Evidence map›Paper›PMID 39090734›Full record

ArticleExperimental hematology & oncology2024

1q jumping translocation as a biomarker in myeloid malignancy: frequently mutated genes associated with bad prognosis and low survival.

Eitan Halper-Stromberg, Victoria Stinnett, Laura Morsberger, Aparna Pallavajjala, Mark J Levis, Amy E DeZern, Michelle Lei, Brian Phan, Rena R Xian, Christopher D Gocke and 2 more

Abstract readLetter
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental hematology & oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. 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

12 authors.

Eitan Halper-StrombergDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
Victoria StinnettDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Laura MorsbergerDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Aparna PallavajjalaDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Mark J LevisDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Amy E DeZernDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michelle LeiDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Brian PhanDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Rena R XianDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Christopher D GockeDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Guilin TangDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, 6565 MD Anderson Blvd, Houston, TX, 77030, USA.
Ying S ZouDepartments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. yzou19@jhmi.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1q jumping translocation (JT) is rare and its molecular profiles in myeloid malignancies are not well-known. This study evaluated gene mutations in 1q-JT cohorts (0.38%) from hematological malignant specimens that underwent genetic analysis at the Johns Hopkins Hospital (n = 11,908) and the MD Anderson Cancer Center. 1q-JT had frequent mutations in eleven genes, most of which are associated with worse prognosis. BCOR mutations significantly co-occurred with others. Patients tended to have mutations in DNA-repair, spliceosome, and epigenetic modification pathways, though genes utilized within each of these pathways were not randomly distributed. Multi-, albeit overlapping, pathway interruptions tended to manifest in mutations of two gene sets. One gene set consisted of SF3B1 (spliceosome) and TET2 (epigenetic modification), while the other consisted of STAG2 (DNA repair), SRSF2, U2AF (spliceosome), ASXL1, KMT2D (epigenetic modification), BCOR, and GATA2 (transcription factors). An "intermediate" JT-like rearrangement may represent an early sign of occurring 1q-JT. Treatments (hypomethylating agents) and unique structures of the short arms of acrocentric chromosomes may contribute to 1q-JT formation in myeloid malignancies. The median overall survival after identification of a JT was 10 months (95% confidence interval, 5-15 months). Our cohort represents the largest number of myeloid malignancies from multi-centers with before and after the 1q-JT event analyzed to date. Overall, this study identified specific molecular profiles that are associated with 1q-JT in myeloid malignancies. 1q-JT could serve as a poor prognosis biomarker in myeloid malignancies, which could be important in making well-informed clinical decisions and treatment strategies.

Indexed as

1q jumping translocationGene mutationMyeloid malignancyPrognosis

Identifiers

PMID39090734
PMCPMC11295323

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