[Chronic gastric ulcer induced by duodenogastric reflux in rats].
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Animals↗
Biomedical subjects
T Oohara
Publications and source records attributed to T Oohara.
Duodenal adenoma with atypia following oral administration of tegafur.
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Adenoma↗
Background mucosal changes of primary advanced large intestinal cancer in patients without familial polyposis coli.
In 337 cases of primary advanced large intestinal cancer in patients without familial polyposis coli, the risk factor for cancer was discussed chiefly from the background mucosa surrounding and apart from the cancers. The following findings were obtained: (1) in the mucosa surrounding cancers, adenoma was seen in 23 cases (6.8 per cent), adenomatous changes of the basal cells in 211 cases (62.6 per cent), and hyperplastic glands in 167 cases (49.6 per cent), (2) in the mucosa at least 10 mm from the cancers, adenoma, adenomatous changes of the basal cells, and hyperplastic glands were seen in 42 cases (12.5 per cent), 129 cases (38.3 per cent), and 40 cases (11.9 per cent), respectively. Therefore, it is suggested that microscopic adenoma and adenomatous changes of the basal cells might be a sign of premalignancy in patients without familial polyposis coli.
Adenocarcinoma↗
Intestinal metaplasia of the regenerative epithelia in 549 gastric ulcers.
Histopathologic changes in the regenerative epithelia of 549 foci of gastric ulcer were studied. About 70 per cent of the regenerative epithelia revealed intestinal metaplasia of the so-called complete or incomplete type. Parietal cells and chief cells were occasionally observed in the regenerative epithelia of ulcers located in fundic gland areas or at fundopyloric gland borders. It is possible that the regenerative epithelium frequently reverts to intestinal epithelium during the regenerative process, later redifferentiating into normal gastric mucosa or remaining as intestinal metaplasia and that, thus, only a few foci of intestinal metaplasia are precancerous lesions.
Cicatrix↗
Minute gastric cancers less than 5 mm in diameter.
Minute gastric cancers with maximum dimensions of less than 5 mm were studied clinicopathologically. There were 49 intramucosal cancers among 46 patients and nine submucosal cancers among nine patients. No lymph node metastasis was found. Macroscopically, eight (13.8%) were evaluated, 12 (20.7%) were flat, and 38 (65.5%) were depressed. Most submucosal cancers were of the depressed type (8/9, 88.9%). Classification of cancers according to association with other large cancers into single group (22 cases) and multiple group (33 cases) revealed that (1) the majority of the minute gastric cancers (20/22, 90.9%) in the single group were the depressed type and (2) submucosal cancers in the single group were 8/22, accounting for 36.4%, a much higher incidence as compared with 1/36 (2.9%) in the multiple group. These facts indicate that gastric cancers should be detected when they are about 5 mm in maximum dimension and before they invade beyond the submucosal layer, especially in single and depressed type.
Adenocarcinoma↗
Simple alkaline treatment induces intestinal metaplasia in the stomach of rats.
By infusing caustic soda (NaOH) into the stomach of rats, the gastric mucosa fell off and regeneration could be induced. In 18 of 26 rats, intestinal metaplasia associated with goblet cells was observed in the regenerative epithelium. Recently, induction of intestinal metaplasia by weak carcinogenic agents are reported with some emphasis on its precancerous meaning. However, our results suggest that, as intestinal metaplasia can be induced by a benign process of regeneration, it is not directly related with carcinogenesis.
Animals↗
[Non-polyposis type neoplasms of the large intestine].
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Adenocarcinoma↗
Studies on the difference of background mucosa among single advanced carcinoma and benign diseases of the large intestine, and familial polyposis coli.
The entire lengths of fixed specimens from 17 single advanced carcinomas of the colon (Cancer Group), four benign lesions (Benign Group), and four familial polyposis coli (Polyposis Group) were step-sectioned. It was found that the tubules of the basal cells were densely packed with rather a small number of goblet cells in the cancer and benign lesion specimens, but clear and loose with completely differentiated goblet cells in the polyposis coli specimens. Microscopic adenomas that were macroscopically unrecognizable and only microscopically detectable were found in 16 lesions in the Cancer Group, one lesion in the Benign Group, and in numerous lesions in the Polyposis Group. All of them developed from the basal cells. These findings indicate that the colonic mucosa of patients in the Cancer and Benign Groups is similar, but differs from that of the Polyposisis Group, and that microscopic adenomas are not uncommon in the Non-Polyposis Groups (Cancer and Benign Groups), findings which were not previously known.
