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Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells

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Transient genomic instability drives tumorigenesis through accelerated clonal evolution.

Ofer Shoshani¹, Bjorn Bakker², Lauren de Haan^1,2

¹Ludwig Cancer Research, Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, California 92093, USA.

Genes & Development

|July 16, 2021

Summary

This summary is machine-generated.

Chromosome instability (CIN) can drive cancer by causing aneuploidy, the abnormal chromosome number. Specific chromosome gains arising from CIN are sufficient to initiate aggressive T-cell lymphomas in mice.

Keywords:

Myc Plk4 aneuploidy cancer chromosome instability p53

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Published on: September 23, 2011

Area of Science:

Genetics
Cancer Biology
Genomics

Background:

Abnormal chromosome number (aneuploidy) is a hallmark of human cancers.
The role of aneuploidy in cancer initiation and progression remains incompletely understood.
Centrosome number, regulated by polo-like kinase 4 (Plk4), is critical for chromosome stability.

Purpose of the Study:

To investigate how aneuploidy induced by chromosome instability (CIN) contributes to tumor initiation and progression.
To determine if specific aneuploidies are selected for during tumorigenesis.
To compare the outcomes of CIN induced by different mechanisms.

Main Methods:

Generation of random aneuploidies in mice via transient induction of polo-like kinase 4 (Plk4).
Assessment of tumor formation, specifically aggressive T-cell lymphomas, in mice with varying p53 gene status.
Single-cell whole-genome DNA sequencing to analyze karyotypic profiles of tumor-initiating cells and tumors.

Main Results:

Transient CIN induced by Plk4 led to aggressive T-cell lymphomas in mice with heterozygous p53 inactivation and accelerated tumor development in p53-deficient mice.
CIN increased the frequency of lymphoma-initiating cells with specific chromosome gains (trisomy of chromosomes 4, 5, 14, and 15) early in tumorigenesis.
Chronic CIN, induced by spindle assembly checkpoint inactivation, gradually trended toward a similar cancer-associated karyotypic profile.

Conclusions:

Transient CIN can generate aneuploid cells, and specific chromosome gains within these cells are sufficient to drive cancer formation.
Distinct mechanisms of CIN can converge on similar karyotypic outcomes that promote cancer development.
This study provides insights into the causal role of aneuploidy in cancer initiation and progression.