Grant: CIHR Fellowship
Direct Payment
$150,000.00
Assessing the contribution of the cGAS-STING defense pathway to autocrine-dependent cancers including multiple myeloma
FY 2016-17
Summary
Important secreted-protein signaling loops exist in several cancers that sustain their growth and promotes cancer cell proliferation. Evidence suggests that persistent DNA damage due to genome instability in certain cancers results in cytoplasmic DNA that causes persistent activation of cellular signaling proteins called cGAS and STING. cGAS is an enzyme present in the cytoplasm that binds cytoplasmic DNA and catalyzes the formation of a small molecule called cGAMP. cGAMP can bind to the adaptor protein STING, which results in the activation of immune signaling and cytokine protein production. There are several cancers, such as multiple myeloma, fibrosarcoma, malignant astrocytoma and a mouse melanoma, that require the constant presence of certain cytokine or growth factor proteins to survive and/or proliferate. From our unpublished and preliminary data, we have discovered that in certain biological contexts the cGAS-STING pathway can cause constant production of some of the same cytokines and growth factor proteins that the aforementioned cancers require. We propose that in several cancers, the cGAS-STING pathway is critical for tumor-promoting protein-secretion loops. Verification of our findings could identify previously unknown signaling network relationships and will suggest the viability of new cancer therapy drugs that block the cGAS-STING pathway.
Department
Program
CIHR Fellowship
Recipient
Location
California, United States of America
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
361491
Name
Hodge Curtis D
Region
California
Country
United States of America
Orgtype
Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Fellowships - Post-PhD
Projecttitle
Assessing the contribution of the cGAS-STING defense pathway to autocrine-dependent cancers including multiple myeloma
Programtype2
Fellowship Programs
Orgnameinp2
Direct Payment
Cihramount2
$150,000
Cihrequipment2
$0
Programname2
CIHR Fellowship
Keyworddelim
Autocrine; Cancer Immunology; Cell Biology; Cgas Sting; Crispr-Cas9; Cyclic Dinucleotides; Cytokine; Cytoplasmic Dna Sensing; Mouse Model; Multiple Myeloma
Abstract
Important secreted-protein signaling loops exist in several cancers that sustain their growth and promotes cancer cell proliferation. Evidence suggests that persistent DNA damage due to genome instability in certain cancers results in cytoplasmic DNA that causes persistent activation of cellular signaling proteins called cGAS and STING. cGAS is an enzyme present in the cytoplasm that binds cytoplasmic DNA and catalyzes the formation of a small molecule called cGAMP. cGAMP can bind to the adaptor protein STING, which results in the activation of immune signaling and cytokine protein production. There are several cancers, such as multiple myeloma, fibrosarcoma, malignant astrocytoma and a mouse melanoma, that require the constant presence of certain cytokine or growth factor proteins to survive and/or proliferate. From our unpublished and preliminary data, we have discovered that in certain biological contexts the cGAS-STING pathway can cause constant production of some of the same cytokines and growth factor proteins that the aforementioned cancers require. We propose that in several cancers, the cGAS-STING pathway is critical for tumor-promoting protein-secretion loops. Verification of our findings could identify previously unknown signaling network relationships and will suggest the viability of new cancer therapy drugs that block the cGAS-STING pathway.
Competitiondate
201611
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Hodge, Curtis D
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $150,000~ $0~