Evidence map›Paper›PMID 26091827›Full record

ArticleCancer discovery2015

Mass Cytometric Functional Profiling of Acute Myeloid Leukemia Defines Cell-Cycle and Immunophenotypic Properties That Correlate with Known Responses to Therapy.

Gregory K Behbehani, Nikolay Samusik, Zach B Bjornson, Wendy J Fantl, Bruno C Medeiros, Garry P Nolan

Open access · greenAbstract read
In one paragraph

Article in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.1field-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

57 citing papers in PubMed, 104 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Gregory K BehbehaniBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California. Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California. Stanford Cancer Institute, Stanford, California.
Nikolay SamusikBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California.
Zach B BjornsonBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California.
Wendy J FantlBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California. Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, California.
Bruno C MedeirosDivision of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California. Stanford Cancer Institute, Stanford, California.
Garry P NolanBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California. gnolan@stanford.edu.
Stanford University · USCancer Prevention Institute of California · USStanford Medicine · US

Funding

Using a tonsil organoid system to probe conditions for the induction of protective antibody and T cell responses to influenza.U19AI057229 · NIAID · STANFORD UNIVERSITY · PI Mark Morris Davis · 2003 to 2026
$88.5M
Systems Biology CoreU19AI100627 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NOLAN, GARRY P · 2012 to 2021
$49.1M
TRIGGERING CELL DEATH IN B CELL LYMPHOMAP01CA034233 · NCI · STANFORD UNIVERSITY · PI LEVY, RONALD · 1985 to 2010
$19.5M
Small Animal ImagingP50CA114747 · NCI · STANFORD UNIVERSITY · PI CONTAG, CHRISTOPHER H · 2005 to 2014
$18.2M
TRANS-NETWORK PROJECTSU54CA143907 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HILLIS, WILLIAM DANIEL · 2009 to 2013
$15.2M
MODELING THE ROLE OF PROGRESSION IN FOLLICULAR LYMPHOMAU54CA149145 · NCI · STANFORD UNIVERSITY · PI PLEVRITIS, SYLVIA KATINA · 2010 to 2014
$12.1M
Software & Hardware Inference Engines for Automated Determination of Primary CellR01CA130826 · NCI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2008 to 2011
$6.7M
(PQD2)New Biomarkers and Pathways to Enhance Cure in Ovarian CancersR01CA184968 · NCI · STANFORD UNIVERSITY · PI FANTL, WENDY JANE, SIKIC, BRANIMIR I · 2014 to 2017
$2.0M
MicroRNAs as T cell sensitivity RheostatsR01AI073724 · NIAID · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2009 to 2013
$2.0M
Mass Cytometry Analysis of Signaling Dysfunction in Duchenne Muscular DystrophyR01NS089533 · NINDS · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2014 to 2017
$1.3M
Multivariate statistical methods, flow cytometry, and network modeling.R01GM109836 · NIGMS · STANFORD UNIVERSITY · PI WONG, WING H. · 2014 to 2017
$1.2M
Highly multiplexed ion-beam tissue molecular imaging with sub-micron resolutionR33CA183654 · NCI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2014 to 2016
$1.2M
NCI NIH HHS 1R01CA130826NCI NIH HHS 5U54CA143907NCI NIH HHS P01 CA034233NCI NIH HHS P50 CA114747NCI NIH HHS R01 CA130826NCI NIH HHS R01 CA184968NCI NIH HHS R01CA184968NCI NIH HHS R33 CA183654NCI NIH HHS R33 CA183692NCI NIH HHS U54 CA143907NCI NIH HHS U54 CA149145NCRR NIH HHS S10 RR027582NHLBI NIH HHS HHSN268201000034CNHLBI NIH HHS N01-HV-00242NHLBI NIH HHS N01 HV028183NIAID NIH HHS 1U19AI100627NIAID NIH HHS 5R01AI073724NIAID NIH HHS HHSN272200700038CNIAID NIH HHS HHSN272201200028CNIAID NIH HHS R01 AI073724NIAID NIH HHS U19 AI057229NIAID NIH HHS U19 AI100627NIGMS NIH HHS R01 GM109836NIH HHS S10 OD016318NINDS NIH HHS 1R01NS089533NINDS NIH HHS R01 NS089533
6 · The paper itself

Abstract

unlabelledAcute myeloid leukemia (AML) is characterized by a high relapse rate that has been attributed to the quiescence of leukemia stem cells (LSC), which renders them resistant to chemotherapy. However, this hypothesis is largely supported by indirect evidence and fails to explain the large differences in relapse rates across AML subtypes. To address this, bone marrow aspirates from 41 AML patients and five healthy donors were analyzed by high-dimensional mass cytometry. All patients displayed immunophenotypic and intracellular signaling abnormalities within CD34(+)CD38(lo) populations, and several karyotype- and genotype-specific surface marker patterns were identified. The immunophenotypic stem and early progenitor cell populations from patients with clinically favorable core-binding factor AML demonstrated a 5-fold higher fraction of cells in S-phase compared with other AML samples. Conversely, LSCs in less clinically favorable FLT3-ITD AML exhibited dramatic reductions in S-phase fraction. Mass cytometry also allowed direct observation of the in vivo effects of cytotoxic chemotherapy. SIGNIFICANCE: The mechanisms underlying differences in relapse rates across AML subtypes are poorly understood. This study suggests that known chemotherapy sensitivities of common AML subsets are mediated by cell-cycle differences among LSCs and provides a basis for using in vivo functional characterization of AML cells to inform therapy selection.

Indexed as

Cell CyclePhenotypeAntineoplastic Combined Chemotherapy ProtocolsBiomarkersBone Marrow CellsBone Marrow ExaminationCluster AnalysisFlow CytometryGenotypeHumansImmunophenotypingKaryotypeLeukemia, Myeloid, AcuteNeoplastic Stem CellsReproducibility of ResultsTreatment OutcomeBiomarkers

Identifiers

PMID26091827
PMCPMC4652947
OpenAlexW2123798150

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.