International registries of families at high risk of pancreatic cancer
Abstract
Aims This study aimed to investigate the effect of caffeic acid phenethyl ester (CAPE), an active component isolated from honeybee propolis, in inducing apoptosis in human pancreatic cancer cells. Methods Inhibition of viability of BxPC-3 and PANC-1 cell lines induced by CAPE was estimated by a trypan blue dye exclusion test. The type of cell death in BxPC-3 after CAPE treatment was characterized by observation of morphology, sub-G1 DNA content, annexin-V/PI staining, caspase-3 and caspase-7 assay, and DNA agarose gel electrophoresis. Results CAPE (10 microg/ml) resulted in marked inhibition of viability of BxPC-3 (80.4 +/- 4.1%) and PANC-1 (74.3 +/- 2.9%) cells. CAPE induced a time-dependent increase in hypodiploid percentage and a significant decrease in mitochondrial transmembrane potential in BxPC-3 cells. It induced morphological changes of typical apoptosis, but no DNA fragmentation was noted by DNA electrophoresis. The inhibition of growth and increased in the proportion of sub-G(1) cells was partially blocked by pretreatment with the pan-caspase inhibitor Z-VAD-fmk (50 microM) in BxPC-3 cells indicating a caspase-related mechanism in CAPE-induced apoptosis. Caspase-3/caspase-7 activity was approximately 2 times greater in CAPE-treated BxPC-3 cells compared with control cells. Conclusions These results suggest that CAPE is a potent apoptosis-inducing agent. Its action is accompanied by mitochondrial dysfunction and activation of caspase-3/caspase-7.
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Registries of high-risk families indicate a roughly 50% lifetime risk of pancreatic ductal adenocarcinoma, regardless of whether a causative mutation is known.
“Registries of such high-risk families indicate a roughly 50% lifetime risk, regardless of whether a causative mutation is known,31”
From Early detection of pancreatic cancer (2020) · cites this paper as [31]
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Lichtenstein, P., Holm, N. V., Verkasalo, P. K., Iliadou, A., Kaprio, J., Koskenvuo, M., Pukkala, E., Skytthe, A., & Hemminki, K. (2000) · New England Journal of Medicine · doi:10.1056/nejm200007133430201 · Cited by 4,114 · see citing works
CDKN2A Germline Mutations in Familial Pancreatic Cancer
Bartsch, D. K., Sina-Frey, M., Lang, S., Wild, A., Gerdes, B., Barth, P., Kress, R., Grützmann, R., Colombo-Benkmann, M., Ziegler, A., et al. (2002) · Annals of Surgery · doi:10.1097/00000658-200212000-00005 · Cited by 186 · see citing works
Self-citationChang, Y.-T., Chang, M.-C., Su, T.-C., Liang, P.-C., Su, Y.-N., Kuo, C.-H., Wei, S.-C., & Wong, J.-M. (2008) · Clinical Chemistry · doi:10.1373/clinchem.2007.093492 · Cited by 83 · see citing works
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Early detection of pancreatic cancer
Pereira, S. P., Oldfield, L., Ney, A., Hart, P. A., Keane, M. G., Pandol, S. J., Li, D., Greenhalf, W., Jeon, C. Y., Koay, E. J., et al. (2020) · The Lancet Gastroenterology & Hepatology · doi:10.1016/s2468-1253(19)30416-9 · Cited by 482 · see citing works
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- Authors
- Greenhalf, W., Malats, N., Nilsson, M., Bartsch, D., & Neoptolemos, J.
- Affiliations
- University of Liverpool (GB)
- Karolinska Institutet (SE)
- Klinikum Bielefeld (DE)
- Corresponding author
- Greenhalf, William
- Venue
- Pancreatology
- Publisher
- Elsevier BV
- Published
- 2008-10
- Volume
- 8
- Issue
- 6
- Pages
- 566-576
- ISSN
- 1424-3903 (ISSN-L)
- OpenAlex
- W2797663228
- Cited by
- 85
- References
- 3
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 5 · 2022: 3 · 2021: 4 · 2020: 7 · 2019: 1 · 2018: 7 · 2017: 4 · 2016: 4 · 2015: 7 · 2014: 6 · 2013: 10 · 2012: 10
- FWCI
- 6.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pancreatology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Agricultural and Biological Sciences › Insect Science › Bee Products Chemical Analysis
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Pharmacology › Healthcare and Venom Research
- Keywords
- caffeic acid phenethyl ester, propolis, pancreatic cancer, apoptosis, caspase-3, caspase-7, mitochondrial membrane potential, mitochondrial dysfunction, BxPC-3 cells, PANC-1 cells, cell viability inhibition, hypodiploidy
- MeSH terms
- Antioxidants, Caffeic Acids, Cell Survival, Dose-Response Relationship, Drug, Humans, Mitochondria, Pancreatic Neoplasms, Phenylethyl Alcohol, Substrate Specificity, Time Factors, Apoptosis, Caspases, Cell Line, Tumor, Membrane Potential, Mitochondrial, DNA Fragmentation
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