Grant: Travel Awards - Institute Community Support
Centre hospitalier de l'Université de Montréal (CHUM)
$1,000.00
Tip60/TRRAP- and MRN/ATM-relayed chromatin stress can mediate senescence-associated inflammatory secretion independently of DNA damage
FY 2015-16
Summary
In recent years it became clear that cancer treatment do not necessarily trigger simple cancer cell death. For example, if prostate cancer cells simply "died" following treatment, tumors should shrink and disappear in a few days, which is not the case. In reality, cancer cells can initiate multiple different responses to treatment varying from rapid programmed cell death to a viable permanent growth arrest reminiscent of cellular aging in normal cells. We now know that this "senescence" response is broadly triggered following cancer therapy in normal and cancer tissues and that these senescent cells can persist for long periods of time (months). Moreover, senescent cells are very active in their host tissue and actively communicate with resident cells, tumor cells and immune cells. Whether these bioactive cells impact the outcome of cancer treatment and whether they can be manipulated remain unknown. Our general goals are to determine the role of senescent cells during cancer evolution and to optimze the senescence response in cancer treatment to improve the long-term outcome.
Department
Program
Travel Awards - Institute Community Support
Location
Quebec, Canada
Recipient Type
Not-for-profit organization or charity
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
331897
Name
Malaquin Nicolas
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Institute of Cancer Research
Projecttitle
Tip60/TRRAP- and MRN/ATM-relayed chromatin stress can mediate senescence-associated inflammatory secretion independently of DNA damage
Programtype2
Undefined
Orgnameinp2
Centre hospitalier de l'Université de Montréal (CHUM)
Cihramount2
$1,000
Cihrequipment2
$0
Programname2
Travel Awards - Institute Community Support
Keyworddelim
Cancer; Dommage À L'Adn; Phenotype Secretoire Asscocié À La Sénescence; Stress De La Chromatine; Sénescence Cellulaire
Abstract
In recent years it became clear that cancer treatment do not necessarily trigger simple cancer cell death. For example, if prostate cancer cells simply "died" following treatment, tumors should shrink and disappear in a few days, which is not the case. In reality, cancer cells can initiate multiple different responses to treatment varying from rapid programmed cell death to a viable permanent growth arrest reminiscent of cellular aging in normal cells. We now know that this "senescence" response is broadly triggered following cancer therapy in normal and cancer tissues and that these senescent cells can persist for long periods of time (months). Moreover, senescent cells are very active in their host tissue and actively communicate with resident cells, tumor cells and immune cells. Whether these bioactive cells impact the outcome of cancer treatment and whether they can be manipulated remain unknown. Our general goals are to determine the role of senescent cells during cancer evolution and to optimze the senescence response in cancer treatment to improve the long-term outcome.
Competitiondate
201505
Approvedterm2
1 yr 0 mth
Pinamesdelim
Malaquin, Nicolas
Approvedterm
1 an 0 mois
Cihrcontribution2
Inst of Cancer Research~ $1,000~ $0~