|Name: Lisa A. Porter
Areas of Expertise: Cancer Cell Biology; Drug Screening; Mouse, Zebrafish and organoid/cell culture models of cancer
Position: Translational Research Director
|Brief Description of Research:|
|Many devastating disorders are caused by the inability of cells to grow and develop properly. The Porter Lab focuses on resolving how key growth regulators control the development and continued maintenance of specific organ systems in our body. They also seek to determine what can go wrong during these processes to initiate tumour development. Some specific projects include:
1) Role of Speedy in Brain Cancers. During her post-doctoral work Dr. Porter discovered the protein Speedy (also called Spy1) which is now known to be a key growth regulator and found at very high levels in a number of different cancers. The Porter lab is determining how this protein participates in the progression of aggressive forms of brain cancer. Importantly, this protein may be involved in driving the growth of a small population of cells known as ‘cancer stem cells’. Data suggests that these cells are highly drug resistant and may be a primary cause of patient relapse. Determining novel ways to stop the growth of these cells may represent extremely effective therapies with little toxicity to the patient.
2) Novel Checkpoint Regulation by Tuberin (TSC2): A number of labs around the world have determined that misregulation of a protein called Tuberin is the leading cause of a hamartoma disorder known as Tuberous Sclerosis that causes tumour growths in several organs including the brain. Our lab has found a unique mechanism for this protein in regulating how cells divide into two daughter cells, a continual process in development and throughout adult life. We are working to determine how specific changes in Tuberin cause tumour formation with a focus on some of the most severe cases of tumours in the central nervous system. Tuberin mutations can be screened in utero to provide early indicators of disease, our work seeks to clarify what the consequences of specific mutations will be as well as to potentially point to therapeutic interventions for these patients.
|5 Select Publications (Porter Lab students/personnel are underlined):|
|D McGrath, B Fifield, AH. Marceau, S Tripathi, LA Porter, and SM Rubin (2017) EMBO J Aug 1;36(15):2251-2262. Mechanism of Cyclin-Dependent Kinase Activation by the Proliferative Factor Spy1.
Lubanska D and Porter LA (2017) Drugs in R&D Jun;17(2):255-263. Revisiting CDK Inhibitors for Treatment of Glioblastoma Multiforme
M Al Sorkhy, B Fifield, D. Myers and LA Porter (2016) Cell Cycle 15(1):128-36. Direct Interactions with both p27 and Cdk2 Regulate Spy1-Mediated Proliferation in vivo and in vitro. Funded by CCS/CBCRA PMID:26771716
D Lubanska and LA Porter (2014) Oncoscience (inaugural edition; cover selection) 1: 336-348. The Atypical Cell Cycle Regulator Spy1 Suppresses Differentiation of the Neuroblastoma Stem Cell Population. PMID: 24434210. Funded by CCS.
D Lubanska, E Fidalgo da Silva, B Market, A deCalvalho, T Mikkelson, and LA Porter (2014) Cancer Cell 13;25(1):64-76. The Novel Cell Cycle Mediator Spy1 Regulates Neurogenesis and is Implicated in Glioblastoma.