Heterotopic pancreatic parenchyma recapitulates the normal pancreas in extrapancreatic locations and, on rare occasions, can even give rise to pancreatic adenocarcinoma. The genetic signatures of pancreatic adenocarcinoma and its precursor lesions are well characterized. We explored the genetic alterations in precursor lesions (intraductal papillary mucinous neoplasms [IPMN], pancreatic intraepithelial neoplasia [PanIN]) in patients with pancreatic heterotopias but without concomitant pancreatic ductal adenocarcinomas. This allowed us to determine whether the stereotypical dysplasia--infiltrating carcinoma sequence also occurs in these extrapancreatic foci. Seven cases of heterotopic pancreas with ductal precursor lesions were identified. These included 2 IPMNs with focal high-grade dysplasia and 5 PanINs with low- to moderate-grade dysplasia (PanIN grades 1-2). Neoplastic epithelium was microdissected and genomic DNA was extracted. Sequencing of commonly mutated hotspots (KRAS, TP53, CDKN2A, SMAD4, BRAF, and GNAS) in pancreatic ductal adenocarcinoma and its precursor lesions was performed. Both IPMNs were found to have KRAS codon 12 mutations. The identification of KRAS mutations suggests a genetic pathway shared with IPMN of the pancreas. No mutations were identified in our heterotopic PanINs. One of the possible mechanisms for the development of dysplasia in these lesions is field effect. At the time of these resections, there was no clinical or pathologic evidence of a prior or concomitant pancreatic lesion. However, a clinically undetectable lesion is theoretically possible. Therefore, although a field effect cannot be excluded, there was no evidence for it in this study.
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http://dx.doi.org/10.1016/j.humpath.2015.09.023 | DOI Listing |
Alzheimers Dement
January 2025
Guangdong Provincial Key Laboratory of Brain Function and Disease, Center for Brain and Mental Well-Being, Department of Psychology, Sun Yat-sen University, Guangzhou, China.
Introduction: Visual short-term memory (VSTM) is a critical indicator of Alzheimer's disease (AD), but whether its neural substrates could adapt to early disease progression and contribute to cognitive resilience in amnestic mild cognitive impairment (aMCI) has been unclear.
Methods: Fifty-five aMCI patients and 68 normal controls (NC) performed a change-detection task and underwent multimodal neuroimaging scanning.
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Adv Exp Med Biol
January 2025
Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Breast cancer (BC) is a profoundly heterogenous disease, with diverse molecular, histological, and clinical variations. The intricate molecular landscape of BC is evident even at early stages, illustrated by the complexity of the evolution from precursor lesions to invasive carcinoma. The key for therapeutic decision-making is the dynamic assessment of BC receptor status and clinical subtyping.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Centre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
Ductal carcinoma in situ (DCIS) accounts for ~20% of all breast cancer diagnoses but whilst known to be a precursor of invasive breast cancer (IBC), evidence suggests only one in six patients will ever progress. A key challenge is to distinguish between those lesions that will progress and those that will remain indolent. Molecular analyses of neoplastic epithelial cells have not identified consistent differences between lesions that progressed and those that did not, and this has focused attention on the tumour microenvironment (ME).
View Article and Find Full Text PDFAm J Gastroenterol
January 2025
Division of Gastroenterology and Hepatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Background And Aims: We sought to develop a minimally-invasive, robust, accessible nonendoscopic strategy to diagnose Barrett's esophagus (BE), esophageal adenocarcinoma (EAC), and its immediate precursor lesion, high-grade dysplasia (HGD) based on methylated DNA biomarkers applied to a retrievable sponge-capsule device in a cohort representative of the BE population (i.e., mostly short-segment, non-dysplastic BE, NDBE).
View Article and Find Full Text PDFCureus
January 2025
College of Dentistry, King Saud University, Riyadh, SAU.
Oral melanocytic nevi (OMN) are rare benign tumors originating from melanocytes with an unclear pathogenesis. The current theory suggests that OMN originate from dormant dendritic melanocytes that become enclosed in the dermis during the embryonic migration of melanoblasts - the precursors of melanocytes - from the neural crest to the epidermis. OMN can be congenital or acquired, with acquired nevi being more common.
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