ReviewOncogene2025
Chromosomal abnormalities of mesenchymal stromal cells in hematological malignancies.
Review in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- An integrated AI pipeline for automated cytogenetic analysis of bone marrow karyograms in hematological malignancies: A Pix2Pix enhancement and deep learning detection approach.Journal of pathology informatics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Historically, hematological malignancies (HMs) and solid cancers were primarily attributed to cell-intrinsic mechanisms. However, overwhelming evidence highlights the crucial role of the tumor microenvironment in this process. Abnormalities in the bone marrow microenvironment (BMM) contribute to the development of HMs and affect patient outcomes. Bone Marrow Mesenchymal Stromal Cells (BM-MSCs) represent one of the key cell types within the BMM. Interestingly, a single specific gene mutation in BM-MSCs is sufficient to disrupt normal hematopoiesis and promote clonal malignant hematopoiesis in mice. Since a particular mutation may be sufficient, attention must also be given to chromosomal abnormalities (CAs), potentially affecting hundreds of genes. Notably, CAs have been identified in the majority of HMs BM-MSCs. CAs have been detected more frequently in BM-MSCs of HMs patients than in healthy donors. The primary explanation for CAs is chromosomal instability (CIN), a phenomenon characterized by increased rates of CAs. CIN can lead to abnormal gene expression, cellular senescence, and inflammation, altering MSCs. It may compromise their anti-tumorigenic functions and shift the BMM towards a supportive or protective state. Despite the importance of CAs and CIN, cytogenetic results in HM-MSCs appear controversial. This review discusses current studies, suggesting that some of the controversies may result from technical limitations. Furthermore, based on the high incidence of CAs and the lack of patterns (randomness), we suggest this is a case of CIN. Therefore, instead of looking for CAs patterns, we must focus on understanding the phenomenon of CIN in these cells. This includes verifying the frequencies of non-clonal CAs, looking for specific CIN mechanisms and distinguishing whether CIN is a driver or a consequence of HMs. To guide future research and address the existing knowledge gaps, we discuss potential approaches to the challenges in studying CAs in HM-MSCs.
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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.