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Grant: Doctoral Re. Award - PA: Sex, Gender and Intersectionality in Health Research

University of British Columbia

$120,000.00

Mechanisms of Neuroproliferation: A Potential Etiology of Endometriosis-Associated Pelvic Pain

EF 2025-26

Résumé
This project investigates the pathways that drive pelvic pain in patients with endometriosis. Endometriosis is a chronic condition in which tissue similar to the inner lining of the uterus grows outside of the uterus. This condition affects approximately 10% of women, girls, and people with a uterus of reproductive age. It is a common cause of infertility and severe pelvic pain, including painful menstruation and penetrative sex, with an estimated annual cost of $1.8 billion to the Canadian healthcare system. Our laboratory has found evidence that patients with endometriosis who experience pain with sex may have a higher number of nerve bundles surrounding their endometriosis lesions, potentially driven by high levels of inflammation, inherited genetic changes, and/or non-inherited gene mutations within the endometriosis lesions. We propose that these patients have a specific type of endometriosis, which we have termed "neuroproliferative endometriosis," that could be identified based on the presence of these inflammatory factors and genetic changes. My research will confirm neuroproliferative endometriosis in a new patient cohort by comparing the inflammatory biomarkers among those with painful sex. I will further investigate whether known inherited and non-inherited genetic changes are driving nerve growth, and therefore, more pain. Finally, I will create a model of neuroproliferative endometriosis by simultaneously culturing human endometriosis cells and sensory neurons to investigate their associations in real-time. Ultimately, this model will be used to test potential drug targets to treat endometriosis. My research will contribute to our understanding of how endometriosis and endometriosis-related pain develop, but also lead to new drug treatments for the neuroproliferative subtype of endometriosis.
Programme
Doctoral Re. Award - PA: Sex, Gender and Intersectionality in Health Research
Emplacement
British Columbia, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
561083
Name
Sreya Mahfuza S
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Gender and Health
Theme2
Biomedical
Prcname2
DT1 (Biomedical and/or Clinical Research) CGRS Doctoral
Projecttitle
Mechanisms of Neuroproliferation: A Potential Etiology of Endometriosis-Associated Pelvic Pain
Programtype2
Studentship Programs
Orgnameinp2
University of British Columbia
Cihramount2
$120,000
Cihrequipment2
$0
Programname2
Doctoral Re. Award - PA: Sex, Gender and Intersectionality in Health Research
Keyworddelim
Co-Culture Modeling; Crispr-Cas9; Dyspareunia; Endometriosis; Immunohistochemistry; Nerve Bundle Density; Nerve Growth Factor (Ngf); Neuroproliferation; Snp Genotyping; Somatic Mutation
Abstract
This project investigates the pathways that drive pelvic pain in patients with endometriosis. Endometriosis is a chronic condition in which tissue similar to the inner lining of the uterus grows outside of the uterus. This condition affects approximately 10% of women, girls, and people with a uterus of reproductive age. It is a common cause of infertility and severe pelvic pain, including painful menstruation and penetrative sex, with an estimated annual cost of $1.8 billion to the Canadian healthcare system. Our laboratory has found evidence that patients with endometriosis who experience pain with sex may have a higher number of nerve bundles surrounding their endometriosis lesions, potentially driven by high levels of inflammation, inherited genetic changes, and/or non-inherited gene mutations within the endometriosis lesions. We propose that these patients have a specific type of endometriosis, which we have termed "neuroproliferative endometriosis," that could be identified based on the presence of these inflammatory factors and genetic changes. My research will confirm neuroproliferative endometriosis in a new patient cohort by comparing the inflammatory biomarkers among those with painful sex. I will further investigate whether known inherited and non-inherited genetic changes are driving nerve growth, and therefore, more pain. Finally, I will create a model of neuroproliferative endometriosis by simultaneously culturing human endometriosis cells and sensory neurons to investigate their associations in real-time. Ultimately, this model will be used to test potential drug targets to treat endometriosis. My research will contribute to our understanding of how endometriosis and endometriosis-related pain develop, but also lead to new drug treatments for the neuroproliferative subtype of endometriosis.
Competitiondate
202511
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Sreya, Mahfuza S
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $120,000~ $0~