging.

Indexed as

acute myeloid leukemiacellular heterogeneityleukemic stem cellsmarkersrelapse

Identifiers

PMID33322769
PMCPMC7764578
OpenAlexW3111839605

What OpenQuestion holds

Textmetadata
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.