Evidence map›Paper›PMID 35499819›Full record

ReviewCancer2022

Defining disease modification in myelofibrosis in the era of targeted therapy.

Naveen Pemmaraju, Srdan Verstovsek, Ruben Mesa, Vikas Gupta, Jacqueline S Garcia, Joseph M Scandura, Stephen T Oh, Francesco Passamonti, Konstanze Döhner, Adam J Mead

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.6field-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

45 citing papers in PubMed, 51 citations in OpenAlex.

  1. Selinexor Plus Ruxolitinib in Janus Kinase Inhibitor-Naïve Myelofibrosis: Phase III SENTRY Trial.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026
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  20. Emerging Therapeutic Approaches for Anemia in Myelofibrosis.Current hematologic malignancy reports · 2025
    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

10 authors at 9 institutions in 5 countries.

Naveen PemmarajuDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.ORCID 0000-0002-1670-6513
Srdan VerstovsekDepartment of Leukemia, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Ruben MesaUT Health San Antonio Cancer Center, San Antonio, Texas, USA.ORCID 0000-0001-5880-7972
Vikas GuptaPrincess Margaret Cancer Centre, University of Toronto, Toronto, Ontario, Canada.
Jacqueline S GarciaDana-Farber Cancer Institute, Boston, Massachusetts, USA.
Joseph M ScanduraDepartment of Medicine, Hematology-Oncology, Weill Cornell Medicine and the New York Presbyterian Hospital, New York, New York, USA.ORCID 0000-0002-9525-143X
Stephen T OhDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Francesco PassamontiDepartment of Medicine and Surgery, University of Insubria, Varese, Italy.
Konstanze DöhnerDepartment of Internal Medicine III, University Hospital, Ulm, Germany.
Adam J MeadMRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, National Institute for Health Research Oxford Biomedical Research Centre, University of Oxford, Oxford, United Kingdom.
The University of Texas MD Anderson Cancer Center · USDana-Farber Cancer Institute · USMays Cancer Center at UT Health San AntonioNational Institute for Health Research · GBNewYork–Presbyterian Hospital · USUniversity Hospital Ulm · DEUniversity of Insubria · ITUniversity of Toronto · CAWashington University in St. Louis · US

Funding

Cancer Research UK 26988Cancer Research UK 27125Cancer Research UK 27723Medical Research Council G84/6443Medical Research Council MC_UU_00016/15Medical Research Council MC_UU_12009/16Medical Research Council MR/L006340/1Medical Research Council MR/M00919X/1
6 · The paper itself

Abstract

The development of targeted therapies for the treatment of myelofibrosis highlights a unique issue in a field that has historically relied on symptom relief, rather than survival benefit or modification of disease course, as key response criteria. There is, therefore, a need to understand what constitutes disease modification of myelofibrosis to advance appropriate drug development and therapeutic pathways. Here, the authors discuss recent clinical trial data of agents in development and dissect the potential for novel end points to act as disease modifying parameters. Using the rationale garnered from latest clinical and scientific evidence, the authors propose a definition of disease modification in myelofibrosis. With improved overall survival a critical outcome, alongside the normalization of hematopoiesis and improvement in bone marrow fibrosis, there will be an increasing need for surrogate measures of survival for use in the early stages of trials. As such, the design of future clinical trials will require re-evaluation and updating to incorporate informative parameters and end points with standardized definitions and methodologies.

Indexed as

Primary MyelofibrosisDisease ProgressionHematopoiesisHumansbone marrow fibrosisdisease modificationmyelofibrosismyelofibrosis pathophysiologytargeted therapy

Identifiers

PMID35499819
PMCPMC9322520
OpenAlexW4225268854

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.