Lisa Porter, Ph.D.
Tel: (519) 253-3000 ext.4775
Tumour growth is 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 Breast, Brain and Blood 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 can initiate specific forms of breast, brain and blood cancer. 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) Regulation of Tuberous Sclerosis (TS).
TS is a disorder characterized by the formation of tumours in various organs throughout the body. The Porter lab are working to determine how specific changes in a protein 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, this work seeks to clarify what the consequences of specific mutations, as well as to potentially point to therapeutic interventions for these patients.
3) Stress Signalling in Breast Cancer Development and Progression.
Stress and other behavioural factors may affect cancer progression and patient survival, yet the underlying mechanisms for this association are poorly understood. This work seeks to determine the effects of the stress-associated steroid hormone cortisol on the growth and function of both normal and cancerous breast cells.
- D Lubanska and LA Porter (2014) Oncoscience (inaugural addition; cover selection) Online advance publication www.impactjournals.com/oncoscience The Atypical Cell Cycle Regulator Spy1 Suppresses Differentiation of the Neuroblastoma Stem Cell Population.
- 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. ISI Impact – 26.566 ** highlighted in Cancer Discovery March 2014 doi:10.1158/2159-8290.CD-RW2014-025. Recommended by F1000Prime.
- Al Sorkhy M*, Ferraiuolo R*, Fratiloiu AR, Jalili E, Sloane B and LA Porter (2012) BMC Cancer 26;12(1):45 Altering Spy1A Protein Stability Represents an Oncogenic Mechanism Mediated Through CDK1.
- E. Fidalgo da Silva, SB Ansari, J Maimaimati, EA Barnes, M Kong-Beltran, DJ Donoghue and Porter LA (2011) Cell Cycle Sep 15;10(18). Tuberin Directly Regulates Entry into Mitosis.
- Sorkhy M, R Craig, B Market, R Ard and LA Porter. (2009) Journal of Biological Chemistry. Jan 30;284(5):2617-27. The CDK Activator, Spy1A, is Targeted for Degradation by the Ubiquitin Ligase Nedd4.