Evidence map›Paper›PMID 35896960›Full record

ArticleClinical proteomics2022

Proteomic and phosphoproteomic measurements enhance ability to predict ex vivo drug response in AML.

Sara J C Gosline, Cristina Tognon, Michael Nestor, Sunil Joshi, Rucha Modak, Alisa Damnernsawad, Camilo Posso, Jamie Moon, Joshua R Hansen, Chelsea Hutchinson-Bunch and 10 more

Open access · goldAbstract read
In one paragraph

Article in Clinical proteomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  9. HighOpen medicine (Warsaw, Poland) · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Role of Biomarkers in the Management of Acute Myeloid Leukemia.International journal of molecular sciences · 2022
    Review
  14. Review
  15. 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

20 authors at 3 institutions in 2 countries.

Sara J C GoslinePacific Northwest National Laboratory, Seattle, WA, USA.
Cristina TognonKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Michael NestorPacific Northwest National Laboratory, Seattle, WA, USA.
Sunil JoshiKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Rucha ModakKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Alisa DamnernsawadKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Camilo PossoPacific Northwest National Laboratory, Seattle, WA, USA.
Jamie MoonPacific Northwest National Laboratory, Seattle, WA, USA.
Joshua R HansenPacific Northwest National Laboratory, Seattle, WA, USA.
Chelsea Hutchinson-BunchPacific Northwest National Laboratory, Seattle, WA, USA.
James C PinoPacific Northwest National Laboratory, Seattle, WA, USA.
Marina A GritsenkoPacific Northwest National Laboratory, Seattle, WA, USA.
Karl K WeitzPacific Northwest National Laboratory, Seattle, WA, USA.
Elie TraerKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Jeffrey TynerKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Brian DrukerKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Anupriya AgarwalKnight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Paul PiehowskiPacific Northwest National Laboratory, Seattle, WA, USA.
Jason E McDermottPacific Northwest National Laboratory, Seattle, WA, USA.
Karin RodlandPacific Northwest National Laboratory, Seattle, WA, USA. Karin.rodland@pnnl.gov.
Pacific Northwest National Laboratory · USOregon Health & Science University · USMahidol University · TH

Funding

Tumor Intrinsic and Microenvironmental Mechanisms Driving Drug Combination Efficacy and Resistance in AMLU54CA224019 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Tothu Q Vu · 2017 to 2026
$13.9M
Proteogenomic Translational Research Center for Clinical ProteomicU01CA214116 · NCI · BATTELLE PACIFIC NORTHWEST LABORATORIES · PI DRUKER, BRIAN J, RODLAND, KARIN D · 2017 to 2021
$6.8M
PNNL Proteome Characterization CenterU24CA210955 · NCI · BATTELLE PACIFIC NORTHWEST LABORATORIES · PI LIU, TAO, SMITH, RICHARD D · 2016 to 2020
$5.3M
Studying drug resistance in AML and PDAC using a novel heterotypic 3D organoid modelR01CA229875 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI AGARWAL, ANUPRIYA · 2019 to 2023
$1.6M
Defining the stromal landscape that sustains AML drug resistanceF30CA239335 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI JOSHI, SUNIL KUMAR · 2019 to 2022
$187k
NCI NIH HHS R01 CA229875NCI NIH HHS U01 CA214116NCI NIH HHS U01CA214116NCI NIH HHS U24 CA210955NCI NIH HHS U54 CA224019
6 · The paper itself

Abstract

Acute Myeloid Leukemia (AML) affects 20,000 patients in the US annually with a five-year survival rate of approximately 25%. One reason for the low survival rate is the high prevalence of clonal evolution that gives rise to heterogeneous sub-populations of leukemic cells with diverse mutation spectra, which eventually leads to disease relapse. This genetic heterogeneity drives the activation of complex signaling pathways that is reflected at the protein level. This diversity makes it difficult to treat AML with targeted therapy, requiring custom patient treatment protocols tailored to each individual's leukemia. Toward this end, the Beat AML research program prospectively collected genomic and transcriptomic data from over 1000 AML patients and carried out ex vivo drug sensitivity assays to identify genomic signatures that could predict patient-specific drug responses. However, there are inherent weaknesses in using only genetic and transcriptomic measurements as surrogates of drug response, particularly the absence of direct information about phosphorylation-mediated signal transduction. As a member of the Clinical Proteomic Tumor Analysis Consortium, we have extended the molecular characterization of this cohort by collecting proteomic and phosphoproteomic measurements from a subset of these patient samples (38 in total) to evaluate the hypothesis that proteomic signatures can improve the ability to predict response to 26 drugs in AML ex vivo samples. In this work we describe our systematic, multi-omic approach to evaluate proteomic signatures of drug response and compare protein levels to other markers of drug response such as mutational patterns. We explore the nuances of this approach using two drugs that target key pathways activated in AML: quizartinib (FLT3) and trametinib (Ras/MEK), and show how patient-derived signatures can be interpreted biologically and validated in cell lines. In conclusion, this pilot study demonstrates strong promise for proteomics-based patient stratification to assess drug sensitivity in AML.

Identifiers

PMID35896960
PMCPMC9327422
OpenAlexW4288726916

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Registered trials

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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.