Evidence map›Paper›PMID 29574002›Full record

ArticleClinical lymphoma, myeloma & leukemia2018

Treatment With JAK Inhibitors in Myelofibrosis Patients Nullifies the Prognostic Impact of Unfavorable Cytogenetics.

Vincent T Ma, Philip S Boonstra, Kamal Menghrajani, Cecelia Perkins, Krisstina L Gowin, Ruben A Mesa, Jason R Gotlib, Moshe Talpaz

Open access · hybridAbstract readComparative StudyMulticenter Study
In one paragraph

Article in Clinical lymphoma, myeloma & leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 97% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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 4 institutions in 1 country.

Vincent T MaUniversity of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI. Electronic address: vma@med.umich.edu.
Philip S BoonstraDepartment of Biostatistics, University of Michigan, Ann Arbor, MI.
Kamal MenghrajaniUniversity of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI.
Cecelia PerkinsDivision of Hematology, Stanford University, Stanford, CA.
Krisstina L GowinDepartment of Hematology and Oncology, Mayo Clinic Arizona, Phoenix, AZ.
Ruben A MesaUniversity of Texas Health San Antonio Cancer Center, San Antonio, TX.
Jason R GotlibDivision of Hematology, Stanford University, Stanford, CA.
Moshe TalpazUniversity of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI.
University of Michigan–Ann Arbor · USStanford University · USMayo Clinic in Florida · USThe University of Texas Health Science Center at San Antonio · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
NCI NIH HHS P30 CA046592
6 · The paper itself

Abstract

introductionIn the era before Janus kinase (JAK) inhibitors, cytogenetic information was used to predict survival in myelofibrosis patients. However, the prognostic value of cytogenetics in the setting of JAK inhibitor therapy remains unknown. PATIENTS AND

methodsWe performed a retrospective analysis of 180 patients with bone marrow biopsy-proven myelofibrosis from 3 US academic medical centers. We fit Cox proportional hazards models for overall survival and transformation-free survival on the bases of 3 factors: JAK inhibitor therapy as a time-dependent covariate, dichotomized cytogenetic status (favorable vs. unfavorable), and statistical interaction between the two. The median follow-up time was 37.1 months.

resultsAmong patients treated with best available therapy, unfavorable cytogenetic status was associated with decreased survival (hazard ratio = 2.31; P = .025). At initiation of JAK inhibitor therapy, unfavorable cytogenetics was (nonsignificantly) associated with increased survival compared to favorable cytogenetics (hazard ratio = 0.292; P = .172). The ratio of hazard ratios was 0.126 (P = .034). These findings were similar after adjusting for standard clinical prognostic factors as well as when measured against transformation-free survival.

conclusionThe initiation of JAK inhibitor therapy appears to change the association between cytogenetics and overall survival. There was little difference in survival between treatment types in patients with favorable cytogenetics. However, the use of JAK inhibitor therapy among patients with unfavorable cytogenetics was not associated with worse survival compared to favorable cytogenetics. Our analyses suggest that initiation of JAK inhibitor therapy nullifies the negative prognostic implication of unfavorable cytogenetics established in the pre-JAK inhibitor therapy era.

Indexed as

AgedBone MarrowCytogenetic AnalysisFemaleHumansJanus Kinase InhibitorsMaleMiddle AgedPrimary MyelofibrosisPrognosisRetrospective StudiesSurvival AnalysisJanus Kinase InhibitorsDIPSSDIPSS-PlusMyeloproliferative neoplasms

Identifiers

PMID29574002
PMCPMC5927833
OpenAlexW2793394789

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Registered trials

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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.