ArticleBioMed research international2014
Cytogenetic as an important tool for diagnosis and prognosis for patients with hypocellular primary myelodysplastic syndrome.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Aberrant Expression ofBioMed research international · 2019Trial
- Cytogenetic Abnormalities in Pediatric Myelodysplastic Syndrome: Insights on the Disease Biology and Impact on Leukemic Evolution.Biomedicines · 2025Article
- Association between Leukemic Evolution and Uncommon Chromosomal Alterations in Pediatric Myelodysplastic Syndrome.Mediterranean journal of hematology and infectious diseases · 2024Article
- A Novel Constitutional t(3;8)(p26;q21) andJournal of clinical medicine · 2023Article
- Clinical, Hematological, and Cytogenetic Profile of Myelodysplastic Syndromes in Adults: A Three-year Cross-sectional Study.Oman medical journal · 2023Article
- Molecular Targeted Therapy and Immunotherapy for Myelodysplastic Syndrome.International journal of molecular sciences · 2021Review
- Aberrant Methylation-Mediated Suppression of APAF1 in Myelodysplastic Syndrome.International journal of hematology-oncology and stem cell research · 2017Article
- Clinico-Pathological Spectrum and Novel Karyotypic Findings in Myelodysplastic Syndrome: Experience of Tertiary Care Center in India.Mediterranean journal of hematology and infectious diseases · 2017Article
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8 authors.
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Abstract
We analyzed cytogenetically 105 patients with hypocellular primary MDS and their clinical implications. The main chromosomal abnormalities found were del(5q)/-5, del(6q)/+6, del(7q)/-7, del(11q), and del(17p). Pediatric patients had a higher frequency of abnormal karyotypes compared with adult patients (P < 0,05). From our patients, 18% showed evolution of the disease. The chromosomal abnormalities presented in the diagnosis of patients who evolved to AML included numerical (-7, +8) and structural del(6q), del(7q), i(7q), t(7;9), i(9q), and del(11q) abnormalities and complex karyotypes. Although the frequency of evolution from hypocellular MDS to AML is low, our results suggest that some chromosomal alterations may play a critical role during this process. We applied the IPSS in our patients because this score system has been proved to be useful for predicting evolution of disease. When we considered the patients according to group 1 (intermediate-1) and group 2 (intermediate-2 and high risk), we showed that group 2 had a high association with respect to the frequency of abnormal karyotypes (P < 0,0001), evolution of disease (P < 0,0001), and mortality (P < 0,001). In fact, the cytogenetic analysis for patients with hypocellular primary MDS is an important tool for diagnosis, prognosis, in clinical decision-making and in follow-up.
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