Ignite Creation Date:
2024-10-26 @ 3:43 PM
Last Modification Date:
2024-10-26 @ 3:43 PM
Study NCT ID:
NCT06649474
Status:
RECRUITING
Last Update Posted:
None
First Post:
2024-09-05
Brief Title:
Evaluation in Humans of the Correlation Between Hepatotoxicity Neurotoxicity Induced by Oxaliplatin and Blood Levels of HMGB1
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Evaluation in Humans of the Correlation Between Hepatotoxicity Neurotoxicity Induced by Oxaliplatin and Blood Levels of HMGB1
Status:
RECRUITING
Status Verified Date:
2024-10
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
HEPATOXALI
Brief Summary:
Oesogastric and pancreatic adenocarcinomas are poor-prognosis cancers Incidence of pancreatic cancer drastically increases to such an extent that it will become the second cause of cancers mortality by 2030 A major challenge is to optimize the therapies for localized setting when oxaliplatin-based chemotherapy is the standard before and after surgical excision Because in 50 of cases oxaliplatin triggers a grade 2-3 sinusoidal obstruction syndrome SOS which increases post-operative morbidity decreases histological response to chemotherapy increases tumor recurrence and aggravates the risk of chemotherapy-induced peripheral neuropathy CIPN
There is an urgent need to better understand the biological processes involved in SOS in order to prevent and treat it without stopping or reducing oxaliplatin administration
The biological link between oxaliplatin and SOS has not been described but recent murine experiments argue for HMGB1 to be the mediator released after exposure to oxaliplatin and inducing SOS and thereafter CIPN To date no biomarker is established between murine and patient analyses and the release of HMGB1 after oxaliplatin treatment and its effect on hepatic parenchyma is not described in patients Investigators hypothesized is that HMGB1 would also been increased in patients after oxaliplatin treatment and correlated to the development of SOS and CIPN If confirmed personalized treatment will be possible to target this pathway
Therefore investigators propose to dynamically explore this hypothesis in localized oesogastric and pancreatic cancer patients who will be routinely managed by an initial laparoscopy and post-oxaliplatin surgical excision
There is an urgent need to better understand the biological processes involved in SOS in order to prevent and treat it without stopping or reducing oxaliplatin administration
The biological link between oxaliplatin and SOS has not been described but recent murine experiments argue for HMGB1 to be the mediator released after exposure to oxaliplatin and inducing SOS and thereafter CIPN To date no biomarker is established between murine and patient analyses and the release of HMGB1 after oxaliplatin treatment and its effect on hepatic parenchyma is not described in patients Investigators hypothesized is that HMGB1 would also been increased in patients after oxaliplatin treatment and correlated to the development of SOS and CIPN If confirmed personalized treatment will be possible to target this pathway
Therefore investigators propose to dynamically explore this hypothesis in localized oesogastric and pancreatic cancer patients who will be routinely managed by an initial laparoscopy and post-oxaliplatin surgical excision
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