FAP-1 Study: FAPi PET in Pancreatic Ductal Adenocarcinoma: A Prospective, Exploratory Study
Conditions: Pancreatic Cancer, Adenocarcinoma Pancreas
Sponsor: Tata Memorial Hospital

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FAPi PET in Pancreatic Ductal Adenocarcinoma:  
A Prospective, Exploratory Study 
 
Principal Investigator: 
Dr Ameya Puranik 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

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Title: 
FAPi PET in Pancreatic Ductal Adenocarcinoma: A Prospective, Exploratory Study 
Introduction: 
The estimated worldwide incidence and cancer associated mortality of pancreatic cancer is 
about 496,000 and 466,000, respectively, according to the 2020 Global Cancer Statistics. (1) 
The most common (90%) histological subtype of pancreatic cancer is pancreatic ductal 
adenocarcinoma (PDAC); which we shall henceforth refer to as ‘pancreatic cancer’; other 
subtypes include neuroendocrine tumor, acinar cell carcinoma,and pancreatoblastoma.(2) 
Pancreatic cancer is typically characterized by intense desmoplastic reactions surrounding the 
cancer cells.(3-5) The characteristic stromal desmoplastic response plays a key role in tumor 
invasion, metastasis, and drug resistance.The stromal component comprises up to 80% of the 
pancreatic tumor mass.(6) 
What is Desmoplasia and its relevance in Pancreatic cancer? 
Desmoplasia, which is also referred to as the desmoplastic reaction, is a fundamental 
characteristic of PDAC. It clinically manifests itself in two ways: (7) significant overproduction of 
extracellular matrix (ECM) proteins, and (8) extensive proliferation of myofibroblast-like cells.(9) 
The resulting dense and fibrous connective tissue therefore is composed of both cellular and 
non-cellular components. Desmoplasia, which is a result of the proliferation of alpha-smooth 
muscle actin-positive fibroblasts (also known as the myofibroblast, or activated pancreatic 
stellate cell (PSC)) and increased deposition of extracellular matrix (ECM) components, leads to 
reduced elasticity of tumor tissue with a concomitant increase in tumor interstitial fluid pressure 
(IFP). Increased IFP results in a decreased rate of perfusion of therapeutic agents and 
consequently decreased efficacy. This physiological chemoresistance has been shown to be a 
major contributor to the reduced efficacy of chemotherapeutics in multiple tumor types.(10) In 

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addition, desmoplasia can result in multiple signaling cascades that increase biological 
chemoresistance to therapeutic agents.  
Fibroblast-Activation Protein and its expression in various cancers: 
Fibroblast activation protein (FAP) is strongly expressed on cancer-associated fibroblasts and is 
a key player in tumor progression (11). High FAP expression is restricted almost exclusively to 
cancer-associated fibroblasts and serves as an independent negative prognostic factor for 
multiple types of cancer (12). In vivo depletion of FAP-positive stromal cells inhibits tumor 
growth by decreasing cancer support, increasing antitumor immunity, and limiting stromal 
barrier effects (13,14). Recently, FAP inhibitor (FAPi)–targeting ligands labeled with 
radioisotopes for PET imaging (e.g., 68Ga and 18F for PET) and therapy (e.g., 177Lu and 90Y) 
have been introduced (15,16). The high tumor uptake that was observed with FAPi PET imaging 
in various cancers suggests that radiolabeled FAPi compounds have promising potential for 
diagnostic and therapeutic applications.(17) 
In a prospective exploratory study by Mona et al (18), , FAPi PET human biodistribution in 
cancer was validated against tumor FAP expression as assessed by immunohistochemistry, on 
a pancancer human tissue microarray (141 patients, 14 different types of cancer). It was 
concluded that FAP biodistribution on imaging strongly correlated with FAP tissue expression. 
Hirmas et al, (19) as a part of interim analysis of prospective trial showed a strong correlation 
between Ga-FAPI SUV max and FAPI IHC scores, especially for sarcoma and pancreatic 
cancer 
Fibroblast-activation protein in Pancreatic Cancer: 
Fibroblast-activation protein (FAP) is a serine protease that contains both dipeptidyl peptidase 
and gelatinase/collagenase activities in vitro [20]. Because of its specific induction in tumor-
associated fibroblasts in over 90% of epithelial tumors, including pancreas and breast among 
others, FAP was used as a platform for studying stromal specific effects on tumor behaviors 
[21]. It is known that FAP exhibits very restricted expression in normal adult tissue and that 

