ArticleDiscover oncology2026
Molecular characterization and improved risk stratification of myelodysplastic syndromes with bone marrow fibrosis through integration of TP53 and MPL mutations.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Myelodysplastic syndromes with moderate-to-severe bone marrow fibrosis (MDS-F) represent a distinct entity with poor prognosis, yet their molecular landscape and precise risk stratification remain poorly defined. This study aimed to characterize the genetic landscape of MDS-F and develop an integrated prognostic model. In this study, clinical and genetic data from 102 treatment-naïve MDS patients with moderate to severe marrow fibrosis (MF-2 and MF-3) were analyzed retrospectively. The cohort comprised 63 MF-2 and 39 MF-3 cases showing comparable clinical characteristics and survival outcomes. Targeted next-generation sequencing of 29 myeloid-associated genes demonstrated distinct mutational patterns: 19.6% harbored TP53 mutations, while 19.6% exhibited JAK-STAT pathway mutations (JAK2: 9.8%, MPL:7.8%, CALR: 2%). Notably, patients with JAK-STAT mutations displayed superior clinical outcomes compared to wild-type counterparts, with the favorable prognostic impact appearing to be primarily driven by MPL mutations (median OS: not reached vs. 24 months, p = 0.004). In the univariate analysis, age, IPSS-R score, as well as TP53, IDH1/2 and MPL mutations were evidently linked with overall survival (OS) and leukemia-free survival (LFS). Of these factors, only IPSS-R score, TP53 mutations and MPL mutations retained independent prognostic significance in the multivariate analysis (p < 0.05). By incorporating IPSS-R and genetic mutations, we generated a novel prognostic model that improved risk stratification, delineating four distinct survival trajectories (median OS: not reached vs. 40 vs. 26 vs. 11 months, log-rank test p < 0.001). In conclusion, MDS patients with MF had specific genetic lesions. The integration of mutational profiling, including the potentially favorable impact of MPL mutations, with conventional scoring systems enables refined prognostic assessment and warrants further validation to guide risk-adapted therapeutic strategies.
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.