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Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

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A Combinatorial Single-cell Approach to Characterize the Molecular and Immunophenotypic Heterogeneity of Human Stem and Progenitor Populations

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Published on: October 25, 2018

Single-cell DNA sequencing reveals pervasive positive selection throughout preleukemic evolution.

Gladys Poon¹, Aditi Vedi², Mathijs Sanders³

¹Early Cancer Institute, University of Cambridge, Cambridge, UK.

|January 22, 2025

Summary

This summary is machine-generated.

Understanding driver mutations in preleukemic hematopoietic stem cells (pHSCs) reveals acute myeloid leukemia (AML) evolution. Identifying early multiple-mutant clones can predict AML risk due to positive selection.

Keywords:

acute myeloid leukemia cancer evolution clonal hematopoiesis early detection evolutionary dynamics pre-cancer somatic mutation

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Published on: December 28, 2015

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VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

Published on: December 28, 2015

Area of Science:

Hematology
Cancer Genomics
Evolutionary Biology

Background:

Driver mutations in preleukemic hematopoietic stem cells (pHSCs) offer insights into the somatic evolution preceding acute myeloid leukemia (AML).
Understanding this evolutionary process is crucial for early detection and intervention strategies.

Purpose of the Study:

To reconstruct phylogenetic trees of driver clones in pHSCs from AML patients.
To develop a computational framework for inferring positive selection during preleukemic evolution.
To assess the potential of identifying early multiple-mutant clones for AML risk prediction.

Main Methods:

Isolation of pHSCs from 16 AML patients.
Single-cell DNA sequencing of thousands of cells per patient.
Development of a computational framework to analyze phylogenetic tree properties and infer positive selection.
Integration of data with 67 previously published phylogenetic trees.

Main Results:

Reconstruction of major driver clone phylogenetic trees from patient pHSCs.
Demonstration that preleukemic tree structures arise from a simple somatic evolution model with pervasive positive selection (9%-24% per year).
Validation that identifying early multiple-mutant clones can predict future AML risk.

Conclusions:

Somatic evolution in preleukemia is characterized by pervasive positive selection.
The variability in preleukemic phylogenetic trees can be explained by a model of positive selection.
Early detection of multiple-mutant clones in pHSCs is a promising biomarker for AML risk stratification.