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Grant: Project Grant

University of Toronto

$745,876.00

Investigating INPP4B signalling as a target for therapy in leukaemia

FY 2017-18

Summary
AML is an aggressive type of leukemia that depends on the function of cells called LSCs (leukemia stem cells). Clinicians believe that leukemia can be cured only when LSCs are completely eliminated. Our research group identified that AML patients with high levels of a protein called INPP4B have a greater likelihood of developing very aggressive disease and shorter survival compared to a patient with low levels of INPP4B. In our studies to understand how INPP4B contributes to leukemia development, we hypothesized that INPP4B plays a critical function in LSCs and thereby promote or accelerate AML progression. In our ongoing work, we have identified lines of evidence to support this hypothesis, and therefore we are proposing to further study the molecular mechanisms and signal transduction pathways impacted by INPP4B in leukemic cells. Ultimately, we hope that our discoveries can generate new AML therapies which can block INPP4B function and eliminate LSCs
Program
Project Grant
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
380561
Name
Salmena Leonardo L
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Cancer Progression & Therapeutics 2
Projecttitle
Investigating INPP4B signalling as a target for therapy in leukaemia
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$745,876
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Aml; Chemoresistance; Inpp4b; Leukaemia Stem Cells; Mouse Model; Phosphoinositide Signalling
Abstract
AML is an aggressive type of leukemia that depends on the function of cells called LSCs (leukemia stem cells). Clinicians believe that leukemia can be cured only when LSCs are completely eliminated. Our research group identified that AML patients with high levels of a protein called INPP4B have a greater likelihood of developing very aggressive disease and shorter survival compared to a patient with low levels of INPP4B. In our studies to understand how INPP4B contributes to leukemia development, we hypothesized that INPP4B plays a critical function in LSCs and thereby promote or accelerate AML progression. In our ongoing work, we have identified lines of evidence to support this hypothesis, and therefore we are proposing to further study the molecular mechanisms and signal transduction pathways impacted by INPP4B in leukemic cells. Ultimately, we hope that our discoveries can generate new AML therapies which can block INPP4B function and eliminate LSCs
Competitiondate
201803
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Salmena, Leonardo L
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $745,876~ $0~