Evidence map›Paper›PMID 26933174›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2016

New Strategies in Myeloproliferative Neoplasms: The Evolving Genetic and Therapeutic Landscape.

Ami B Patel, Nadeem A Vellore, Michael W Deininger

Abstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Nuclear-Cytoplasmic Transport Is a Therapeutic Target in Myelofibrosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  8. Article
  9. 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

3 authors.

Ami B PatelUniversity of Utah Huntsman Cancer Institute, Salt Lake City, Utah.
Nadeem A VelloreUniversity of Utah Huntsman Cancer Institute, Salt Lake City, Utah.
Michael W DeiningerChief of Hematology, University of Utah Huntsman Cancer Institute, Salt Lake City, Utah. Michael.deininger@hci.utah.edu.

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI KATHARINE S ULLMAN · 1986 to 2026
$72.6M
TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SHPALL, ELIZABETH J · 1990 to 2014
$41.8M
Mechanisms of resistance to ponatinib therapy in chronic myeloid leukemiaR01CA178397 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W., O'HARE, THOMAS J. · 2014 to 2018
$2.6M
Biology of Imatinib-Resistant Mutants of BCR-ABLR01HL082978 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DEININGER, MICHAEL W. · 2005 to 2009
$1.5M
NCI NIH HHS P01 CA049639NCI NIH HHS P30 CA042014NCI NIH HHS P30CA042014NCI NIH HHS R01 CA178397NCI NIH HHS R01CA178397NHLBI NIH HHS R01 HL082978
6 · The paper itself

Abstract

The classical BCR-ABL1-negative myeloproliferative neoplasms (MPN) include essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Although these clonal disorders share certain clinical and genetic features, MF in particular is distinct for its complex mutational landscape, severe disease phenotype, and poor prognosis. The genetic complexity inherent to MF has made this disease extremely challenging to treat. Pharmacologic JAK inhibition has proven to be a transformative therapy in MPNs, alleviating symptom burden and improving survival, but has been hampered by off-target toxicities and, as monotherapy, has shown limited effects on mutant allele burden. In this review, we discuss the genetic heterogeneity contributing to the pathogenesis of MPNs, focusing on novel driver and epigenetic mutations and how they relate to combination therapeutic strategies. We discuss results from ongoing studies of new JAK inhibitors and report on new drugs and drug combinations that have demonstrated success in early preclinical and clinical trials, including type II JAK inhibitors, antifibrotic agents, and telomerase inhibitors.

Indexed as

Evolution, MolecularFusion Proteins, bcr-ablHumansJanus Kinase 2Myeloproliferative DisordersNeoplasmsPolycythemia VeraPrimary MyelofibrosisThrombocythemia, EssentialBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablJanus Kinase 2

Identifiers

PMID26933174
PMCPMC4826348

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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.