Four-Timepoint Multi-tracer PET Imaging to Characterize Metastatic prOstate Cancer Heterogeneity
Trial statusRecruiting
Trial phaseNot applicable
Trial typeInterventional
Biological sexMale
Age18+
SponsorFrederic Pouliot
About this trial
Imaging modalities currently used in the clinics do not image cancer, but the effect ofncancer on bone (bone scan) or on the anatomy (CT-scan). Bone scan and CT-scan are therefore named conventional imaging (CI) modalities. Positron Emission Tomography (PET) is an imaging technique that uses tracers to measure cancer activity in each lesion and is therefore quantitative. Usually, treatment changes in metastatic prostate cancers are based on the appearance of new lesions on CI, named metastases. Prostate cancer metastases have been shown to be clonal, which means that there are several cancers within each patient, potentially with divergent behaviors under therapy. In other words, some metastases might be resistant to a systemic therapy like chemotherapy, while others might be sensitive. The study proposes here to use molecular imaging by positron emission tomography to image and quantify the activity of prostate cancer cells in each metastasis before start, after 3 months and after progression during systemic therapy.
Each metastasis will then be measured to assess whether there is an increase (resistance) or a decrease (response) in prostate cancer cell activity. The analysis will determine how many metastases progress or remain stable when new metastases appear on conventional imaging (polyclonal resistance), as well as the impact of a change in therapy on metastases that were previously stable when cancer progressed elsewhere. In addition, the genes expressed in responding and non-responding metastases will be analyzed to identify gene expression patterns associated with resistance and/or response. Overall, this study aims to characterize metastatic prostate cancer clonal resistance mechanisms using serial PET molecular imaging and imaging-guided genomics.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
Assign male at birth, any gender ≥ 18 years old;
Histologically or cytologically proven adenocarcinoma of the prostate;
Metastatic disease documented by at least 3 metastatic active lesions*, ** on whole body bone scan and/or measurable soft tissue on CT-scan (lymph nodes and visceral lesions);
CRPC & post-androgen receptor pathway inhibitor (ARPI) defined by progression under continuous castration (measured serum testosterone ≤50 ng/dL [1.73 nM]) AND an ARPI (darolutamide, apalutamide, enzalutamide or abiraterone acetate);
Disqualifiers
1. Another non-cutaneous malignancy or melanoma diagnosed in the past 5 years; 2. Currently under a randomized controlled trial with unknown allocation; 3-Any disease or condition limiting the patient's capacity to execute the study procedures, based on the investigators' opinion;
Trial design
Design model
Single group
Treatments tested in this trial
PET Tracer
Diagnostic testMulti-tracer PET imaging to characterize metastatic prOstate Cancer heterogeneity
Treatment groups
45 Participants
are divided into 1 treatment groupGroup A: PET with FDG, PSMA and DOTATATEExperimental treatment 1 intervention
Trial outcomes
Primary outcomes
1
Determine the change in prevalence of IIH of mCRPC undergoing consecutive lines of systemic therapy.
Percentage of patients that show heterogeneous FDG and PSMA tracer uptakes between at least two metastases at baseline and at each progression following consecutive lines1 of study systemic therapies.
Time frame
At Baseline and at the date of first and second documented progression, assessed up to 60 months2
Determine intrapatient intermetastasis therapeutic heterogeneous response (IIHR) in mCRPC patients.
Percentage of patients that show opposite FDG and/or PSMA tracer uptake and/or ratio responses between two metastases after first and second study systemic therapy.
Time frame
At the date of first and second documented progression, assessed up to 60 monthsSecondary outcomes
1
Evaluate the impact of systemic treatment change on progressing and non-progressing FDG or PSMA PET lesions under last treatment.
Percentage of metastases per patient that will show a significant increase or decrease of FDG or PSMA tracer uptake or ratio after subsequent treatment change for progression.
Time frame
At the date of first and second documented progression, assessed up to 60 months2
Correlate histopathology of biopsies to imaging phenotypes.
Associate histopathology and immunohistochemistry (IHC) with double tracer imaging phenotypes of biopsied patients.
Time frame
At the date of first and second documented progression, assessed up to 60 monthsOther outcomes
1
Link radiomic, and genomic features of single-timepoint and sequential multitracer PET imaging with clinical outcomes. Characterize the biological features of FDG positive/DOTATATE any/PSMA negative lesions (poor prognosis) vs PSMA positive/FDG any/DO
1. Molecular imaging parameters (including DOTATATE data) and genomics that will predict radiographic or clinical failure to systemic therapy from data at baseline, 3 months and at progression. 2. Molecular characterization of aggressive and less aggressive cancer by fresh frozen analysis (omics) and organoid cultures harvested from corresponding lesions.
Time frame
At the date of randomization, then 3 months after randomizaton and at the date of first and second documented progression, assessed up to 60 monthsSponsors and contacts
Click on the lead sponsor to view all of their trials.
Frederic Pouliot
Lead sponsor
CHU de Quebec-Universite Laval
Sponsor institution
Source ClinicalTrials.gov