Kimberly J Bussey, Ph.D.

Assistant Professor
Glendale, AZ

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Dr. Bussey is a cancer cytogeneticist, applied bioinformatician, and an assistant professor in the Precision Medicine Program. She is passionate about educating healthcare professionals about genomics and how to integrate genomics into their current medical decision making. Her research centers around understanding how large-scale chromosome alterations in tumors lead to cancer. Her motivation, the observation that cancer is an evolutionary process characterized by chromosome evolution, has led her to interdisciplinary collaborations with engineers, theoretical physicists, and artists to study both common and rare cancers in academic, government, non-profit, and industry settings. An alumna of the University of Arizona, Dr. Bussey received her PhD in Medical and Molecular Genetics from Oregon Health and Science University in 2000 and completed a post-doctoral fellowship in bioinformatics at the National Cancer Institute. She has published 40+ scientific papers and has been granted four patents for her work in rare tumors, with an additional four patent applications pending.

Assistant Professor

Glendale, AZ

College of Graduate Studies - AZ

Precision Medicine

Master of Science in Precision Medicine
Post-Graduate Certificate in Precision Medicine

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Oregon Health Sciences University | 2000 | Ph.D.
University of Arizona | 1994 | B.S.

Courses Taught

PMMSG 501: Introduction to Genetics and Genomics

PMMSG 502: Genomics of Rare and Complex Diseases

PMMSG 503: Introduction to Bioinformatics, Statistics, and Data Interpretation

PMGCG 501: Introduction to Genetics and Genomics

PMGCG 502: Genomics of Rare and Complex Diseases

PMGCG 503: Introduction to Bioinformatics, Statistics, and Data Interpretation


Cancers or cancer-like phenomena are found across the tree of life in multicellular organisms. The hallmarks of cancer describe the functions a cell or group of cells must express to become a cancerous tumor, including uncontrolled growth, uninhibited mobility, and resistance to cell death. The current paradigm ascribes the acquisition of such behavior to the gradual accumulation of genomic changes. This gene-centric view has been useful up to a point, but it suffers from the problem that most oncogenic changes are neither necessary, sufficient, nor context-independent. Furthermore, such behaviors can be suppressed in a physiologically normal environment.

We propose thinking about cancer as an atavism, in this case the re-expression of single-cell biology in a multicellular context. The re-expression of unicellular behavior is the consequence of a speciation event. Cancer is not normal gone wrong. It is the emergence of a new unicellular parasitic collective where adaptability is itself a selected trait. Under this context, we hypothesize that we can detect evidence of single-cell stress-responses, such as stress-induced mutation (SIM), in cancer genomes, identify how unicellular information flows have been restored through integrating “omic” data sets and testing the resulting predictions in the lab, and apply this understanding clinically. 


American Society of Human Genetics

American Association for Cancer Research

American Association for the Advancement of Science

American Society of Clinical Oncology

International Society for Ecology, Evolution, and Cancer

European Society of Human Genetics

More Information


US 9,198,910: Methods for the Treatment of Cancer

US 9,222,138: Therapeutic Targets for Adrenocortical Carcinoma

US 9,745,634: Systems and Methods for Diagnosing and Treating Cancer

US 10,066,270B2: Methods and Kits Used in Classifying Adrenocortical Carcinoma