Pierre Billon

Dr. Pierre Billon

Pronouns: He/Him


Assistant Professor

Cumming School of Medicine, Department of Biochemistry and Molecular Biology


Arnie Charbonneau Cancer Institute

Contact information

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Phone number

Office: 403.220.7289


Laboratory: HRIC2B26
Office: HRIC2A20

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Susana Escobedo
Email: susana.escobedo@ucalgary.ca

Office: 403.220.2954


Educational Background

M.Sc. Molecular Biology and Biotechnology, Paul Sabatier University, 2009

Ph.D. Cellular and Molecular Biology, Laval University, 2015

Postdoc Genetics and Development, Columbia University Irving Medical Center, 2020


Dr. Pierre Billon completed his Ph.D. in the laboratory of Pr. Jacques Côté at the Cancer Research Center at Laval University. The main focus of his work was to study the functional roles of post-translational modifications of DNA replication and repair factors.

Next, Pierre joined the laboratory of Dr. Alberto Ciccia at the Columbia University Irving Medical Center for his postdoctoral training. He studied the connection between cellular DNA repair mechanisms and genome editing technologies. He developed new tools, methods, and technologies each of which resulted in an expansion and improvement of the genome editing toolbox, with applications in cancer detection and treatment.

In November 2020, he opened his own laboratory at the University of Calgary in the Cumming School of Medicine. He is a member of the Robson DNA Science Centre at the Arnie Charbonneau Cancer Institute.


Areas of Research

Area of Focus
  • Genome stability
  • Genome editing
Summary of Research

i. Investigating the mechanisms that promote CRISPR-based precision genome editing

DNA is the precious hereditary material of biological systems. Genomes contain genetic variants that can cause or predispose humans to disease. Emerging genome editing technologies have the potential to prevent or cure human disorders by eliminating pathogenic variants.

Genome editing technologies operate by triggering cellular DNA repair systems to resolve site-specific DNA lesions in living systems. The ability to introduce site-specific double-strand breaks by engineered nucleases or natural CRISPR-associated nucleases laid the foundations for the recent genome editing revolution. Modern sophisticated DSB-free genome editing agents, such as programmable base editors, prime-editors, and integrases, are exploited to generate precise base modifications, and insertions and deletions of desired sequences by inducing genomic lesions and by stabilizing certain repair intermediates at specific genomic sequences. These include single-strand breaks, deaminated bases, abasic sites, mismatched nucleotides, and flap structures. Accurate, specific, and predictable editing can be modulated by manipulating cellular DNA repair effectors. The lab aims to control DNA repair to improve the efficiency, accuracy, and safety of modern precision genome editing technologies.

The manipulation of the cellular DNA repair mechanisms will enable fine control of editing in therapeutic cellular systems. The insights gained from this work will not only improve the applications of genome editing technologies but also help generate important knowledge on the fundamental mechanisms of DNA repair. Adequate control of the cellular response to DNA damage will lay the foundation for precise therapeutic genome editing and contribute to precisely modeling and functionally studying pathogenic variants.

ii. Investigating DNA repair in cancer

Genomic instability is an enabling characteristic of cancer, a leading cause of death and disease worldwide.

Cells have developed highly sophisticated and complex mechanisms, collectively referred to as the DNA Damage Response (DDR), that detect and repair DNA damage. The DDR suppresses tumorigenesis and modulates the response to cancer therapies by conferring exploitable vulnerabilities to tumor cells. The targeting of the DDR, which protects against genomic instability, has proven to be an effective strategy for counteracting cancer development and improving therapy. Consequently, it is crucial to comprehensively study the fundamental mechanisms regulating the DDR under physiological and pathological conditions in order to develop targeted therapeutic strategies. The lab aims to leverage the DDR to better understand cancer development and to enhance therapy.

Recent advances in genome editing technologies enable the interrogation of encoded regulatory information with single-base resolution. This provides new opportunities for the development of a range of approaches to elucidating the fundamental molecular mechanisms underlying cancer progression and to enhance the efficiency of DNA damage-based cancer treatments. Deciphering the regulatory mechanisms that maintain genome stability is crucial not only for allowing new insights into the cellular response to conventional cancer therapies but also for developing new strategies to facilitate drug discovery.

More information on our research projects and recent publications on these topics can be found here: https://www.billonlab.com/researchprojects


Course number Course title Semester
MDGE 625 Chromatin Dynamics and Epigenetics Winter
MDGE 722 Nucleic Acids, DNA Replication, Transcription and RNA Signalling Fall


Investigating the mechanisms that promote DNA Repair and Genome Editing

The Billon Laboratory is studying the mechanisms that promote DNA Repair and Genome Editing.

We employ cutting-edge genome editing technologies (CRISPR-associated transposons, base editing, and prime editing), high-throughput genetic screens in cell lines and in vivo, biochemical assays, cell biology experiments, and mouse models to interrogate and manipulate the cellular mechanisms that protect our genome.

Studying and controlling the cellular DNA damage response will not only provide new insights into the mechanisms that promote genome stability to enhance cancer treatments, but also to improve the accuracy, efficiency, and safety of modern precision genome editing technologies for the treatment of human genetic diseases.