Welcome to the Wei Qiu Lab!
The Wei Qiu lab is located in the Cardinal Bernardin Cancer Center, Stritch School of Medicine, Loyola University of Chicago. The lab is focused on understanding the molecular mechanisms involving in hepatocellular carcinoma and alcohol liver disease.
Dr. Wei Qiu
Professor
Department of Surgery & Department of Cancer biology
School of Medicine, Loyola University Chicago
Link for Dr. Wei Qiu: https://ssom.luc.edu/surgery/faculty/profile/index.cfm?id=4410
https://ssom.luc.edu/cancerbiology/ourpeople/faculty/wei%20qiu/
Research Interest Areas: liver cancer and Alcohol liver Disease
Research Description
I am a tenured Professor at Department of Surgery and Department of Cancer Biology. I am engaged in both basic and translational liver disease research. Over the last 18 years, I have been studying the molecular mechanisms of tissue injury, inflammation and tumorigenesis using a number of in vitro and mouse models. I have published 47 peer-reviewed papers in high-profile journals, including Cell Stem Cell, JCI, PNAS, Hepatology, Cancer Research, and Oncogene. I am currently funded by NCI, NIAAA and American Cancer Society.
In last several years, we have been focusing on investigating the functions of tyrosine kinases in hepatocellular carcinoma (HCC) development. HCC is the major form of liver cancer. It is the fifth most common malignancy globally and is third in total cancer-related deaths annually. The five year overall survival of patients with a new diagnosis of HCC is less than 18%, and a majority of HCC patients present with advanced disease so that treatment options are limited. It is imperative to develop new and more effective therapeutic strategies and agents to treat HCC, but achieving this goal requires better understanding of the molecular signaling pathways that drive or mediate the development of the disease. We have discovered that a number of tyrosine kinases, such as FAK, EphA2, and ABL kinases, play critical roles in liver tumorigenesis. These important findings provide a basis for targeting these kinases to treat HCC. In addition, we are also interested in studying the resistance mechanisms of FDA-approved targeted therapies (e.g. sorafenib, cabozantinib and immunotherapy) for HCC, which shall help to improve the efficacy of these drugs in treating HCC.
We are also interested in understanding molecular signaling pathways which are critical for the development of Alcoholic liver disease (ALD). ALD is one of the primary causes of chronic liver disease worldwide and cirrhosis associated deaths in the United States. There are currently no FDA-approved pharmacological or nutritional therapies for treating patients with ALD. Novel therapeutic strategies are desperately needed. The goal of our research is to advance our understanding of how ALD initiate and develop, which is critical for identifying effective therapeutic strategies for the prevention and treatment of ALD.
A wide variety of approaches are employed in my studies, including molecular and cell biology techniques, state-of-art cell imaging, transgenic and knockout mouse models, injury and cancer models, and correlative studies using clinical samples.
I am a tenured Professor at Department of Surgery and Department of Cancer Biology. I am engaged in both basic and translational liver disease research. Over the last 18 years, I have been studying the molecular mechanisms of tissue injury, inflammation and tumorigenesis using a number of in vitro and mouse models. I have published 47 peer-reviewed papers in high-profile journals, including Cell Stem Cell, JCI, PNAS, Hepatology, Cancer Research, and Oncogene. I am currently funded by NCI, NIAAA and American Cancer Society.
In last several years, we have been focusing on investigating the functions of tyrosine kinases in hepatocellular carcinoma (HCC) development. HCC is the major form of liver cancer. It is the fifth most common malignancy globally and is third in total cancer-related deaths annually. The five year overall survival of patients with a new diagnosis of HCC is less than 18%, and a majority of HCC patients present with advanced disease so that treatment options are limited. It is imperative to develop new and more effective therapeutic strategies and agents to treat HCC, but achieving this goal requires better understanding of the molecular signaling pathways that drive or mediate the development of the disease. We have discovered that a number of tyrosine kinases, such as FAK, EphA2, and ABL kinases, play critical roles in liver tumorigenesis. These important findings provide a basis for targeting these kinases to treat HCC. In addition, we are also interested in studying the resistance mechanisms of FDA-approved targeted therapies (e.g. sorafenib, cabozantinib and immunotherapy) for HCC, which shall help to improve the efficacy of these drugs in treating HCC.
We are also interested in understanding molecular signaling pathways which are critical for the development of Alcoholic liver disease (ALD). ALD is one of the primary causes of chronic liver disease worldwide and cirrhosis associated deaths in the United States. There are currently no FDA-approved pharmacological or nutritional therapies for treating patients with ALD. Novel therapeutic strategies are desperately needed. The goal of our research is to advance our understanding of how ALD initiate and develop, which is critical for identifying effective therapeutic strategies for the prevention and treatment of ALD.
A wide variety of approaches are employed in my studies, including molecular and cell biology techniques, state-of-art cell imaging, transgenic and knockout mouse models, injury and cancer models, and correlative studies using clinical samples.