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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

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What biologic factors predict for transformation to AML?

¹UC San Diego Moores Cancer Center, 3855 Health Sciences Drive, San Diego, CA, 92093, USA.

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|November 24, 2018

Summary

Myelodysplastic syndromes (MDS) transformation to secondary acute myeloid leukemia (sAML) may be better defined by biological changes than blast percentage. Genetic markers and gene expression profiles can identify MDS patients at high risk for sAML transformation.

Keywords:

Clonal evolution Clonal expansion Clonal hematopoiesis Gene expression Growth signaling pathways MDS Mutations Myelodysplastic syndromes Progression Secondary acute myeloid leukemia Signature Transformation sAML

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Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Transformation of myelodysplastic syndromes (MDS) to secondary acute myeloid leukemia (sAML) is currently defined by an arbitrary threshold of ≥20% bone marrow blasts.
This definition may not accurately reflect the biological transition, with a clearer distinction existing between MDS with isolated bone marrow failure and those with excess blasts.

Purpose of the Study:

To propose a more biologically relevant subtyping of MDS.
To identify predictors of transformation from MDS to sAML.
To improve risk stratification for MDS patients.

Main Methods:

Analysis of clonal evolution and somatic mutations (variant allele frequencies).
Identification of genetic abnormalities including gene mutations (NRAS, KRAS, PTPN11, FLT3, NPM1, WT1, IDH2) and cytogenetic abnormalities (monosomy 7, complex karyotype, loss of 17p).
Evaluation of gene expression profiles to identify subtypes associated with AML transformation risk.

Main Results:

MDS can be more accurately stratified into clonal cytopenias and oligoblastic leukemias based on dysplasia and blast percentage, respectively.
Mutations in growth signaling pathways, AML-associated genes, and specific cytogenetic abnormalities are predictors of transformation.
A progenitor gene signature subtype identified by gene expression profiles is associated with a high risk of sAML transformation.

Conclusions:

The ≥20% bone marrow blast threshold for sAML transformation is arbitrary and may not represent a true biological transition.
Subtyping MDS into clonal cytopenias and oligoblastic leukemias, using genetic and cytogenetic markers, can improve risk stratification.
Assessing specific genetic abnormalities and gene expression profiles can better identify MDS patients at high risk for transformation to sAML.