Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

Koei Chin; Sandy DeVries; Jane Fridlyand; Paul T. Spellman; Ritu Roydasgupta; Wen Lin Kuo; Anna Lapuk; Richard M. Neve; Zuwei Qian; Tom Ryder; Fanqing Chen; Heidi Feiler; Taku Tokuyasu; Chris Kingsley; Shanaz Dairkee; Zhenhang Meng; Karen Chew; Daniel Pinkel; Ajay Jain; Britt Marie Ljung; Laura Esserman; Donna G. Albertson; Frederic M. Waldman; Joe W. Gray

doi:10.1016/j.ccr.2006.10.009

Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

Koei Chin
, Sandy DeVries
, Jane Fridlyand
, Paul T. Spellman
, Ritu Roydasgupta
, Wen Lin Kuo
, Anna Lapuk
, Richard M. Neve
, Zuwei Qian
, Tom Ryder
, Fanqing Chen
, Heidi Feiler
, Taku Tokuyasu
, Chris Kingsley
, Shanaz Dairkee
, Zhenhang Meng
, Karen Chew
, Daniel Pinkel
, Ajay Jain
, Britt Marie Ljung

Laura Esserman, Donna G. Albertson, Frederic M. Waldman, Joe W. Gray

Research output: Contribution to journal › Article › peer-review

1103 Scopus citations

Abstract

This study explores the roles of genome copy number abnormalities (CNAs) in breast cancer pathophysiology by identifying associations between recurrent CNAs, gene expression, and clinical outcome in a set of aggressively treated early-stage breast tumors. It shows that the recurrent CNAs differ between tumor subtypes defined by expression pattern and that stratification of patients according to outcome can be improved by measuring both expression and copy number, especially high-level amplification. Sixty-six genes deregulated by the high-level amplifications are potential therapeutic targets. Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism.

Original language	English (US)
Pages (from-to)	529-541
Number of pages	13
Journal	Cancer Cell
Volume	10
Issue number	6
DOIs	https://doi.org/10.1016/j.ccr.2006.10.009
State	Published - Dec 2006
Externally published	Yes

Funding

This work was supported by the NIH (CA58207, CA90421, and CA101359), the Office of Health and Environmental Research of the U.S. Department of Energy (contract DE-AC03-76SF00098), and the Avon Foundation. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. For full disclaimer, see http://www-library.lbl.gov/public/tmRco/howto/RcoBerkeleyLabDisclaimer.htm .

Funders	Funder number
Office of Health and Environmental Research
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	CA58207, CA101359
U.S. Department of Energy	DE-AC03-76SF00098
National Institute of Health-National Cancer Institute	R01CA090421
Avon Foundation for Women

Keywords

CELLCYCLE
HUMDISEASE

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

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10.1016/j.ccr.2006.10.009

Cite this

Chin, K., DeVries, S., Fridlyand, J., Spellman, P. T., Roydasgupta, R., Kuo, W. L., Lapuk, A., Neve, R. M., Qian, Z., Ryder, T., Chen, F., Feiler, H., Tokuyasu, T., Kingsley, C., Dairkee, S., Meng, Z., Chew, K., Pinkel, D., Jain, A., ... Gray, J. W. (2006). Genomic and transcriptional aberrations linked to breast cancer pathophysiologies. Cancer Cell, 10(6), 529-541. https://doi.org/10.1016/j.ccr.2006.10.009

Chin, K, DeVries, S, Fridlyand, J, Spellman, PT, Roydasgupta, R, Kuo, WL, Lapuk, A, Neve, RM, Qian, Z, Ryder, T, Chen, F, Feiler, H, Tokuyasu, T, Kingsley, C, Dairkee, S, Meng, Z, Chew, K, Pinkel, D, Jain, A, Ljung, BM, Esserman, L, Albertson, DG, Waldman, FM & Gray, JW 2006, 'Genomic and transcriptional aberrations linked to breast cancer pathophysiologies', Cancer Cell, vol. 10, no. 6, pp. 529-541. https://doi.org/10.1016/j.ccr.2006.10.009

