The association between Campylobacter-like organisms (CLOs) and lesions of the gastric mucosa was studied in 59 consecutive biopsies. Hematoxylin and eosin and Warthin-Starry silver stains, as well as high-resolution light microscopy (HRLM) and transmission electron microscopy (TEM), were used. The organisms were found in intimate contact with foveolar cells showing abundant phagolysosomes and alterations of the intercellular complexes. CLOs also were seen in close proximity of parietal cells in resting phase, some of which showed degenerative changes. The findings are discussed in light of recent reports linking CLOs to the cause of gastritis. (Key words: Campylobacter; Ultrastructure; Gastritis; Peptic ulcer; Parietal cells; Fovelor cells). Am J Clin Pathol 1986; 86: 575-582 SPIRAL MICROORGANISMS have been reported in the gastric mucosa since 1940, 3 but their possible role as pathogens has not been clarified. Recently, these organisms have been found to share many characteristics with the Campylobacter genus, and the term Campylobacterlike organisms (CLOs) has been widely used in referring to them.8 It has been postulated that these organisms may play an etiologic role in peptic ulcer disease, and a hypothetical mechanism has been offered to explain that role.9 This study was conducted to provide morphologic and bacteriologic data on the infection of the gastric mucosa with CLOs and to explore possible mechanisms responsible for lesions and symptoms. Materials and MethodsBiopsies from the gastric antrum and corpus were taken from 59 consecutive patients attending the endoscopy clinic at Charity Hospital in New Orleans between March and September 1985. One tissue fragment was fixed in buffered formalin, embedded in paraffin, and sectioned and stained with hematoxylin and eosin and WarthinStarry silver technics. A second fragment was used for high-resolution light microscopy (HRLM); if CLOs were identified (33 cases), the block was further processed for Departments of Pathology and Internal Medicine (Gastroenterology), Louisiana State University MedicalCenter, New Orleans, Louisiana transmission electron microscopy (TEM) according to methods described previously. 5 In 23 cases, a third tissue fragment was used to prepare smears for Gram's stain and for bacteriologic cultures.For HRLM and TEM, intact biopsies from antrum and corpus were immediately fixed in paraformaldehyde and postfixed in osmium tetroxide according to previously described standard methods.5 After dehydration, the tissue was embedded in Spurr's epoxy, and l-/um sections were cut for HRLM. They were stained with toluidine blue and counterstained with basic fuchsin. This method allowed the microorganisms to be readily recognizable. Four TEM grids per block were stained with uranyl acetate and lead citrate and studied in a Zeiss® electron microscope. The presence of CLOs and their relationship with normal cells was assessed. A systematic search for the presence of microorganisms and for degenerative changes in the epithelial cells was made. Bo...

The recently identified tumor-suppressor gene TSLC1 on chromosome 11q23.2 is frequently inactivated in human non-small cell lung adenocarcinoma by DNA methylation-associated silencing. The aim of this study was to determine if TSLC1 is inactivated in adenocarcinoma of the pancreas. We analyzed 17 pancreatic cancer cell lines, 91 primary pancreatic adenocarcinoma, 46 pancreatic intraepithelial (PanIN) precursor lesions and 15 microscopically normal pancreata for methylation of the 5' CpG island of the TSLC1 gene through methylation-specific PCR. We observed 5' CpG methylation of TSLC1 in 4 of 17 cell lines (24%). In each cell line the aberrant methylation was associated with loss of TSLC1 expression by RT-PCR that was reversible after treatment with the DNA methyl-transferase inhibitor 5-aza-2'- deoxycytidine. Furthermore, we observed that TSLC1 was methylated in 25 of 91 primary pancreatic adenocarcinomas (27%), and in 2 of 7 highgrade PanIN-3 lesions (29%), but not in low-grade PanIN (0 of 9 PanlN-2 and 0 of 30 PanIN-1) lesions or in normal pancreata (n=15). We conclude that epigenetic silencing of TSLC1 expression through 5' CpG island associated methylation is common in pancreatic adenocarcinoma and is a late event in pancreatic neoplastic development.

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A pancreatoduodenectomy specimen is complex, and there is much debate on how it is best approached by the pathologist. In this review, we provide an overview of topics relevant for current clinical practice in terms of gross dissection, and macro- and microscopic assessment of the pancreatoduodenectomy specimen with a suspicion of suspected pancreatic cancer. Tumor origin, tumor size, degree of differentiation, lymph node status, and resection margin status are universally accepted as prognostic for survival. However, different guidelines diverge on important issues, such as the diagnostic criteria for evaluating the completeness of resection. The macroscopic assessment of the site of origin in periampullary tumors and cystic lesions is influenced by the grossing method. Bi-sectioning of the head of the pancreas may offer an advantage in this respect, as this method allows for optimal visualization of the periampullary area. However, a head-to-head comparison of the assessment of clinically relevant parameters, using axial slicing versus bi-sectioning, is not available yet and the gold standard to compare both techniques prospectively might be subject of debate. Further studies are required to validate the various dissection protocols used for pancreatoduodenectomy specimens and their specific value in the assessment of pathological parameters relevant for prognosis.