Catherine K. L. Too, PhD, Dalhousie University

Catherine K. L. Too
Catherine K. L. Too, PhD

Dr. Too's laboratory is interested in prolactin receptor (PRLR) action in PRL-responsive tumor cells such as breast and prostate cancers, and lymphomas. Their long-term goal is to elucidate the signal-transduction pathways of the PRLR and identify crosstalk between the PRLR and other signaling pathways. Their current studies focus on the roles of alpha4-phosphoprotein of the mTOR pathway that regulates the initiation of translation and on carboxypeptidase-D (CPD) that contributes to nitric oxide production to promote the survival of tumour cells.

Additionally, the lab is actively involved in studying the action of androgens in prostate cancer (pCa). Their current studies are directed towards understanding the relative contribution of Steroid 5-alpha-reductase (5aR) 1 and 2 to the development and progression of pCa, the synthesis and secretion of prostate-specific antigen (PSA), and in determining the efficacy of specific inhibitors of these isozymes in chemoprevention of pCa.

Products

References

  1. Thomas LN, Douglas RC, Lazier CB, Gupta R, Norman RW, Murphy PR, Rittmaster RS and Too CKL. Levels of 5α-reductase type 1 and type 2 are increased in localized high grade compared to low grade prostate cancer. J Urol. 2008;179(1):147-51.
  2. Lunacek A, Schwentner C, Oswald J, Fritsch H, Sergi C, Thomas LN, Rittmaster RS, Klocker H, Neuwirt H, Bartsch G and Radman C. Fetal distribution of 5α-reductase 1 and 5α-reductase 2, and their imput on human prostate development. J Urol. 2007;178(2):716-721.
  3. Thomas LN, Lazier CB, Gupta R, Norman RW, Troyer DA, O'Brien SP and Rittmaster RS. Differential alterations in 5α-reductase type 1 and type 2 levels during development and progression of prostate cancer. Prostate. 2005;63(3):231-239.
  4. Titus MA, Gregory CW, Ford III OH, Schell MJ, Maygarden SJ and Mohler JL. Steroid 5α-reductase isoenzymes I and II in recurrent prostate cancer. Clin Cancer Res. 2005;11(12):4365-4371.
  5. Thomas LN, Douglas RC, Vessey JP, Gupta R, Fontaine D, Norman RW, Thompson IM, Troyer DA, Rittmaster RS and Lazier CB. 5α-Reductase type 1 immunostaining is enhanced in some prostate cancers compared with benign prostatic hyperplasia epithelium. J Urol.2003:170(5):2019-2025.
  6. Too CKL, Vickaryous N, Boudreau RTM and Sangster SM (2001) Identification and nuclear localization of a novel prolactin and cytokine-responsive carboxypeptidase D. Endocrinology 142: 1357-1367.
  7. O'Malley PGP, Sangster SM, Abdelmagid SA, Bearne SL and Too CKL (2005) Characterization of a novel, cytokine-inducible carboxypeptidase-D isoform in haematopoietic tumor cells. Biochemical Journal 390: 665- 673.
  8. Abdelmagid SA and Too CKL (2008) Estrogen and prolactin upregulate carboxypeptidase-D to promote nitric oxide production and survival of MCF-7 breast cancer cells. Endocrinology 149: 4821-4828.
  9. Thomas LN, Morehouse TJ and Too CKL (2012) Testosterone and prolactin increase carboxypeptidase-D and nitric oxide levels to promote survival of prostate cancer cells. The Prostate 72: 450-460.
  10. Koirala S, Thomas L.N. and Too CKL (2014). Prolactin/Stat5 and androgen R1881 co-activate carboxypeptidase- D gene in breast cancer cells. Molecular Endocrinology 28: 331-343.
  11. Thomas LN, Merrimen J, Bell DG, Rendon R, Goffin V and Too CKL (2014). Carboxypeptidase-D is elevated in prostate cancer and its anti-apoptotic activity is abolished by combined androgen and prolactin receptor targeting. The Prostate 74: 732-742.
  12. Thomas LN, Merrimen J, Bell DG, Rendon R, and Too CKL (2015) Prolactin- and testosterone-induced carboxypeptidase-D correlates with increased nitrotyrosines and Ki67 in prostate cancer. The Prostate 75: 1726-1736.