Ignite Creation Date:
2024-05-06 @ 8:57 AM
Last Modification Date:
2024-10-26 @ 12:07 PM
Study NCT ID:
NCT02863900
Status:
UNKNOWN
Last Update Posted:
2016-08-11
First Post:
2016-08-01
Brief Title:
From the Characterization of the Cholesterol-epoxide Pathway Deregulation to New Therapeutic Perspectives in Breast Cancers
Sponsor:
Institut Claudius Regaud
Organization:
Institut Claudius Regaud
Study Overview
Official Title:
From the Characterization of the Cholesterol-epoxide Pathway Deregulation to New Therapeutic Perspectives in Breast Cancers
Status:
UNKNOWN
Status Verified Date:
2016-08
Last Known Status:
NOT_YET_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
BREASTEROL
Brief Summary:
The main objective of our project is to further characterize the deregulation of CE Cholesterol Epoxides metabolism in different moleculars subtypes of BC BCBreast Cancer luminal A and B HER2 and triple negative We will study not only the level of expression of the enzymes involved in this pathway by immuno-histochemistry all the enzymes involved were identified in our preclinical work GSTA1 Glutathione S-Transferase A1 DHCR7 D8D7I 11βHSD2 11β-hydroxysteroid dehydrogenase of type 2 but also the metabolite rates of CE hydrolyses cholesterols-56-epoxide CT into cholestane-3β 5α 6β triol DDA Dendrogenin Aand OCDO 6-oxo-cholestan-3β 5α-diol Our preliminary results demonstrate the feasibility of these dosages We will also establish whether these deregulations are i correlated with different histo-prognostic parameters pN N Node pT T Tumor EV TIL but also clinical ii an independent prognostic parameter of BC in terms of disease-free survival metastasis-free survival and overall survival The cohort consists of 350 cases of BC treated between 2009 and 2011 as well as all relevant clinical informations In parallel we will continue our preclinical work by characterizing the targets and mechanisms of action of OCDO Our preliminary results indicate that OCDO is a modulator of the glucocorticoid receptor GR which could be target to inhibit this pathway On the other hand we will characterize in the same manner as in human tumors the deregulations of the CE metabolism in vitro and in vivo including xenografts in mice of human tumors in collaboration with Roman-Roman S on a representative panel of BC molecular subtypes sensitive or not usually administered in clinical treatment and study the anti-tumor effect of various anti-OCDO therapies therapies preventing its production such as Tam tamoxifen or DDA inhibitor of the enzyme producing OCDO or an inhibitor of the GR glucocorticoid receptor alone or in combination with conventional therapies
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None