Related Experiment Video
Updated: Jan 3, 2026

11:15
Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
Published on: September 20, 2016
24.9K
Does mutational burden add to other prognostic factors in MDS?
1Department of Hematology and Medical Oncology, Cleveland Clinic, Taussig Cancer Center, OH, USA; Center of Clinical Artificial Intelligence, Cleveland Clinic, OH, USA.
Best Practice & Research. Clinical Haematology
|November 30, 2019
Summary
Myelodysplastic syndromes (MDS) are bone marrow disorders with varied outcomes. Genomic mutations are emerging as key factors for personalized prognosis, potentially improving patient predictions.
Area of Science:
- Hematology
- Oncology
- Genetics
Background:
- Myelodysplastic syndromes (MDS) are clonal bone marrow disorders.
- Genomic abnormalities significantly influence MDS phenotype, prognosis, and progression.
- Patient outcomes in MDS are highly heterogeneous, ranging from months to years.
Purpose of the Study:
- To review the evolving landscape of prognostic models in MDS.
- To highlight the impact of somatic mutations on MDS outcomes.
- To explore the development of personalized prediction models for MDS.
Main Methods:
- Review of current literature on MDS prognostication.
- Analysis of the role of genomic mutations in MDS progression.
- Discussion of emerging personalized prediction strategies.
Main Results:
- International Prognostic Scoring System (IPSS) and its revised version (IPSS-R) are established risk stratification tools.
- Somatic mutations are increasingly recognized as critical determinants of overall survival and acute myeloid leukemia progression.
- Newer personalized models are being developed to refine MDS prognostication.
Conclusions:
- Genomic insights are transforming MDS risk stratification.
- Personalized prediction models hold promise for improved patient management and outcomes in MDS.
- The optimal integration of genomic data into prognostic frameworks is an active area of research.
Related Concept Videos
Mismatch Repair
6.2K
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...
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...
6.2K
Mismatch Repair
43.4K
Overview
43.4K
Abnormal Proliferation
5.0K
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...
5.0K
Mutations in Microorganisms
453
Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
453
Mutagenicity and Carcinogenicity
1.8K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.8K
Mutations
94.2K
Overview
94.2K

