Evidence map›Paper›PMID 27252511›Full record

ReviewHaematologica2016

Bone marrow fibrosis in myelofibrosis: pathogenesis, prognosis and targeted strategies.

Abdallah Abou Zahr, Mohamed E Salama, Nicole Carreau, Douglas Tremblay, Srdan Verstovsek, Ruben Mesa, Ronald Hoffman, John Mascarenhas

Open access · goldAbstract readReview
In one paragraph

Review in Haematologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

101 citing papers in PubMed, 2 syntheses or guidelines pooled it, 186 citations in OpenAlex.

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  4. Myelofibrosis symptom assessment form total symptom score version 4.0: measurement properties from the MOMENTUM phase 3 study.Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation · 2025
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41 more citing papers are in PubMed but not listed here.

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 5 institutions in 1 country.

Abdallah Abou ZahrDivision of Hematology Oncology, Mount Sinai Beth Israel, New York, NY, USA.
Mohamed E SalamaAssociated Regional University Pathologists Laboratories, Department of Pathology, University of Utah, Salt Lake City, UT, USA.
Nicole CarreauDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Douglas TremblayDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Srdan VerstovsekDepartment of Leukemia, MD Anderson Cancer Center, Houston, TX, USA.
Ruben MesaDivision of Hematology & Medical Oncology, Mayo Clinic Cancer Center, Scottsdale, AZ, USA.
Ronald HoffmanTisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
John MascarenhasTisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA john.mascarenhas@mssm.edu.
Icahn School of Medicine at Mount Sinai · USMayo Clinic in Arizona · USMount Sinai Beth Israel · USThe University of Texas MD Anderson Cancer Center · USUniversity of Utah · US

Funding

Tissue BankP01CA108671 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Ronald Hoffman · 2006 to 2026
$82.0M
NCI NIH HHS P01 CA108671
6 · The paper itself

Abstract

Bone marrow fibrosis is a central pathological feature and World Health Organization major diagnostic criterion of myelofibrosis. Although bone marrow fibrosis is seen in a variety of malignant and non-malignant disease states, the deposition of reticulin and collagen fibrosis in the bone marrow of patients with myelofibrosis is believed to be mediated by the myelofibrosis hematopoietic stem/progenitor cell, contributing to an impaired microenvironment favoring malignant over normal hematopoiesis. Increased expression of inflammatory cytokines, lysyl oxidase, transforming growth factor-β, impaired megakaryocyte function, and aberrant JAK-STAT signaling have all been implicated in the pathogenesis of bone marrow fibrosis. A number of studies indicate that bone marrow fibrosis is an adverse prognostic variable in myeloproliferative neoplasms. However, modern myelofibrosis prognostication systems utilized in risk-adapted treatment approaches do not include bone marrow fibrosis as a prognostic variable. The specific effect on bone marrow fibrosis of JAK2 inhibition, and other rationally based therapies currently being evaluated in myelofibrosis, has yet to be fully elucidated. Hematopoietic stem cell transplantation remains the only curative therapeutic approach that reliably results in resolution of bone marrow fibrosis in patients with myelofibrosis. Here we review the pathogenesis, biological consequences, and prognostic impact of bone marrow fibrosis. We discuss the rationale of various anti-fibrogenic treatment strategies targeting the clonal hematopoietic stem/progenitor cell, aberrant signaling pathways, fibrogenic cytokines, and the tumor microenvironment.

Indexed as

AnimalsBone MarrowBone Marrow CellsCell Transformation, NeoplasticCellular MicroenvironmentDisease ProgressionGenetic Predisposition to DiseaseHumansMolecular Targeted TherapyPrimary MyelofibrosisPrognosisSeverity of Illness Index

Identifiers

PMID27252511
PMCPMC5013940
OpenAlexW2416281109

What OpenQuestion holds

Textmetadata
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.