BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//CERN//INDICO//EN
BEGIN:VEVENT
SUMMARY:Temporal dynamics of macrophages plasticity in the bone microenvir
 onment
DTSTART;VALUE=DATE-TIME:20180709T050000Z
DTEND;VALUE=DATE-TIME:20180709T052000Z
DTSTAMP;VALUE=DATE-TIME:20210228T011325Z
UID:indico-contribution-347@conferences.maths.unsw.edu.au
DESCRIPTION:Speakers: Etienne Baratchart (Integrated Mathematical Oncology
  Dept\, H Lee Moffitt Cancer Center)\nTumour associated macrophages have l
 ong been implicated in the progression of primary solid malignancies inclu
 ding prostate cancer. Metastatic prostate cancer typically manifests in th
 e bone where it induces painful osteogenic lesions that are incurable. Bon
 e is naturally rich in myeloid derived macrophages whose temporal polariza
 tion into pro- (M1) and anti-inflammatory (M2) phenotypes is critical for 
 regulating the program of bone injury repair mediated by bone resorbing os
 teoclasts (OCL) and bone building (OBLs). However\, the dynamics of macrop
 hage polarization in the context of bone metastatic prostate cancer is und
 erexplored and difficult to address with traditional biological approaches
 . In order to address it we built a mathematical model describing bone res
 ident cell population dynamics during bone injury response through a set o
 f coupled ordinary differential equation (ODE). We informed this model by 
 analyzing macrophage plasticity *in vivo* subsequent to intratibial injury
 . Bone marrows were isolated at several time points and profiled by flow c
 ytometry for pro- and anti-inflammatory macrophage content. Contralateral 
 tibias were analyzed for bone volume\, osteoblast and osteoclast numbers. 
 The ODE model was able to predict experimental observations of M1/M2\, OBL
 \, OCL and bone dynamics. Generation of the ODE model required testing a n
 umber of assumptions regarding macrophage polarization behaviour. For exam
 ple\, it is unknown whether M1 resolve at the initial stages of bone injur
 y repair through death\, or by re-polarizing into M2. For each aspect\, co
 mpeting mechanistic assumptions were proposed and simulated mathematically
  by sets of ODEs. The best fitting assumptions for each aspect were integr
 ated into a comprehensive ODE model to fully describe the dynamics of the 
 bone resident cell populations during bone repair. This experimentally val
 idated model is now being exploited to address how bone population dynamic
 s respond to metastatic prostate cancer cells and subsequently identify th
 e resultant impact on bone formation and cancer growth.\n\nhttps://confere
 nces.maths.unsw.edu.au/event/2/contributions/347/
LOCATION:University of Sydney New Law School/--107
URL:https://conferences.maths.unsw.edu.au/event/2/contributions/347/
END:VEVENT
END:VCALENDAR