Genomic and Functional Approaches to Understanding Cancer Aneuploidy
2018
- Alison M. Taylor
- Juliann Shih
- Gavin Ha
- Galen F. Gao
- Xiaoyang Zhang
- Ashton C. Berger
- Steven E. Schumacher
- Chen Wang
- Hai Hu
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- John A. Demchok
- Ina Felau
- Melpomeni Kasapi
- Martin L. Ferguson
- Carolyn M. Hutter
- Heidi J. Sofia
- Roy Tarnuzzer
- Zhining Wang
- Liming Yang
- Jean C. Zenklusen
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- Rashi Naresh
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- Eva Giné
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- Nguyen Van Bang
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- Therese Bocklage
- Lisa M. Landrum
- Robert S. Mannel
- Kathleen N. Moore
- Katherine Moxley
- Russel Postier
- Joan L. Walker
- Rosemary Zuna
- Michael Feldman
- Federico Valdivieso
- Rajiv Dhir
- James D. Luketich
- Edna M. Mora Pinero
- Mario Quintero-Aguilo
- Carlos Gilberto Carlotti
- José Sebastião dos Santos
- Rafael Kemp
- Ajith Sankarankuty
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- Eryn M. Godwin
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- Laura S. Rozek
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- Rayleen Bowman
- Kwun M. Fong
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- Robert Korst
- W. Kimryn Rathmell
- J. Leigh Fantacone-Campbell
- Jeffrey A. Hooke
- Albert J. Kovatich
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- John F. DiPersio
- Bettina F. Drake
- Ramaswamy Govindan
- Sharon Heath
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- Brian A. Van Tine
- Peter Westervelt
- Mark A. Rubin
- Jung-Il Lee
- Natália D. Aredes
- Armaz Mariamidze
Summary Aneuploidy, whole chromosome or chromosome arm imbalance, is a near-universal characteristic of human cancers. In 10,522 cancer genomes from The Cancer Genome Atlas, aneuploidy was correlated with TP53 mutation, somatic mutation rate, and expression of proliferation genes. Aneuploidy was anti-correlated with expression of immune signaling genes, due to decreased leukocyte infiltrates in high-aneuploidy samples. Chromosome arm-level alterations show cancer-specific patterns, including loss of chromosome arm 3p in squamous cancers. We applied genome engineering to delete 3p in lung cells, causing decreased proliferation rescued in part by chromosome 3 duplication. This study defines genomic and phenotypic correlates of cancer aneuploidy and provides an experimental approach to study chromosome arm aneuploidy.
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