平特五不中

Juliana Cavalcante de Moura

M.Sc. Research Assistant

As a research assistant at Dr. Bailey鈥檚 lab, I am responsible for supporting research activities related to gastro-esophageal adenocarcinoma, training new students, conducting wet lab experiments such as ChIP-seq, DNA and RNA extraction, cell culture, RT-qPCR, cloning and more. Additionally, I take care of regular maintenance and upkeeping of the laboratory such as stock solutions preparation, inventory management, lab glassware cleaning and general autoclaving.

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Eftyhios Kirbizakis (Aki)

PhD student

Cancer is a disease caused by genomic alterations. Our understanding cancer biology, biomarkers, and therapeutic targets have been driven by gene-centric approaches, where protein coding regions of the genome are significantly altered. Most genomic alterations occur in the non-coding regions of the genome, which contain gene regulatory elements that can modulate gene expression. However, the effects of genomic alterations and their downstream effects on gene modulation remain poorly explored. My research focuses on computationally predicting how these non-coding alterations affect gene expression through their effects on interacting gene regulatory elements. With these approaches, we aim to identify potentially cancer genes, which could lead to future potential therapeutic targets.听

Ansley Gnanapragasam

PhD candidate

The development of peritoneal metastasis (PM) is the most common progression of gastroesophageal adenocarcinoma (GEA) and leads to an exceptionally poor prognosis with a median survival rate of less than four months. This poor prognosis results from the late presentation of the disease, the inability to surgically resect the cancerous lesions and the absence of therapeutic options. The lack of actionable target genes involved in the progression of GEA has made it difficult to understand and treat its progression. Through deep whole exome sequencing of patient-matched primary GEA tumors, peritoneal metastases and adjacent normal we aim to identify potential causal gene variations promoting the transition from GEA to PM. We are further functionally characterizing significant candidate variants, through in-vivo and in-vitro assays, to elucidate and target the mechanisms of progression to PM, ultimately aiming to improve the survival of GEA patients.

Kyle White

M.Sc.

CRISPR screening and characterizing chromatin using chipmentation.