Evidence map›Paper›PMID 29148847›Full record

ReviewExpert opinion on therapeutic targets2018

Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas.

Anna Orlova, Bettina Wingelhofer, Heidi A Neubauer, Barbara Maurer, Angelika Berger-Becvar, György Miklós Keserű, Patrick T Gunning, Peter Valent, Richard Moriggl

Open access · hybridAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  9. A RecurrentCancers · 2021
    Article
  10. STAT5 as a Key Protein of Erythropoietin Signalization.International journal of molecular sciences · 2021
    Review
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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

9 authors at 5 institutions in 3 countries.

Anna Orlovaa Institute of Animal Breeding and Genetics , University of Veterinary Medicine Vienna , Vienna , Austria.
Bettina Wingelhofera Institute of Animal Breeding and Genetics , University of Veterinary Medicine Vienna , Vienna , Austria.
Heidi A Neubauera Institute of Animal Breeding and Genetics , University of Veterinary Medicine Vienna , Vienna , Austria.
Barbara Maurerc Institute of Pharmacology and Toxicology , University of Veterinary Medicine Vienna , Vienna , Austria.
Angelika Berger-Becvarg Department of Chemical & Physical Sciences , University of Toronto Mississauga , Mississauga , Canada.
György Miklós Keserűd Medicinal Chemistry Research Group, Research Centre for Natural Sciences , Hungarian Academy of Sciences , Budapest , Hungary.
Patrick T Gunningg Department of Chemical & Physical Sciences , University of Toronto Mississauga , Mississauga , Canada.
Peter Valente Department of Internal Medicine I, Division of Hematology and Hemostaseology , Medical University of Vienna , Vienna , Austria.
Richard Moriggla Institute of Animal Breeding and Genetics , University of Veterinary Medicine Vienna , Vienna , Austria.
University of Veterinary Medicine Vienna · ATLudwig Boltzmann Institute for Cancer Research · ATUniversity of Toronto · CAHUN-REN Research Centre for Natural Sciences · HULudwig Boltzmann Cluster for Cardiovascular Research · AT

Funding

CIHR 495468CIHR 497203
6 · The paper itself

Abstract

introductionHematopoietic neoplasms are often driven by gain-of-function mutations of the JAK-STAT pathway together with mutations in chromatin remodeling and DNA damage control pathways. The interconnection between the JAK-STAT pathway, epigenetic regulation or DNA damage control is still poorly understood in cancer cell biology. Areas covered: Here, we focus on a broader description of mutational insights into myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas, since sequencing efforts have identified similar combinations of driver mutations in these diseases covering different lineages. We summarize how these pathways might be interconnected in normal or cancer cells, which have lost differentiation capacity and drive oncogene transcription. Expert opinion: Due to similarities in driver mutations including epigenetic enzymes, JAK-STAT pathway activation and mutated checkpoint control through TP53, we hypothesize that similar therapeutic approaches could be of benefit in these diseases. We give an overview of how driver mutations in these malignancies contribute to hematopoietic cancer initiation or progression, and how these pathways can be targeted with currently available tools.

Indexed as

AnimalsAntineoplastic AgentsDisease ProgressionDNA DamageEpigenesis, GeneticHumansJanus KinasesLeukemia, T-CellLymphoma, T-Cell, PeripheralMolecular Targeted TherapyMutationMyeloproliferative DisordersSTAT Transcription FactorsAntineoplastic AgentsJanus KinasesSTAT Transcription FactorsEpigenetic targethematopoietic cancerMPNmutational landscapePTCLtherapeutic target

Identifiers

PMID29148847
PMCPMC5743003
OpenAlexW2769549375

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.