Ignite Creation Date:
2024-05-06 @ 3:56 PM
Last Modification Date:
2024-10-26 @ 2:00 PM
Study NCT ID:
NCT04813913
Status:
UNKNOWN
Last Update Posted:
2021-03-24
First Post:
2020-06-25
Brief Title:
VASCular Impact of Angiogenic Treatment in Patients With Advanced Colorectal Cancer
Sponsor:
University Hospital Rouen
Organization:
University Hospital Rouen
Study Overview
Official Title:
VASCular Impact of Angiogenic Treatment in Patients With Advanced Colorectal Cancer
Status:
UNKNOWN
Status Verified Date:
2020-06
Last Known Status:
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:
VASCATAQ
Brief Summary:
Antiangiogenic treatments are used in many tumor locations such as metastatic colorectal cancer mCRC with a significant improvement in carcinological results on overall survival and or progression-free survival However their use is characterized by an increase in side effects and in particular cardiovascular effects such as high blood pressure hypertension One of the main classes of antiangiogens used in this indication is that of monoclonal antibodies the leader of which is bevacizumab Avastin Roche Bale Switzerland Bevacizumab works by inhibiting endothelial vascular growth factor-dependent neoangiogenesis vascular endothelial growth factor VEGF In the reference studies the inhibition of VEGF whether extracellular monoclonal antibody directed against VEGFA or intracellular receptor inhibitors with tyrosine kinase activity induces hypertension of all grades observed in 25 to 40 of patients including 8 to 17 of severe grades grade 3 NCI-CTCAE In terms of pathophysiology inhibition of VEGFA results in a decrease in the availability of nitric oxide NO at the endothelial level and the appearance of arteriolar rarefaction This induces an increase in peripheral resistance responsible ultimately for an increase in blood pressure The occurrence of hypertension induced by anti-VEGF treatment seems to be predictive of the carcinological response in certain oncological situations such as metastatic breast cancer9 glioblastoma and mRCC Furthermore it has also been shown that there is an early attack on the elastic conductance arteries branches of the aorta and its main ones characterized by an increase in their rigidity in patients exposed to a VEGF receptor inhibitor with tyrosine activity kinase or bevacizumab This increase whose poor prognostic impact is known at the cardiovascular level is largely independent of the rise in blood pressure and reflects a direct toxicity of treatments at the level of the artery wall This increase in rigidity refused when the pressure rises would be predictive of a low carcinological response rate at 6 months However these data are based on populations that are heterogeneous in terms of carcinology and the position prior to or concomitant with other antineoplastic treatments
In this context the evaluation of arterial stiffness in the same patient population would make it possible to better define the involvement of the conductive arteries in a clearly defined clinical situation Joint measurements of the plasma concentration of the treatment as well as those of factors derived from the endothelium and circulating tumor markers which to our knowledge have never been carried out in these patients would make it possible to better specify the mechanisms of involvement and the links between exposure arterial toxicity and carcinologic efficacy of bevacizumab Of course in order to assess more precisely the inherent impact of chemotherapy on the conductance arteries the evolution of arterial stiffness must take into account the possible effects in patients receiving for essentially clinical and biological reasons systemic treatment without antiangiogenic
In this context the evaluation of arterial stiffness in the same patient population would make it possible to better define the involvement of the conductive arteries in a clearly defined clinical situation Joint measurements of the plasma concentration of the treatment as well as those of factors derived from the endothelium and circulating tumor markers which to our knowledge have never been carried out in these patients would make it possible to better specify the mechanisms of involvement and the links between exposure arterial toxicity and carcinologic efficacy of bevacizumab Of course in order to assess more precisely the inherent impact of chemotherapy on the conductance arteries the evolution of arterial stiffness must take into account the possible effects in patients receiving for essentially clinical and biological reasons systemic treatment without antiangiogenic
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
False
Is an FDA AA801 Violation?:
None