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pancreatic stellate cells are the ‘normal’ fibroblastic cells found in the exocrine pancreas. 
Activated pancreatic stellate cells are believed to be responsible for the fibrosis in chronic 
pancreatitis and the desmoplastic reactions in pancreatic adenocarcinomas [22]. 
The experimental approach used to study the role of FAP in tumor invasion utilized an in vivo-
like 3D matrix system that has been shown to effectively recapitulate stromal ECMs from 
various murine and human tissues.[23] In this study, it has been observed that FAP+ fibroblast-
derived matrices presented higher organization levels of fibers when compared to FAP- 
matrices. Importantly, it was shown that FAP+ matrices contain parallel fiber organization 
features that are reminiscent of tumor-associated ECMs of pancreatic desmoplastic tissues 
associated with pancreatic adenocarcinoma looking at human normal and tumor ECMs both in 
vivo and in vitro. 
Imaging of Pancreatic Cancer: 
Contrast-enhanced Computed Tomography (ceCT) is recommended as the primary imaging 
modality for resectability evaluation according to the National Comprehensive Cancer Network 
(NCCN) and European Society for Medical Oncology (ESMO) guidelines.[24,25] Pancreatic 
cancer is usually seen as a mass lesion that exhibits hypoenhancement compared to the 
adjacent parenchyma in the pancreatic phase. It may cause interruption and upstream dilatation 
of the pancreatic or bile duct, abutment or encasement of adjacent vascular structures, direct 
invasion of adjacent organs, and regional lymph node enlargement. In meta-analyses, ceCT has 
shown sensitivity of 89–91% and specificity of 85–90% for the diagnosis of pancreatic 
cancer.[26] Also, for assessment of resectability, ceCT has shown a better diagnostic 
performance than MRI.[27] 
PET/CT imaging for Pancreatic Cancer: 
Although it is the most widely used PET tracer in nuclear oncology, 18F-
fluorodeoxyglucose(18F FDG) has several limitations in the diagnosis and staging of pancreatic 

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cancer.[28] First, 18F-FDG PET/CT sometimes yields false-negative results in the detection of 
small, isodense 
pancreatic cancers. Second, 18F-FDG PET/CT has a low-to-moderate sensitivity in the 
evaluation of metastatic lymph nodes (LNs). It underestimates the N (node) stage, limiting its 
utility in the surgical planning for patients with pancreatic cancer.[29] Furthermore, 18F-FDG 
PET/CT exhibits poor performance in the detection of liver metastases and peritoneal 
carcinomatosis, which are common forms of metastasis in pancreatic cancer.[30] 
FAPI PET/CT in Pancreatic Cancer: 
As FAP is overexpressed on the CAFs of 90% of the types of malignant epithelial cancer and 
exhibits negative/low expression in healthy tissues, it has attracted much attention as a tracer of 
choice where FDG has limited utility. Recently, a series of quinoline-based FAP inhibitors 
(FAPIs) have been developed and these have yielded encouraging results in preclinical 
and clinical molecular imaging studies.[31,32] In a preclinical study, a patient-derived orthotopic 
xenograft model of pancreatic adenocarcinoma displayed a significantly higher tumor-to-muscle 
ratio with 68Ga-FAPI-04 than with 18F-FDG.[33] The favorable image contrast obtained with 
68Ga-FAPI PET/CT may allow its clinical use for the detection of early-stage pancreatic cancer. 
In a subsequent clinical investigation of a larger patient cohort, 68Ga-FAPI (FAPI-04) PET/CT 
exhibited intense radiotracer uptake and favorable tumor-to-background contrast ratios in 
various cancers, including pancreatic cancer (maximum standardized uptake value [SUVmax] > 
10 in pancreatic cancer, n 5 51).[34] In a study reported by Rohrich and colleagues,[35] 19 
patients with PDAC (7 primary, 12 progressive/recurrent) demonstrated intense 68Ga-FAPI 
(FAPI-04) uptake in the primary tumors (SUVmax: 13.37  5.45), LN metastases (SUVmax: 
14.13  8.50), and distant metastases (SUVmax: 7.34  2.48). These first experiences of 68Ga-
FAPI PET/CT in pancreatic cancer highlight its potential use in tumor staging, recurrence 
detection, and individual oncologic management. 
Comparison of FDG PET and FAPI PET: 

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In the first head-to-head comparative study in pancreatic cancer (68Ga-FAPI-04 vs 18F-FDG), 
68Ga-FAPI PET/CT exhibited significantly higher radiotracer uptake than 18F-FDG in primary 
tumors (SUVmax, 21.4 vs 4.8; P < .001), involved LNs (SUVmax, 8.6 vs 2.7; P < .001), liver 
metastases (SUVmax, 7.4 vs 3.7; P < .001), peritoneal metastases (SUVmax, 8.4 vs 2.8; P < 
.001), and bone metastases (SUVmax, 10.6 vs 2.3; P 5 .001).[36] In contrast to 18F-FDG, 
68Ga-FAPI was not taken up by the brain tissue, and exhibited lower background activity in the 
liver, heart, and gastrointestinal tract. 68Ga-FAPI PET/CT yielded a favorable image contrast 
with low background activity throughout the body. [37] Regarding the diagnostic accuracy, 
68Ga-FAPI PET/CT exhibited significantly higher sensitivity than 18F-FDG PET/CT in the 
detection of primary tumors (100% vs 73%), involved LNs (82% vs 59%), and bone and 
visceral metastases (92% vs 44%).[38] 
Conclusion: FAP expression has been documented in pancreatic cancers, in animal models as 
well as human studies, which has formed the basis of using the FAP inhibitor - FAPi radioligand 
for imaging. This needs systematic prospective study of Ga-68-labeled FAPi PET/CT imaging in 
pancreatic lesions suspicious of malignancy as well as biopsy proven pancreatic ductal 
adenocarcinomas for staging and restaging to assess the imaging parameters. 
Current status of FAPi PET: 
FAPi PET is an established imaging modality in Europe and United States with majority of the 
literature involves studies realted to gastro-intestinal cancers. In the Indian scenario, FAPi 
peptide was made available in India in 2021 and is routinely used in clinical practice, with the 
earliest multi-center study in 2021 involved All India Institute of Medical Sciences [39],wherein 
they showed increased tumor accumulation and retention time, with no abnormal 
biosdistribution at other sites. Since then, FAPi has been extensively used in almost 15-20 
centres, both in public and private hospitals. In Department of Nuclear Medicine at Tata 