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title = "Genomic and transcriptional aberrations linked to breast cancer pathophysiologies",

abstract = "This study explores the roles of genome copy number abnormalities (CNAs) in breast cancer pathophysiology by identifying associations between recurrent CNAs, gene expression, and clinical outcome in a set of aggressively treated early-stage breast tumors. It shows that the recurrent CNAs differ between tumor subtypes defined by expression pattern and that stratification of patients according to outcome can be improved by measuring both expression and copy number, especially high-level amplification. Sixty-six genes deregulated by the high-level amplifications are potential therapeutic targets. Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism.",

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author = "Koei Chin and Sandy DeVries and Jane Fridlyand and Spellman, \{Paul T.\} and Ritu Roydasgupta and Kuo, \{Wen Lin\} and Anna Lapuk and Neve, \{Richard M.\} and Zuwei Qian and Tom Ryder and Fanqing Chen and Heidi Feiler and Taku Tokuyasu and Chris Kingsley and Shanaz Dairkee and Zhenhang Meng and Karen Chew and Daniel Pinkel and Ajay Jain and Ljung, \{Britt Marie\} and Laura Esserman and Albertson, \{Donna G.\} and Waldman, \{Frederic M.\} and Gray, \{Joe W.\}",

note = "Funding Information: This work was supported by the NIH (CA58207, CA90421, and CA101359), the Office of Health and Environmental Research of the U.S. Department of Energy (contract DE-AC03-76SF00098), and the Avon Foundation. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. For full disclaimer, see http://www-library.lbl.gov/public/tmRco/howto/RcoBerkeleyLabDisclaimer.htm . ",

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doi = "10.1016/j.ccr.2006.10.009",

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T1 - Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

AU - Chin, Koei

AU - DeVries, Sandy

AU - Fridlyand, Jane

AU - Spellman, Paul T.

AU - Roydasgupta, Ritu

AU - Kuo, Wen Lin

AU - Lapuk, Anna

AU - Neve, Richard M.

AU - Qian, Zuwei

AU - Ryder, Tom

AU - Chen, Fanqing

AU - Feiler, Heidi

AU - Tokuyasu, Taku

AU - Kingsley, Chris

AU - Dairkee, Shanaz

AU - Meng, Zhenhang

AU - Chew, Karen

AU - Pinkel, Daniel

AU - Jain, Ajay

AU - Ljung, Britt Marie

AU - Esserman, Laura

AU - Albertson, Donna G.

AU - Waldman, Frederic M.

AU - Gray, Joe W.

N1 - Funding Information: This work was supported by the NIH (CA58207, CA90421, and CA101359), the Office of Health and Environmental Research of the U.S. Department of Energy (contract DE-AC03-76SF00098), and the Avon Foundation. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. For full disclaimer, see http://www-library.lbl.gov/public/tmRco/howto/RcoBerkeleyLabDisclaimer.htm .

PY - 2006/12

Y1 - 2006/12

N2 - This study explores the roles of genome copy number abnormalities (CNAs) in breast cancer pathophysiology by identifying associations between recurrent CNAs, gene expression, and clinical outcome in a set of aggressively treated early-stage breast tumors. It shows that the recurrent CNAs differ between tumor subtypes defined by expression pattern and that stratification of patients according to outcome can be improved by measuring both expression and copy number, especially high-level amplification. Sixty-six genes deregulated by the high-level amplifications are potential therapeutic targets. Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism.

AB - This study explores the roles of genome copy number abnormalities (CNAs) in breast cancer pathophysiology by identifying associations between recurrent CNAs, gene expression, and clinical outcome in a set of aggressively treated early-stage breast tumors. It shows that the recurrent CNAs differ between tumor subtypes defined by expression pattern and that stratification of patients according to outcome can be improved by measuring both expression and copy number, especially high-level amplification. Sixty-six genes deregulated by the high-level amplifications are potential therapeutic targets. Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism.

KW - CELLCYCLE

KW - HUMDISEASE

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M3 - Article

C2 - 17157792

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SN - 1535-6108

VL - 10

SP - 529

EP - 541

JO - Cancer Cell

JF - Cancer Cell

IS - 6

ER -

Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

Abstract

Funding

Keywords

ASJC Scopus subject areas

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