Grant: CIHR Fellowship
University of Alberta
$135,000.00
Biological significance of SALL4, a novel homeobox gene that is aberrantly expressed in ALK-expressing anaplastic large cell lymphoma
FY 2008-09
Summary
Tyrosine kinase is a type of enzyme that provides many important biological functions in our body. When abnormally activated, tyrosine kinases are known to cause cancer. It is important to fully understand the mechanisms by which these over-active enzymes cause cancer, since one can design new anti-cancer therapy based on these information. In this proposal, the fellow will explore one novel pathway by which an over-active tyrosine kinase, NPM-ALK, can cause a specific childhood cancer. We believe that NPM-ALK allows SALL4 to be expressed in cells in which SALL4 expression should have been shut-off. SALL4 in turns mediates the tumor-forming effects for NPM-ALK. If our hypothetical model turns out to be correct, we may be able to treat this type of cancer by interrupting the interaction between NPM-ALK and SALL4.
Department
Program
CIHR Fellowship
Recipient
Location
Alberta, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
181122
Name
Molavi Ommoleila
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Fellowships - Post-PhD
Projecttitle
Biological significance of SALL4, a novel homeobox gene that is aberrantly expressed in ALK-expressing anaplastic large cell lymphoma
Programtype2
Fellowship Programs
Orgnameinp2
University of Alberta
Cihramount2
$135,000
Cihrequipment2
$0
Programname2
CIHR Fellowship
Keyworddelim
Apoptosis Assay; Clonogenic Assay; Immunohistochemistry; Npm-Alk; Oncogenic Tyrosine Kinase; Sall4; Sirna; Stat3
Abstract
Tyrosine kinase is a type of enzyme that provides many important biological functions in our body. When abnormally activated, tyrosine kinases are known to cause cancer. It is important to fully understand the mechanisms by which these over-active enzymes cause cancer, since one can design new anti-cancer therapy based on these information. In this proposal, the fellow will explore one novel pathway by which an over-active tyrosine kinase, NPM-ALK, can cause a specific childhood cancer. We believe that NPM-ALK allows SALL4 to be expressed in cells in which SALL4 expression should have been shut-off. SALL4 in turns mediates the tumor-forming effects for NPM-ALK. If our hypothetical model turns out to be correct, we may be able to treat this type of cancer by interrupting the interaction between NPM-ALK and SALL4.
Competitiondate
200902
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Molavi, Ommoleila
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $135,000~ $0~
