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Grant: Doctoral: Vanier Canada Graduate Scholarships

University of British Columbia

$150,000.00

Chronic obstructive pulmonary disease contributes to a tumour-promoting microenvironment and the development of lung cancer

FY 2017-18

Summary
Lung cancer is the leading cause of cancer death worldwide. Inflammation is a well-known cause of cancer, and inflammatory lung diseases (such as chronic obstructive pulmonary disease (COPD)) have been associated with an increased risk of developing lung cancer. While the two diseases share known risk factors, the reasons why COPD airway damage leads to lung cancer are unknown. This includes the understudied role of inflammation in inducing damage, which could be an important factor in cancer development. We believe that COPD-related damage promotes cancer formation by causing gene expression changes in both airway cells and immune cells. Further, we believe gene expression changes crucial to cancer growth will be shared between the damaged tissues and the tumours themselves. We will test our theories by assessing the lungs of 15 individuals with COPD and lung cancer (rare samples collected at St. Paul's Hospital). We will identify changes in gene expression, along with differences in immune cell content, throughout the lung, and compare them to tumours in order to identify the changes most associated with cancer formation. This will reveal previously unknown gene expression changes and immune cell responses that are most likely driving cancer development. Additionally, we will build off the work our lab has previously conducted on the airways of COPD patients with and without lung cancer. We will first see if gene disruptions observed in the airways of COPD patients with lung cancer are also found in this rare lung tissue dataset. Second, we will determine if these genes can initiate cancer in normal lung cells by using CRISPR and virus-based gene editing techniques. Finally, we will test whether inhibition of these genes in mice can prevent the development of cancer. My project will lead to scientific discoveries that will help explain why COPD predisposes patients to lung cancer, and will reveal new targets for cancer therapy and methods of cancer prevention.
Program
Doctoral: Vanier Canada Graduate Scholarships
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
376210
Name
Marshall Erin A
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Vanier Canada Graduate Scholarships CIHR
Projecttitle
Chronic obstructive pulmonary disease contributes to a tumour-promoting microenvironment and the development of lung cancer
Programtype2
Studentship Programs
Orgnameinp2
University of British Columbia
Cihramount2
$150,000
Cihrequipment2
$0
Programname2
Doctoral: Vanier Canada Graduate Scholarships
Keyworddelim
Bioinformatics; Chronic Obstructive Pulmonary Disease; Crispr; Genomics; Lentivirus; Non-Small Cell Lung Cancer; Rna; Tumour Field
Abstract
Lung cancer is the leading cause of cancer death worldwide. Inflammation is a well-known cause of cancer, and inflammatory lung diseases (such as chronic obstructive pulmonary disease (COPD)) have been associated with an increased risk of developing lung cancer. While the two diseases share known risk factors, the reasons why COPD airway damage leads to lung cancer are unknown. This includes the understudied role of inflammation in inducing damage, which could be an important factor in cancer development. We believe that COPD-related damage promotes cancer formation by causing gene expression changes in both airway cells and immune cells. Further, we believe gene expression changes crucial to cancer growth will be shared between the damaged tissues and the tumours themselves. We will test our theories by assessing the lungs of 15 individuals with COPD and lung cancer (rare samples collected at St. Paul's Hospital). We will identify changes in gene expression, along with differences in immune cell content, throughout the lung, and compare them to tumours in order to identify the changes most associated with cancer formation. This will reveal previously unknown gene expression changes and immune cell responses that are most likely driving cancer development. Additionally, we will build off the work our lab has previously conducted on the airways of COPD patients with and without lung cancer. We will first see if gene disruptions observed in the airways of COPD patients with lung cancer are also found in this rare lung tissue dataset. Second, we will determine if these genes can initiate cancer in normal lung cells by using CRISPR and virus-based gene editing techniques. Finally, we will test whether inhibition of these genes in mice can prevent the development of cancer. My project will lead to scientific discoveries that will help explain why COPD predisposes patients to lung cancer, and will reveal new targets for cancer therapy and methods of cancer prevention.
Competitiondate
201711
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Marshall, Erin A
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $150,000~ $0~