Evidence map›Paper›PMID 36181657›Full record

ReviewInternational journal of hematology2023

Chronic myeloid leukemia (CML) evolves from Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) with unexpected frequency.

Michael J Hochman, B Douglas Smith, Theodoros Karantanos, Evan M Braunstein, Ivana Gojo, Tania Jain, Michael B Streiff, Alison R Moliterno, Amy E DeZern

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Co-occurrence ofFrontiers in oncology · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Michael J HochmanDivision of Hematological Malignancies and Bone Marrow Transplantation, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, CRBI Room 3M87, Baltimore, MD, 21287-0013, USA.
B Douglas SmithDivision of Hematological Malignancies and Bone Marrow Transplantation, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, CRBI Room 3M87, Baltimore, MD, 21287-0013, USA.
Theodoros KarantanosDivision of Hematological Malignancies and Bone Marrow Transplantation, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, CRBI Room 3M87, Baltimore, MD, 21287-0013, USA.
Evan M BraunsteinDivision of Hematology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD, USA.
Ivana GojoDivision of Hematological Malignancies and Bone Marrow Transplantation, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, CRBI Room 3M87, Baltimore, MD, 21287-0013, USA.
Tania JainDivision of Hematological Malignancies and Bone Marrow Transplantation, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, CRBI Room 3M87, Baltimore, MD, 21287-0013, USA.
Michael B StreiffDivision of Hematology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD, USA.
Alison R MoliternoDivision of Hematology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD, USA.
Amy E DeZernDivision of Hematological Malignancies and Bone Marrow Transplantation, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, 1650 Orleans Street, CRBI Room 3M87, Baltimore, MD, 21287-0013, USA. adezern1@jhmi.edu.
Johns Hopkins Hospital · USJohns Hopkins University · USSidney Kimmel Comprehensive Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloproliferative neoplasms (MPN) are chronic clonal disorders characterized by overproduction of myeloid-lineage blood cells and potential risk of evolution to acute myeloid leukemia (AML). Chronic myeloid leukemia (CML) is distinct from other MPNs in that its pathophysiology stems from the BCR-ABL fusion protein of the Philadelphia chromosome (Ph +). Though there are known cases of Ph- and Ph + MPNs coexisting in a single patient, overall prevalence has never been quantified in a prospective cohort. Here, we review our center's MPN registry, which shows 0.6% of Ph- MPN patients later developed CML. This development occurred no less than 10 and up to 36 years after Ph- MPN diagnosis. This rate of chronic transformation exceeds what is expected, as the incidence of CML in the United States is 2 per 100,000 people-years. The probability of this CML case rate in an average-risk population is less than 0.001%, suggesting there are shared risk factors between Ph- and Ph + MPNs. We speculate that these risk factors may include exposures, genetic predispositions, or be inherent to disease biology. Abrupt-onset leukocytosis heralded post-MPN CML in all cases here and suggests this salient clinical feature should trigger hematologists to consider this diagnosis and perform appropriate testing.

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveMyeloproliferative DisordersChronic DiseaseHumansPhiladelphia ChromosomeProspective StudiesCancer epidemiologyChronic myeloid leukemiaJAK2Myeloproliferative neoplasms

Identifiers

PMID36181657
OpenAlexW4298326645

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.