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Background: Pancreatic cancer is among the malignancies with the poorest prognosis, largely due to its aggressive nature and resistance to conventional therapies. Case Summary: This report describes the case of a 69-year-old male patient with stage IV primary lung adenocarcinoma presenting with high levels of programmed death-ligand 1 (PD-L1). Simultaneously, abdominal computed tomography (CT) showed a dilated pancreatic duct at the level of the pancreatic head and a hypodense lesion in the uncinate process involving the superior mesenteric artery. Fine-needle aspiration (FNA) of the pancreatic lesions was negative. After three cycles of chemoimmunotherapy, positron emission tomography–computed tomography (PET-CT) showed complete remission of the lung nodules, lymphadenopathy, and pleural thickening, as well as a decrease in the size of the pancreatic lesion. After another six months, a PET-CT scan showed a focal increased uptake in the pancreatic mass in the same location, indicating disease progression. A core biopsy of the pancreatic tumor showed atypical spindle cell morphology with positive staining for vimentin, characteristic of mesenchymal differentiation with no apparent epithelial features. Comprehensive molecular profiling through Caris Molecular Intelligence® revealed four genes with actionable mutations in the pancreatic tissue, including KRAS (p.G12D) and TP53 (p.R175H). These molecular findings suggested the diagnoses of sarcomatoid carcinoma and conventional pancreatic ductal adenocarcinoma with epithelial–mesenchymal transition. Primary mesenchymal tumors and neuroendocrine neoplasms were excluded because immunohistochemistry was negative for anaplastic lymphoma kinase (ALK), smooth muscle actin (SMA), desmin, CD34, signal transducer and activator of transcription 6 (STAT6), S100, HMB45, CD117, discovered on GIST-1 (DOG1), CD56, progesterone, and synaptophysin. However, despite multiple rounds of systemic chemotherapy, immunotherapy, and radiation, his pancreatic disease rapidly deteriorated and metastasized to the liver and bone. Conclusions: Despite multiple lines of treatment, the patient's condition worsened and he succumbed to his pancreatic malignancy. This study highlights the clinical characteristics, diagnosis, and treatment of rare pancreatic cancer, emphasizing the importance of molecular testing and histopathological biomarkers in personalizing treatment. It also provides insights into promising therapeutic approaches for similar cases with an unusual presentation. [ABSTRACT FROM AUTHOR]

Fibroblast Activation Protein Inhibitor (FAPI) positron emission tomography (PET) imaging has emerged as a useful method for identifying pancreatic disorders, notably pancreatitis. Unlike Fluorine-18 fluorodeoxyglucose (FDG), FAPI uptake is directly proportional to the degree of fibrosis, making it very useful in separating pancreatic tumors from inflammation. Recent investigations have shown that FAPI positron emission tomography/computer tomography (PET/CT) can identify pancreatic inflammation with great sensitivity, providing vital diagnostic information. In this case study, a 52-year-old male with a history of Ewing sarcoma presented with epigastric pain. Pancreatitis was confirmed on a computer tomography (CT) scan showing mild fat stranding in the pancreatic body and tail, in addition to a significant increase in pancreatic head mass, necessitating further evaluation with FDG PET/CT and FAPI PET/CT, as the patient was known to have metastatic sarcoma. While FDG PET/CT revealed an avid infiltrative lesion in the duodenal/pancreatic head area, FAPI PET/CT showed diffuse uptake in the pancreatic body and tail, indicating fibroblast-mediated inflammation consistent with pancreatitis. This case demonstrates the usefulness of FAPI imaging in discriminating between pancreatic metastasis and pancreatitis, with FAPI PET/CT providing crucial diagnostic information when FDG uptake is ambiguous. [ABSTRACT FROM AUTHOR]