Grant: Project Grant
McGill University
$837,675.00
Investigating LKB1-mediated inflammation as a mediator of tumour progression
FY 2017-18
Summary
It is now appreciated that the immune system plays an important role in controlling cancer progression. Recent work in understanding how T cells respond to the tumour microenvironment has led to transformative therapies - so called "immune checkpoint blockade" therapies - used to treat cancer by unleashing anti-tumour immune responses. However, inflammation is a double-edged sword. Tumour-associated inflammation has been shown to be an important contributing factor to cancer progression. Understanding how inflammation is regulated in the tumour microenvironment may help us to design rational therapies that circumvent the tumour-promoting effects of inflammation while maintaining or enhancing anti-tumour immune responses.
Current models propose that immune cell interaction with the tumour microenvironment promotes cancer-associated inflammation. Our results indicate that the tumour suppressor LKB1, mutated in multiple cancers including lung, breast, and pancreatic cancer, can regulate tumour-intrinsic and tumour-extrinsic effects on cancer-associated inflammation. This proposal investigates the role that inflammation controlled by LKB1 has on cancer development and progression, and whether we can use existing drugs to block inflammation and reduce cancer incidence.
Department
Program
Project Grant
Recipient
Location
Quebec, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
368921
Name
Jones Russell G
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Cancer Biology & Therapeutics
Projecttitle
Investigating LKB1-mediated inflammation as a mediator of tumour progression
Programtype2
Operating Grants
Orgnameinp2
McGill University
Cihramount2
$837,675
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Cancer; Cancer Metabolism; Gastrointestinal Polyps; Inflammation; Lkb1; Mtor; Peutz Jeghers Syndrome (Pjs); Stat3; T Cells; Tumour Suppressor
Abstract
It is now appreciated that the immune system plays an important role in controlling cancer progression. Recent work in understanding how T cells respond to the tumour microenvironment has led to transformative therapies - so called "immune checkpoint blockade" therapies - used to treat cancer by unleashing anti-tumour immune responses. However, inflammation is a double-edged sword. Tumour-associated inflammation has been shown to be an important contributing factor to cancer progression. Understanding how inflammation is regulated in the tumour microenvironment may help us to design rational therapies that circumvent the tumour-promoting effects of inflammation while maintaining or enhancing anti-tumour immune responses.
Current models propose that immune cell interaction with the tumour microenvironment promotes cancer-associated inflammation. Our results indicate that the tumour suppressor LKB1, mutated in multiple cancers including lung, breast, and pancreatic cancer, can regulate tumour-intrinsic and tumour-extrinsic effects on cancer-associated inflammation. This proposal investigates the role that inflammation controlled by LKB1 has on cancer development and progression, and whether we can use existing drugs to block inflammation and reduce cancer incidence.
Competitiondate
201709
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Jones, Russell G
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $837,675~ $0~