Senny Wong

Buxton Lab

Senny Wong, a graduate student in the Department of Biochemistry, is studying breast cancer metastasis in Dr. Iain Buxton's lab. She has been researching on how purinergic mechanisms influence breast cancer metastasis. The fundamental protein of interest is a secreted factor that has been shown to be released by breast cancer cells but not normal breast cells. This factor has a role in elevating nucleotide pools (particularly of interest is ATP) in the extracellular microenvironment. We propose this elevation of ATP near the blood vessels can contribute to the generation of new blood vessel formation and a pathway for breast cancer cells to escape to distant regions of the body. Understanding these mechanisms can be utilized for pharmacologic methods to target and treat breast cancer. She is currently interested in exosomes, small lipid vesicles secreted from cells, as biomarker carriers for the diagnostics of breast cancer.

Senny has received her B.Sc. in Biochemistry at the University of Nevada, Reno.

Senny has mentored students; Katie Speirs and Suzann Duan. Below are their achievements and current statuses.


Katie Speirs (2012-2014)

  • GURA 2012-13: Preventing Metastases of Human Breast Cancer Cells in an Immunocompromised Mouse Model of Human Cancer
  • Summer INBRE 2013: Development and Optimization of a Luciferin-Luciferase Activity Assay for the Detection of Nucleoside Diphosphate Kinase
  • GURA 2013-14: Optimization of Detection Methods for Nucleotide Diphosphate Kinase in Human Breast Cancer Tissues
  • Current status: Accepted for medical school

Suzaan Duan (2013-2014)

  • Current status: Accepted in the CMPP graduate program

Breast Cancer Research

Breast cancer is a heterogeneous disease comprised of many dysregulated pathways and is the most common cancer diagnosed in women. Within the developed world, breast cancer patients usually succumb due to metastasis of the cancer and not from the primary tumor. This demonstrates the importance of understanding and treating metastasis. There is strong evidence that breast cancer metastasizes away from the breast early on during tumor development. Cells at distant sites can remain dormant for an extended period of time despite loco-regional treatment including surgical removal of the primary tumor. These secondary metastases can then grow large enough to attract their own blood supply by a process known as angiogenesis.

Several studies have shown that nucleoside diphosphate kinase (NM23 or NDPK) may have a pathological role in cancer. NDPK-A was detected in the serum of patients diagnosed from lymphoma, neuroblastoma, and melanoma. Our lab has shown that NDPK-A and B is elaborated outside breast cancer cells. NDPK has been shown to promote cell migration, proliferation, and tumor-mediated angiogenesis that would support metastasis. The functional role of NDPK generates extracellular ATP from ADP thus elevating ATP/ADP levels. Nucleotide release has been established to have signaling roles in many organ systems. Extracellular ATP can activate purinergic (P2Y) receptors leading to transactivation of vascular endothelial growth factor receptor (VEGFR) on endothelial cells, which promotes angiogenesis, tubulogenesis, and cell proliferation. This activation can occur in the absence of VEGF. Another role for ATP is the dilation of arterial vessels. Activation of P2Y receptors can release nitric oxide, prostaglandins, and more ATP from endothelial cells leading to vasodilation in arterioles. Stimulating P2Y on endothelial cells may also cause cell contraction leading to vascular permeability to support cancer cell intravasation and extravasation for migrating to secondary sites in the body. Thus, NDPK provides a means for the cancer cell to travel to distant sites in the body and propagate during metastasis.