|Monday, April 11th|
9:15 AM - 9:30 AM
Head and neck cancer patients often lose their sense of taste after receiving radiation therapy. Understanding the physiological mechanisms of taste and smell has the potential to improve these patients’ sense of taste. Previously it was accepted that taste buds only lived for 10-14 days, however, here I present research that suggests otherwise. Transgenic mice were first generated to express fluorescent markers in taste buds. Mice were then sacrificed, their tongues were sectioned and these sections were immunostained for confocal microscopy. Confocal analysis revealed taste bud cells that survived for up to 14 weeks. These startling results help to provide insight into taste bud cell turnover rates in humans, and may also help to improve the quality of life of cancer patients.
9:30 AM - 9:45 AM
Meningioma tumors are the most common primary brain tumor, yet there is no effective chemotherapy treatment; surgery is the only option. These tumors are classified into three WHO grades according to histopathy. Ninety percent of meningioma cases are benign, but can evolve to become cancerous unexpectedly. This research was conducted to find a biomarker for meningioma malignancy by investigating five potential biomarker proteins (AKAP12, Rb-1, p53, SMAD2/3, and Merlin) based on protein expression in benign compared to malignant tumors. Using western blot methods, these proteins were tested in specimen tissue samples and cell lines to determine differences in regulation across the grades. We found that AKAP12 and Rb-1 were down-regulated. These findings and prior research of other cancers led to the theory that AKAP12 and Rb-1 may be in the same phosphorylation cascade that is involved with the cell aggressiveness in meningiomas via CDKs and cyclin kinases, particularly cyclin D.
9:45 AM - 10:00 AM
In recent years, antibody-drug conjugates (ADCs) have become an effective tool for treating various types of cancer. ADCs are complex molecules composed of a monoclonal antibody specific for a tumor-associated antigen, a highly potent, synthetic, cytotoxic agent, and a stable protein linker that connects the cytotoxic agent to the antibody. Upon antibody-antigen recognition on surface of cancer cells, ADCs are internalized by a process known as receptor-mediated endocytosis. Endosomes transport the ADC/antigen complex to lysosomes, in which lysosomal proteolytic enzymes cleave the antibodydrug linker, thereby activating the cytotoxic agent and inducing cell death. By combining the unique targeting of monoclonal antibodies with the potent, cancer-killing ability of cytotoxic drugs, ADCs allow for sensitive discrimination between healthy and cancerous tissue. My research explores ADC design optimization, and the efficacy of ADC treatment across various cancer types.
10:00 AM - 10:15 AM
Autophagy is traditionally thought of as a cellular recycling pathway used to regularly turn-over organelles and proteins found within the cell, as well as to eliminate dysfunctional organelles like mitochondria. The autophagy pathway has recently been shown to also function as a secretion pathway, raising the possibility for a role in signaling between cells. Recent studies suggest that the autophagy-dependent secretion pathway may play an important role in cancer metastasis. This raises exciting new possibilities for anti-cancer drugs targeting these secreted proteins or the process that secretes them. However, the autophagy secretion pathway is still poorly understood. My summer research project at the Debnath Lab at UCSF was to investigate a specific protein, IRGQ, that was screened as a possible player in the autophagy secretion pathway. IRGQ was found to be secreted in an autophagy-dependent manner and was found to interact with previously-known players in the autophagy pathway.
|Tuesday, April 12th|
9:00 AM - 9:15 AM
Regulatory T cells (Tregs) make up a population of T cells in the immune system that are crucial for preventing autoimmunity and promoting immune homeostasis. It is well established that during infection Tregs function to prevent autoimmunity and dampen over exuberant immune responses. Although less well known, it is hypothesized that Tregs also play an important role in the facilitation of pathogen clearance. Here we explore this hypothesis by analyzing how Tregs function in immune responses to influenza, a virus that affects 5 million people across the world annually. Specifically, we examine how immune responses to influenza virus are impaired in the absence of regulatory T cells, and evaluate mechanisms that could lead to the observed impairment.