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Related Concept Videos

Karyotyping01:17

Karyotyping

Overview
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Meiosis vs. Mitosis02:57

Meiosis vs. Mitosis

Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is...
Nondisjunction01:29

Nondisjunction

During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...

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Updated: May 10, 2026

Use of Hematopoietic Stem Cell Transplantation to Assess the Origin of Myelodysplastic Syndrome
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Published on: October 3, 2018

Monosomal karyotype in MDS: explaining the poor prognosis?

J Schanz1, H Tüchler, F Solé

  • 1Department of Hematology and Oncology, University of Göttingen, Göttingen, Germany.

Leukemia
|June 22, 2013
PubMed
Summary

Monosomal karyotype (MK) impacts myelodysplastic syndromes (MDS) survival, but only when fewer than five abnormalities are present. High numbers of complex abnormalities, not MK alone, predict the worst prognosis in MDS patients.

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Area of Science:

  • Hematology
  • Clinical Genetics
  • Oncology

Background:

  • Monosomal karyotype (MK) is a known adverse prognostic factor in acute myeloid leukemia (AML).
  • The prognostic significance of MK in myelodysplastic syndromes (MDS) requires further investigation.
  • Understanding prognostic markers is crucial for tailoring MDS treatment strategies.

Purpose of the Study:

  • To evaluate the prognostic impact of monosomal karyotype (MK) in a cohort of primary, untreated myelodysplastic syndromes (MDS) patients.
  • To determine if MK is an independent prognostic marker for overall survival (OS) and AML-free survival in MDS.
  • To explore the interaction between MK and the number of chromosomal abnormalities in predicting MDS outcomes.

Main Methods:

  • Analysis of cytogenetic and clinical data from 431 primary, untreated MDS patients from an international database.
  • Univariate and multivariate regression models were used to assess overall survival (OS) and AML-free survival.
  • Patients were stratified based on the presence of MK and the number of chromosomal abnormalities.

Main Results:

  • Monosomal karyotype (MK) was identified in 47.3% of MDS patients.
  • MK showed prognostic significance for OS only in patients with four or fewer chromosomal abnormalities.
  • In patients with five or more abnormalities, MK did not differentiate prognostic subgroups (median OS 4.9 months vs. 5.6 months).
  • MK-positive karyotypes with increasing numbers of abnormalities showed decreasing OS (e.g., 2 abnormalities: 13.4 months; ≥5 abnormalities: 4.9 months).
  • Multivariate analysis indicated that MK was not an independent prognostic factor in MDS.

Conclusions:

  • The number of complex chromosomal abnormalities, rather than monosomal karyotype (MK) alone, is a critical determinant of poor prognosis in myelodysplastic syndromes (MDS).
  • An unstable clone, suggested by a high number of abnormalities, defines the subgroup with the worst survival outcomes in MDS.
  • MK's prognostic value in MDS is context-dependent, particularly influenced by the total number of chromosomal aberrations.