Analyzing the post-contrast attenuation of the esophageal wall on routine contrast-enhanced MDCT examination can improve the diagnostic accuracy in response evaluation of the squamous cell esophageal carcinoma to neoadjuvant chemoradiotherapy in comparison with the esophageal wall thickness.

PURPOSE: To evaluate the accuracy of the multidetector computed tomography (MDCT) in the response evaluation of the esophageal squamous cell carcinoma (ESCC) to neoadjuvant chemoradiotherapy (nCRT) by analyzing the thickness and post-contrast attenuation of the esophageal wall after the nCRT. METHODS: Contrast-enhanced (CE)-MDCT examinations in portal venous phase of one hundred patients with locally advanced ESCC who received nCRT and underwent esophageal resection and histopathology assessment of tumor regression grade (TRG) were retrospectively analyzed by measuring the maximal thickness and mean density of the esophageal wall in the segment involved by tumor and visually searching for hyperdense foci within it. Diagnostic performance was evaluated using the ROC analysis. RESULTS: Average attenuation of the esophageal wall had stronger diagnostic performance for predicting pathologic complete regression (pCR) (AUC = 0.994; p < 0.001) in relation to maximal esophageal wall thickness (AUC = 0.731; p < 0.001). Maximal esophageal wall thickness ≤ 9 mm and average attenuation of the esophageal wall ≤ 64 HU predicted pCR with the sensitivity, specificity, and overall accuracy of 62.5%, 77.9%, and 73%, and 96.9%, 98.5%, and 98%, respectively. Combination of both cutoff values enabled correct assessment of pCR with the 100% accuracy. Visual detection of the hyperdense focus within the esophageal wall predicted pCR with the sensitivity, specificity, and overall accuracy values of 100%, 94.1%, and 96%, respectively. CONCLUSION: Visual analysis and measurement of post-contrast attenuation of the esophageal wall after the nCRT can improve diagnostic accuracy of MDCT in the response evaluation of the ESCC to nCRT in comparison with measuring the esophageal wall thickness.

[Pathology and pathobiology of the gastric carcinoma].

Recent epidemiological studies in Serbia revealed that gastric carcinoma is the third and the fifth main cause of cancer morbidity in men and women, respectively. Despite the declining incidence of gastric cancer, it remains the second most common cause of cancer-related deaths as it is worldwide. A well-defined carcinogenic inflammation-metaplasia-dysplasia-cancer sequence typically precedes the development of most gastric adenocarcinomas. Alterations such as gastric mucosal atrophy and intestinal metaplasia are merely markers of increased risk, while gastric epithelial dysplasia (GED) represent a direct precursor of cancer. DNA damage and increased mucosal proliferation secondary to H pylori infection, combined with a suitable host susceptibility phenotype (eg, genetic polymorphisms in interleukin IL-1B, IL-1RN, and tumor necrosis factor a TNF-alpha genes), are important factors in this progression pathway. However, only a small minority of patients infected with H. pylori eventually develops gastric cancer, and eradication of H pylori in these patients does not seem to eliminate the risk of cancer completely. It has been shown that atrophy may be a better indicator of risk of cancer than intestinal metaplasia, and remains to be validated in routine clinical practice according to recent proposal for new quantitative methods. It is often associated with pseudopyloric gland metaplasia in the gastric corpus mucosa, which expresses a type of trefoil peptide, the spasmolytic polypeptide (termed spasmolytic polypeptide-expressing metaplasia or SPEM) and has been shown to be linked more closely to gastric cancer than intestinal metaplasia. Better histological characterization of adenomatous (or type I), hyperplastic (foveolar or type II) and tubule-neck (mucocellular or type III) GED, two-tiered grading system (low and high grade dysplasia) as well as the introduction of Padova and Vienna international classifications of dysplasia seem to be more helpful in GED surveillance and comparative studies. A combination of histopathological features, serum markers such as pepsinogen I, and molecular tests that analyze host susceptibility polymorphisms and bacterial virulence factors, may allow development of strategies for early detection of cancer in the future. At present, pathobiology of gastric cancerogenesis is far from known, despite the progressive knowledge on predisposing environmental conditions and genetic and epigenetic abnormalities, including tumour suppressor genes, oncogenes, microsatellite instability and hypermethylation or the significance of E-cadherin mutational status association with hereditary diffuse gastric cancer syndrome. Recent evidence regarding the importance of several histopathologically derived prognostic factors, such as resection margin status and lymph node metastases and their implications have also been discussed. We aim to review these aspects, with special relevance to gastric cancer specimen reporting.

[Two cases of pancreatic head polypeptide tumors, one with a central cavity which fistulized into the duodenum]. / Dva slucaja polipeptidnog tumora glave pankreasa od kojih je jedan s centralnom supljinom koja je fistulizirala u duodenum.

PP omas are rare, usually malignant tumours of the PP cells of the Langerhan's islets which secrete pancreatic polypeptide. The authors present two women operated for PP-omas of the pancreas. The first was 55 year-old woman in whom we did a cephalic duodenopancreatectomy (Whipple's procedure) for the tumor of the head of the pancreas with central cavity containing gas due to communication with the duodenum. Immunohistochemistry showed a PP oma with strong generalised immunoreactivity with antibodies against Chromogramin A, neuron specific enolasa and PP with more the 95% of tumor cells and coexpression of somatostatine in 35% and VIP in less then 5% of tumor cells. Following uneventful recovery the patient stayed symptom free so far and put 20 kilograms in weight. The second patient was 19 year-old girl with a multinodal tumor of almost the entire pancreas in whom a local excision of the nodal mass of the head of the pancreas had been carried out in the other hospital, three years ago and relaparotomy and tumor biopsy a month before admission to our institution. In her we did a total duodenopancreatectomy and standard lymphadenectomy for a multinodal mass occupying almost the entire pancreas. Immunohistochemistry showed a strong generalised immunoreactivity with antibodies against Chromographin A, Neuron specific enolasa and PP for more then 95% of tumors, cells. Glucagon was expressed in few focuses (in less then 1% of cells), somatostatin was expressed very rarely in single cells while the rest of tumor markers did not show a visible immunologic reactions in the majority of tumors, cells. Three years after surgery she died due to multiple liver secondaries.