Whole Body Dynamic 68Ga-DOTATOC PET/CT in Neuroendocrine Tumors

Neuroendocrine Tumors Clinical Trial

— GAPET-NET  

Official title:

Prognostic Interest of a Whole Body Dynamic PET Acquisition in Pre-therapeutic 68Ga-DOTATOC PET/CT for Neuroendocrine Tumors

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT03576040
• Other study ID #: GAPET-NET (29BRC17.0036)
• Status: Recruiting
• Start date: July 19, 2018
• Est. completion date: July 2023

Study information

• Verified date: July 2019
• Source: University Hospital, Brest
• Contact: Philippe Thuillier
• Phone: 02-98-34-71-19
• Email: philippe.thuillier[@]chu-brest.fr
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

Neuroendocrine tumors (NET) are a network of rare tumors with common embryological origin. Functional imaging plays a major role in the extension assessment and tumor characterization of NETs. SPECT/CT with 111In-pentetreotide is the recommended test when tumors are well differentiated (grade G1 or G2). It has a real interest in diagnosis, in therapeutic decision-making (in particular by cold somatostatin analogues or in PRRT) and in the systematic follow-up of patients. Nevertheless, SPECT/CT procedure makes for a relatively long review. In addition, scintigraphy has a lower spatial resolution than PET technology and remains of limited interest for signal quantification.

However, the ability to locate and quantitatively measure the absorption of radiopharmaceuticals in the target tissues is a major challenge in oncology for the characterization of the disease.

Recent developments in radiopharmacy have made it possible to target NETs in PET imaging through the use of somatostatin analogues coupled with positron emitters, called 68Ga-DOTA peptides. The diagnostic performance of 68Ga-DOTApeptide PET/CT appears to be superior to SPECT/CT with 111In-pentetreotide. A marketing authorization has thus recently been issued in France for the use of 68Ga-DOTATOC.

Historically, the recommended quantification method in PET was based on the instantaneous measurement in static acquisition (3D) of the maximum of the standardized uptake value (SUVmax). This approach has the disadvantage to measure the signal at a time "t" for a single voxel of the image. Dynamic acquisition methods (4D) have been proposed to extract a radiotracer absorption coefficient (Ki) for a lesion. Several studies have demonstrated the superiority of Ki versus SUVmax in 18FDG PET/CT for the diagnostic management, therapeutic evaluation and prognosis of various solid cancers.

However, no work has validated this approach in PET / CT at 68Ga-DOTATOC as part of the prognostic evaluation of NETs.

The objective of the study is to evaluate the prognostic value of the tumor absorption coefficient Ki resulting from a 4D whole-body dynamic acquisition in PET / CT at 68Ga-DOTATOC in patients with well-differentiated NETs grade I or II according to the WHO classification

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 120
• Est. completion date: July 2023
• Est. primary completion date: July 2023
• Gender: All
• Age group: 18 Years to 100 Years

Eligibility

Inclusion Criteria:

• Patient majeur = 18 year old

• Présenting a well differentiated neuroendocrine tumor (G1 ou G2)

• Indication performing a68Ga-DOTATOC PET/CT

• non-opposition

Exclusion Criteria:

• Patient <18 years old

• Breastfeeding/ pregnancy

• Other type of tumor

• Refusal of participation

Related Conditions & MeSH terms

• Neuroendocrine Tumors

Intervention

Device:
• Whole Body Dynamic 68Ga-DOTATOC PET/CT
68Ga-DOTATOC PET-CT will be performed in the nuclear medicine department of the University Hospital of Brest on a Biograph mCT S64 machine (Siemens medical, Erlangen, Germany) "Time of Flight" system after intravenous injection of 150MBq of 68Ga-DOTATOC. In the usual conditions for performing this exam, the patient must remain at a strict rest for 60 minutes following the injection of the tracer and before a static 3D acquisition. For this protocol, a complementary 4D dynamic acquisition (15-60 minutes post-injection) will be performed during this usual rest period.

Locations

Country	Name	City	State
France	CHRU de Brest	Brest

Sponsors (1)

Lead Sponsor	Collaborator
University Hospital, Brest

Country where clinical trial is conducted

France, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Progression free survival (PFS)	To evaluate the prognostic value of lesionnal Ki on progression-free survival at 2 years and compare it with SUVmax (static 3D acquisition) in patients with metastatic well-differentiated NET	2 years
Primary	Recidive free survival (RFS)	To evaluate the prognostic value of Ki lesion on progression-free survival at 2 years and compare it with SUVmax (static 3D acquisition) in patients with localised well-differentiated NET	2 years
Secondary	Correlation between lesionnal Ki and immunochemistry markers	Evaluate the statistical correlation between lesional Ki versus SUVmax with NET immunohistochemistry markers expression (SSTR2, SSTR3, and SSTR5; BCL2, Phospho-MTOR expression PD-L1 by tumor cells and immune cells, intra-tumor CD8 + lymphocytes, tumor necrosis surface)	0 to 2 years
Secondary	Predictive value of non-event survival (PFS+RFS)	To evaluate the predictive value of non-event survival (PFS+RFS) with a ?Ki approach in patients receiving an intermediate therapeutic assessment examination (somatostatin analogues or PRRT with 177Lu-DOTATATE), and compare it with a ?SUVmax approach	6 months to 2 years
Secondary	Correlation between 68Ga-DOTATOC PET/CT and/or 111In-pentetréotide SPECT/CT and 177Lu-DOTATATE SPECT/CT	Evaluate the statistical correlation between the SUVmax assessed with 68Ga-DOTATOC PET/CT and/or 111In-pentetréotide SPECT/CT and 177Lu-DOTATATE SPECT/CT	0 to 2 years
Secondary	Prognostic value of Ki versus usual prognostic parameters	To evaluate the prognostic value on non-event survival (PFS+RFS) at 2 years of Ki and clinical parameters (sex, age), biological (CgA assay), pathology (grade, differentiation, Ki67 expression, BCL2, phospho-MTOR).	2 years