A5103158580- CRISPR and Genetic Engineering
- PARP inhibition in cancer therapy
- Cancer Genomics and Diagnostics
- DNA Repair Mechanisms
- Cancer, Hypoxia, and Metabolism
- Neuroscience of respiration and sleep
- Male Breast Health Studies
- Prostate Cancer Diagnosis and Treatment
- Chemotherapy-related skin toxicity
- Cancer and Skin Lesions
- Respiratory Support and Mechanisms
- Prostate Cancer Treatment and Research
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Genomic variations and chromosomal abnormalities
- Growth Hormone and Insulin-like Growth Factors
- Chromosomal and Genetic Variations
- Epigenetics and DNA Methylation
- Metabolism and Genetic Disorders
Lunenfeld-Tanenbaum Research Institute
2013-2022
Mount Sinai Hospital
2013-2022
University of Toronto
2013-2016
University of British Columbia
2007
Amplification of the CCNE1 locus on chromosome 19q12 is prevalent in multiple tumour types, particularly high-grade serous ovarian cancer, uterine tumours and gastro-oesophageal cancers, where high cyclin E levels are associated with genome instability, whole-genome doubling resistance to cytotoxic targeted therapies
Abstract Amplification of the gene encoding cyclin E ( CCNE1 ) is an oncogenic driver in several malignancies and associated with chemoresistance poor prognosis. To uncover therapeutic targets for -amplified tumors, we undertook genome-scale CRISPR/Cas9-based synthetic lethality screens cellular models amplification. Here, report that increasing dosage engenders a vulnerability to inhibition PKMYT1 kinase, negative regulator CDK1. inhibit PKMYT1, developed RP-6306, orally bioavailable...