Evidence map›Paper›PMID 35182376›Full record

ReviewInternational journal of hematology2022

Novel treatments for myelofibrosis: beyond JAK inhibitors.

Douglas Tremblay, Ruben Mesa

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.8field-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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases.International journal of molecular sciences · 2023
    Review
  9. 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

2 authors at 2 institutions in 1 country.

Douglas TremblayTisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Ruben MesaMays Cancer Center at UT Health San Antonio MD Anderson, Mays Family Foundation Distinguished University Presidential Chair, San Antonio, TX, USA. mesar@uthscsa.edu.ORCID http://orcid.org/0000-0001-5880-7972
Icahn School of Medicine at Mount Sinai · USThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelofibrosis is a chronic hematologic malignancy characterized by constitutional symptoms, bone marrow fibrosis, extramedullary hematopoiesis resulting in splenomegaly and a propensity toward leukemic progression. Given the central role of the JAK-STAT pathway in the pathobiology of myelofibrosis, JAK inhibitors are the mainstay of current pharmacologic management. Although these therapies have produced meaningful improvements in splenomegaly and symptom burden, JAK inhibitors do not significantly impact disease progression. In addition, many patients are ineligible because of disease-related cytopenias, which are exacerbated by JAK inhibitors. Therefore, there is a continued effort to identify targets outside the JAK-STAT pathway. In this review, we discuss novel therapies in development for myelofibrosis. We focus on the preclinical rationale, efficacy and safety data for non-JAK inhibitor therapies that have published or presented clinical data. Specifically, we discuss agents that target epigenetic modification (pelabresib, bomedemstat), apoptosis (navitoclax, navtemdalin), signaling pathways (parsaclisib), bone marrow fibrosis (AVID200, PRM-151), in addition to other targets including telomerase (imetelstat), selective inhibitor of nuclear transport (selinexor), CD123 (tagraxofusp) and erythroid maturation (luspatercept). We end by providing commentary on the ongoing and future therapeutic development in myelofibrosis.

Indexed as

Janus Kinase InhibitorsPrimary MyelofibrosisHumansJanus KinasesProtein Kinase InhibitorsSignal TransductionSplenomegalySTAT Transcription FactorsJanus Kinase InhibitorsJanus KinasesProtein Kinase InhibitorsSTAT Transcription FactorsBCL-2/xLBETCD123LSD1MDM2MyelofibrosisPI3KPRM-151SINETelomeraseTGFb

Identifiers

PMID35182376
OpenAlexW4213041869

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.