ArticleClinical epigenetics2022
Identification of clinical implications and potential prognostic models of chromatin regulator mutations in multiple myeloma.
Article in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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.
Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- A positive feedback loop between YTHDC1 and EP300 drives multiple myeloma tumorigenesis.Oncogene · 2026Article
- Decreased Expression of FAT4 Promotes Multiple Myeloma Proliferation and Migration by Targeting the Hippo/YAP Pathway.Cancer science · 2026Article
- High diffuse bone marrow uptake in 18F-FDG PET/CT may reflect the diverse mutational characteristics of multiple myeloma.The Korean journal of internal medicine · 2026Article
- Genome-wide copy number profiling enhances risk stratification in multiple myeloma by shallow whole-genome sequencing.Blood advances · 2026Article
- Leveraging a disulfidptosis-based signature to characterize heterogeneity and optimize treatment in multiple myeloma.Frontiers in immunology · 2025Article
- Construction of a Clinical Prediction Model for Complications After Femoral Head Replacement Surgery.Journal of clinical medicine research · 2024Article
- The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies.Cancers · 2023Review
- High-risk multiple myeloma predicted by circulating plasma cells and its genetic characteristics.Frontiers in oncology · 2023Article
- Molecular Crosstalk between Chromatin Remodeling and Tumor Microenvironment in Multiple Myeloma.Current oncology (Toronto, Ont.) · 2022Review
- Integrated single-cell and transcriptome sequencing analyses determines a chromatin regulator-based signature for evaluating prognosis in lung adenocarcinoma.Frontiers in oncology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWith the rapid development of next-generation sequencing (NGS) technologies, researchers are making efforts to reveal the genomic landscape of multiple myeloma (MM). However, the clinical significance of many mutations remains poorly defined due to the genetic heterogeneity of MM. To systematically explore the clinical implications of gene mutations and build practical prognostic models, we performed DNA sequencing in newly diagnosed MM patients.
methodsMM cells were purified from bone marrow aspirates using CD138 microbeads and subjected to sequencing with a 387-gene Panel. Nomogram was developed using Cox's proportional hazards model, and candidate variables were screened by stepwise regression. Internal validation was carried out by the bootstrap method.
resultsBetween July 2016 and December 2020, a total of 147 patients were included in our study. We found patients with a higher mutational load had a significantly shorter progress-free survival (PFS) (19.0 vs. 32.0 months, P = 0.0098) and overall survival (OS) (3-year OS rates were 66.1% and 80.0%, P = 0.0290). Mutations in chromatin regulators (CRs) including KMT2C (14.3%), KMT2D (14.3%), EP300 (11.6%) and ARID gene family (31.3%) were highly frequent in newly diagnosed MM patients. Interestingly, proteins encoded by these genes could form a complex called KMT2C/D COMPASS (K
conclusionOur findings emphasized the importance of CRs mutations in newly diagnosed MM patients and indicated the mutations affecting K
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.