Biliary-tract-carcinomas (BTC), pancreatic-ductal-adenocarcinomas (PDAC) and adenoidcystic-carcinomas (AC) have in common that they are traditionally treated with large clinical-target-volumes (CTV). The aim of this study is to examine the impact of pretreatment-[Ga]FAPI-PET/CT on target-volume-definition and posttreatment-[Ga]FAPI-PET/CT-response-assessment for BTC-, PDAC- and AC-patients referred to radiation-therapy. All consecutive BTC-, PDAC-, and AC-patients who received pretreatment-[Ga]FAPI-PET/CT±[F]FDG-PET/CT were included from 01.01.2020 to 01.03.2022. MTV and SUV were separately generated based on [Ga]FAPI- and [F]FDG-PET/CT-images. A [Ga]FAPI- and [F]FDG-based-CTV was defined. Treatment-plans were compared. Treatment-response was reassessed by a second [Ga]FAPI-PET/CT and [F]FDG-PET/CT after treatment-completion. Intermodality comparison of lesion-to-background-ratios [SUV/SUV] for individual timepoints t and t revealed significant higher values for [Ga]FAPI compared to [F]FDG (t, p = 0.008; t, p = 0.005). Intermodality comparison of radiation-therapy-plans showed that [Ga]FAPI-based planning resulted in D100% = 97.2% and V95% = 98.8% for the [F]FDG-MTV. [F]FDG-based-planning resulted in D100% = 35.9% and V95% = 78.1% for [Ga]FAPI-MTV. [F]FDG-based-planning resulted only in 2 patients in V95% > 95% for [Ga]FAPI-MTV, and in 1 patient in D100% > 97% for [Ga]FAPI-MTV. GTV-coverage in terms of V95% was 76.4% by [F]FDG-based-planning and 99.5% by [Ga]FAPI-based-planning. Pretreatment [Ga]FAPI-PET/CT enhances radiation-treatment-planning in this particular group of patients. While perilesional and tumoral follow-up [F]FDG-uptake behaved uniformly, perilesional and tumoral reaction may differ in follow-up [Ga]FAPI-imaging. Complementary [Ga]FAPI- and [F]FDG-imaging enhance treatment-response-assessment.
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http://dx.doi.org/10.1038/s41598-022-20447-6 | DOI Listing |
Signal Transduct Target Ther
December 2024
Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Advanced biliary tract cancer (BTC) and pancreatic ductal adenocarcinoma (PDAC) have poor prognoses and limited treatment options. Here, we conducted this first-in-class phase II study to evaluate the efficacy and safety of SHR-1701, a bifunctional fusion protein targeting programmed death-ligand 1 (PD-L1) and transforming growth factor-beta (TGF-β), combined with famitinib, a multi-targeted receptor tyrosine kinase inhibitor, in patients with advanced BTC or PDAC who failed previous standard treatment (trial registration: ChiCTR2000037927). Among 51 enrolled patients, the BTC cohort showed an objective response rate (ORR) of 28% (including 2 complete responses) and a disease control rate (DCR) of 80%, with a median progression-free survival (mPFS) of 5.
View Article and Find Full Text PDFDig Liver Dis
January 2025
Department of Medical and Surgical Sciences - DIMEC, Alma Mater Studiorum - University of Bologna, Bologna, Italy; Morgagni, Pierantoni Hospital, Forlì, Italy. Electronic address:
Cancer Discov
November 2024
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Cancer Discov
November 2024
Cancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Intratumoral heterogeneity in pancreatic ductal adenocarcinoma (PDAC) is characterized by a balance between basal and classical epithelial cancer cell states, with basal dominance associating with chemoresistance and a dismal prognosis. Targeting oncogenic KRAS, the primary driver of pancreatic cancer, shows early promise in clinical trials, but efficacy is limited by acquired resistance. Using genetically engineered mouse models and patient-derived xenografts, we find that basal PDAC cells are highly sensitive to KRAS inhibitors.
View Article and Find Full Text PDFJ Pers Med
April 2024
Department of Surgery, "Iuliu Hațieganu" University of Medicine and Pharmacy, Croitorilor Street, No. 19-21, 400162 Cluj-Napoca, Romania.
Pancreatic cancer is one of the most aggressive, heterogeneous, and fatal types of human cancer; therefore, more effective therapeutic drugs are urgently needed. Human epidermal growth factor receptor 2 (HER2) overexpression and amplification have been identified as a cornerstone in this pathology. The aim of this review is to identify HER2 membrane overexpression in relation to pancreatic cancer pathways that can be used in order to develop a targeted therapy.
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