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Aims: Although it is necessary to measure the invasive size of lung adenocarcinoma with a lepidic component, it is not uncommon to have trouble in measuring the invasive size of lung adenocarcinoma. This study examined whether there were other stronger prognostic factors than invasive size., Methods: We characterised the clinicopathological features associated with recurrence-free survival (RFS) of 686 patients with the pathological stage (p-Stage) I lung adenocarcinoma. Moreover, we compared the area under the curve (AUC) values for recurrence between various combinations of pathological-baseline (age & sex & p-Stage based on invasive size) (B(i)) and several prognostic factors, and various combinations of p-baseline based on total tumour size (B(t)) and several prognostic factors., Results: AUC showed no significant differences between B(i) & new International Association for the Study of Lung Cancer grade (G) or vascular invasion (V), and B(t) & G or V. AUC was the highest in B & G & lymphatic invasion (L) & V. RFS was significantly shorter in patients with G3 OR L(+) OR V(+) than in those with G≤2 AND L(-) AND V(-) in each p-Stage based on invasive size (p-Stage(i)) and p-Stage based on total tumour size (p-Stage(t)) (p<0.05), and there were no significant differences in RFS between each p-Stage(i) and p-Stage(t)., Conclusions: In any invasive size or total tumour size of p-Stage I lung adenocarcinoma, G, L and V are more powerful prognostic factors than the size criteria of p-Stage. Therefore, pathologists should focus on these pathological findings., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective: To clarify the significance of neuroendocrine differentiation in prostate cancer., Methods: We immunohistochemically examined 96 samples of prostatic cancers obtained from radical prostatectomies using a specific neuroendocrine marker and various neuropeptides, as well as markers for cell proliferation, angiogenesis and androgen-receptor expression., Results: We frequently found neuroendocrine cells in atrophic glands with or without chronic inflammation in nontumorous tissues. Neuroendocrine cells were detected in 36.5% of prostate cancer samples overall, but had no significant correlation to angiogenesis, cell proliferation or biochemical recurrence. However, patients with a high frequency of neuroendocrine cells (9.4%) tended to undergo preoperative hormonal therapy (p = 0.060), which led to their cancers being atrophic with inflammation. The neuroendocrine cells in these patients contained calcitonin-positive cells (p

A santorinicele is defined as a focal cystic dilatation of the terminal portion of the dorsal pancreatic duct at the minor papilla; most cases have been reported in patients with pancreas divisum. It has been suggested that a santorinicele results from a combination of a minor papilla obstruction which prevents the flow of pancreatic juice and a weakness of the duodenal wall where the dorsal pancreatic duct terminates. However, these conditions can occur in patients with invasive ductal cancer in the pancreatic head. We encountered a rare case of a santorinicele with unresectable adenocarcinoma of the pancreatic head in an 81-year-old woman.

The incidence of prostate cancer has increased in Japan recently and is developing into a life-threatening disease for many Japanese men. This is a result of several convergent factors including the adoption of a Western lifestyle, the widespread use of prostate-specific antigen (PSA) testing, and an increased population of advanced years in Japanese men. Although there is much information to date relating to molecular events underlying the etiology of prostate cancer, it is still unclear as to how and when these genetic alterations occur in each step of tumorigenesis. One fruitful area of investigation has been in the analysis of chromosomal abnormalities commonly observed in prostate cancer. However, no single candidate gene has been definitely identified in cancer initiation and/or progression; in addition, less research has been devoted to understanding the molecular events that underlie tumor histogenesis in terms of likely precursor lesions, such as prostatic intraepithelial neoplasia (PIN). This article reviews the current knowledge of the molecular pathology of prostate cancer, including its histogenesis, genetic and epigenetic alterations, and hereditary factors.

Using 19 radical prostatectomy specimens, we studied the histological distribution of free prostate specific antigen (PSA), total PSA, alpha1-antichymotrypsin (ACT) and prostate secretory granules (PSG) in both normal and cancerous cells of the prostate. After glutaraldehyde fixation, numerous fine eosinophilic droplets of PSG could be found mainly in the apical portions of normal acinous epithelial cells, but was markedly decreased in cancer cells. With antibodies against free PSA, normal acinous cells were granularly positive in the apical portion of the epithelium, which corresponded to the PSG, whereas cancer cells were diffusely positive. With antibodies against ACT, normal duct cells and cancer cells were often positive, but few normal acinous cells were positive. Presumably, these findings indicate that free PSA is secreted into the lumen as PSG in normal glands, but not by the same pathway in cancers where free PSA appears to accumulate due to a decrease of PSG, then leak into the blood producing complexed PSA to some extent in the cytoplasm. One factor analysis of variance (ANOVA) on the correlation of tumor differentiation or Gleason score with serum values of total PSA, free PSA and a free/total PSA ratio demonstrated no significant links. Elucidation of secretory mechanisms should provide better comprehension of various PSA indices for prostate cancer screening.

Multiple genetic mutations and epigenetic methylation are believed to be involved in prostate carcinogenesis, but it is not known whether these events are independent or correlated in some fashion. We therefore studied 32 prostate adenocarcinomas not only for deletions and / or mutations of multiple suspect genes, but also for aberrant DNA methylation using methylation-specific PCR (MSP). Of those genes examined, p16(INK4a), O(6)-MGMT, and GST-P were found to be the most frequently methylated (66%, 25% and 75% of cases, respectively), while methylations of p14(ARF), RB1, p21(Waf1), and p27(Kip1) were far less common (3%, 6%, 6% and 6% of cases, respectively). Methylation of O(6)-MGMT and GST-P genes was defective in about 19% of the cases and there were occasional simultaneous deletions and methylations of p14(ARF) and p16(INK4a) genes (13% and 3% of cases, respectively). In p16(INK4a), methylation occurred in the promoter region in 9% of samples and in exon 2 in 66% of tumors. Hypermethylation of O(6)-MGMT with concurrent p53 and ras gene mutations were found in 6% and 13% of specimens, respectively; among those tumors with high Gleason scores were 2 carcinomas showing hypermethylated O(6)-MGMT with G-to-A transitions in K-ras. Our results demonstrate that multiple genes of a subset common in prostate carcinomas are methylated and not infrequently show concurrent deletions. Further, there is a suggestion that specific combinations of hypermethylation and mutation correlate to tumor malignancy.