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Background: We have previously demonstrated a relationship between the depth of submucosal invasion (SM depth) and the frequency of lymph node metastasis in resected submucosal invasive colorectal cancers (SICRCs). Here, we assessed the desmoplastic reaction (DR) in pretreatment biopsy specimens of SICRC to predict the SM depth., Methods: A total of 359 patients with SICRCs, who had undergone surgical or endoscopic mucosal resection, were enrolled. The SM depth of the SICRC lesions was evaluated according to the procedure established by the Japanese Society for Cancer of the Colon and Rectum, and the patients' corresponding pretreatment biopsy specimens were examined histologically to evaluate the prevalence of DR., Results: For pedunculated SICRCs, the prevalence of DR in pretreatment biopsy specimens was significantly higher in moderately differentiated than in well-differentiated adenocarcinomas, but was not significantly related to SM depth. For nonpedunculated SICRCs, the prevalence of DR in pretreatment biopsy specimens was significantly related to histological type, tumor size, and SM depth. When non-pedunculated SICRCs were further divided using a specific cutoff value of 1000 μm for SM depth, the DR positivity rate in pretreatment biopsy specimens was significantly higher in SICRCs with an SM depth of ≥1000 μm (termed "SM massive CRCs") than in cases where the SM depth was <1000 μm (termed "SM slight CRCs")., Conclusions: Detection of DR in pretreatment biopsy specimens is useful for the prediction of SM depth in nonpedunculated SICRCs, and may be useful for the selection of such cases that would be treatable by endoscopic mucosal resection and endoscopic submucosal dissection (EMR/ESD).

Gastric carcinoma is thought to develop via the actions of inducers and promoters of carcinogenesis. Tryptophan in charred fish or animal meat, ultraviolet rays, and irradiation, which damage genes of normal cells, have long been regarded as inducers of carcinoma, and agents such as alcohol, tobacco, aflatoxin, and nitrosoamine as promoters, with tobacco having both activities. The interaction between these environmental factors, principally diet, and Helicobacter pylori (Hp) is important in the genesis of gastric carcinoma. In this report, the histopathological feature of the Hp gastritis-carcinoma sequence is outlined, and the pathological characteristics of gastroesophageal reflux disease (GERD) and endoscopically negative reflux disease (ENRD) and the risk factors for lower esophageal carcinoma after Hp eradicated status in particular are discussed regarding aspects of cell cycle-associated factors. We conclude that (1) Infection with Hp increases the risk of gastric cancer in two histological phenotypes (i.e., diffuse undifferentiated type and intestinal differentiated type). Excessive cell replication and interrupting the mucus secretion mechanism may result in a large proportion of cells with genetic abnormalities. (2) Genetic alterations in gastric carcinogenesis may differ from those in colonic carcinogenesis. (3) The degree of GERD in Japanese patients is milder than that in patients from Western countries, although the incidence of GERD increases the status after successful eradication of Hp. It is also possible that accumulation of genetic abnormalities increases the number of cardiac and lower esophageal cancers. Investigation of cell cycle factors in GERD including ENRD can be expected to reveal the risk of carcinogenesis.

Background: The present study was undertaken to investigate the role of cathepsin D in the invasiveness of human gastric cancer., Methods: Immunohistochemical cathepsin D staining was performed in samples from 29 early gastric adenocarcinomas (papillary or tubular adenocarcinoma) and 15 gastric adenomas, and their adjacent nonneoplastic gastric mucosa. We classified the patterns of cathepsin D immunostaining into four types; type A, fine granular staining in the apical portion: type B, intense coarse granular staining in the apical portion; type C, fine granular staining in the basal portion; and type D, diffuse granular staining throughout the cytoplasm., Results: All of the nonneoplastic mucosa showed an apical cytoplasmic distribution pattern (type A or type B). However, 20% (2/10) of low-grade gastric adenomas and 60% (3/5) of high-grade gastric adenomas showed an abnormal staining pattern. i.e., types C and D. Moreover, 82% (9/11) definite intramucosal gastric adenocarcinomas, and the majority of gastric adenocarcinomas with submucosal invasion [83% (15/18) of those in the mucosal part and 100% (14/ 14) of those in the invasive submucosal part] showed an abnormal staining pattern (types C and D). Interestingly, most of the carcinoma cells invading the stroma and lymphatics showed the type D staining pattern., Conclusions: These results indicate that an abnormal cytoplasmic staining pattern of cathepsin D may reflect the invasive potential of gastric carcinoma cells.