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Memorial Hospital, we have been using FAPi in select cases since 2021, and our retrospective 
audit is already in process which is an TMC IEC approved project (No - 4167). 
Rationale of our study: 
● Tata Memorial Hospital is an apex referral center for pancreatic cancer, with 
approximately 200-250 new patients visiting the out-patient department every year. 
● In current western literature, FAPi labeled PET imaging has shown strong potential for 
diagnosis, staging and restaging of pancreatic cancers. 
● There is availability of this radioligand in our facility which has provided us with the 
opportunity to design this study. 
Aims and Objectives: 
Aim: To evaluate utility of FAPI PET/CT in  
- 
Histopathologically proven pancreatic cancer for staging/restaging 
- 
Post neoadjuvant therapy response assessment 
Objective: To calculate sensitivity, specificity, positive predictive value and negative predictive 
value of quantitative and semi-quantitative parameters on FAPi PET 
Methodology: 
Type of Study: Prospective, exploratory 
Centers -  
Dept of Nuclear Medicine, Tata Memorial Hospital, Mumbai and ACTREC, Navi Mumbai  
Sample Size - Since this is an exploratory study, a sample size of 60 (approximately 30 each 
for diagnosis/staging and restaging) 
Study Duration:  
Recruitment: From the date of approval to 12 months 
Follow-up period: 12 months from the recruitment of last patient 
Inclusion Criteria: 

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- 
Any gender with age more than 18 years 
- 
Patients with pancreatic cancer referred to TMH and ACTREC 
- 
Patient willing to participate in study 
Exclusion criteria:  
- 
Patient with concurrent malignancy 
Imaging Time-points: 
Baseline and post NACT response assessment -  within 2 weeks of ceCT 
Imaging Protocol: 
Patients referred from GI-OPD shall be explained the procedure and consent will be taken 
After detailed history taking, an intravenous access will be secured. In-house synthesis and 
labeling of Ga-68-FAPi shall be performed. As is recommended, 3-4 mCi of radiotracer shall be 
injected IV and the patient shall be asked to wait in the radiation waiting facility for 45-60 mins. 
Patients then will be positioned supine in PET/CT scanner for scan acquisition. 
Acquisition protocol: 
After obtaining a scout image whole body CT will be performed first in craniocaudal direction 
(120kV, slice thickness 5mm,pitch-0.83, voltage 120kV, FOV 600mm, rotation time - 0.5sec, 
automated mA, image matrix-512x512). Non-contrast CT was used for diagnostic purposes and 
for attenuation correction of the PET data. PET scanning was performed immediately after the 
CT acquisition, without changing the patient position. Approximately twelve bed positions shall 
be used for imaging, with an acquisition time of 60-90 seconds for each position. PET shall be 
acquired in 3D mode. Fusion PET/CT images will be generated and can be viewed on 
workstation.  
Image Interpretation: 
Lesion detection: 
 
ceCT (size) 
Interpretation  
 
FAPI PET 
(SUV max) 
Interpretation 

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Primary 
 
 
 
 
Nodes 
 
 
 
 
Metastases 
 
Liver 
 
Other 
 
 
 
 
 
Semi-quantitative parameters: 
Maximum standardised uptake value (SUV max) and FAPi metabolic volume: 
System-generated automated region of interest will be drawn on the lesion  
Tumor-to-normal liver ratio: SUV max of lesion in liver and normal liver will be calculated with 
automated ROI 
Gold Standard: Follow-up imaging or histopathology 
Statistical analysis: 
Data analysis will be performed using SPSS software Version 25 (IBM) 
Following variables will be analyzed for the calculation of sensitivity, specificity, PPV & NPV of 
FAPI PET/CT; 
1. SUVmax of the primary and metastatic sites. 
2. Ratio of SUVmax of the lesion to the SUVmax in the mediastinal blood pool. 
Optimal cutoffs will be derived using ROC curve and Youden's index 
Above mentioned continuous variables will be stratified based on the optimal cutoffs obtained 
from the ROC curve. 
FAPI PET/CT findings will be confirmed either with follow up imaging or histopathological 
correlation wherever available. 
 
 
 

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