Adenoma↗
Comparative study of familial polyposis coli and nonpolyposis coli on the histogenesis of large-intestinal adenoma.
The entire length of the large intestine resected from six patients with familial polyposis coli (FPC) was step-sectioned, and microscopic adenomas composed of one to several glands were prepared into complete serial sections. Histopathologic comparison of these microscopic adenomas was made between FPC and nonpolyposis coli (those not included in the special disease group of FPC). The histogenesis of adenomas in FPC and nonpolyposis coli was considered as follows. (1) In nonpolyposis coli, adenomas arise from basal cells of the deep layer of the mucosa. (2) In FPC, most of the adenomas (81.2 per cent) arise in the same manner as described above, although there are some (18.8 per cent) that appear to have arisen in the middle or superficial layer of the mucosa. (3) Therefore, it is believed that the morphologic difference of the large-intestinal mucosa between FPC and nonpolyposis coli comes not from the difference in the number of adenomas present but from the difference in the position and/or timing of appearance of adenomas.
Adenoma↗
Histogenesis of microscopic adenoma and hyperplastic (metaplastic) gland in nonpolyposis coli.
Histogenesis of microscopic adenoma in nonpolypoid colons (those not included in the special disease group of familial polyposis coli) was investigated using complete serial sections with the following results: Adenoma arises from basal cells in the deep layer of the mucosa; and two types of basal cells found were 1) those which had already undergone changes to adenoma and 2) those which are in their transitional stage to adenomas. Early-phase growth of adenoma is brought about by branching. Individual hyperplastic (metaplastic) glands constituting so-called hyperplastic (metaplastic) polyps are considered to be only an expression of one variant in the growing process of adenomas and the glands showing these changes most characteristically have a serrated pattern. Based on these findings, the histogenesis of adenoma in nonpolypoid colons is shown schematically.
Adenoma↗
Microscopic adenoma in nonpolyposis coli: incidence and relation to basal cells and lymphoid follicles.
Six microscopic adenomas found in four patients of nonpolyposis coli (namely, not included in the group of familial polyposis coli) which had been detectable microscopically but not macroscopically, were examined by preparing complete serial section. With respect to the histogenesis of large-intestinal adenomas in nonpolyposis coli, they are considered to originate from the basal cells. As the background for this, a great number of adenomatous changes in basal cells were seen, and the microscopic adenomas showed a tendency of multiplicity (in the present study a total of 36 microscopic adenomas were detected). The above-described adenomatous changes in basal cells and development of microscopic adenomas are considered to be closely related to lymphoid follicles on the muscularis mucosa, with 20 (55.6 per cent) of 36 microscopic adenomas originating in the basal cell upon the lymphoid follicles.
Adenoma↗
Dual roles of peptic ulcer in the carcinogenesis or extension of early gastric cancer.
BACKGROUND: Early gastric cancer (EGC) often coexists with peptic ulcer. In this study we investigated the roles of peptic ulcer in the carcinogenesis and extension of gastric cancer. METHODS: The clinicopathological characteristics of EGC and peptic ulcer and their relationship, as well as that of the background intestinal metaplasia, were compared among the following three groups: patients with peptic ulcer only inside the EGC (Contained group, 53 patients); patients with peptic ulcer only outside the EGC (Separate group, 26 patients); and patients of EGC with no peptic ulcer (Absent group, 43 patients). RESULTS: In the Separate group, a male preponderance was observed (P = .006), and all EGCs developed in the middle or lower third of the stomach (P = .06). Most of the EGCs were an intestinal type of cancer with severe background intestinal metaplasia. Topographically, 88% of the peptic ulcers in the Separate group developed proximal to the EGC. On the other hand, in the Contained group, most EGCs developed in the middle third of the stomach with an intestinal/diffuse type ratio of 1:1. Peptic ulcers inside the EGC were significantly more shallow than those that developed outside the EGC (P = 0.008). Although the incidences of submucosal cancer were nearly the same among the three groups, the maximum cancer diameter tended to be increased in the Contained group compared to that in the Absent group, and the incidence of lymph node involvement tended to be higher in the Contained group (8%) as compared with the other two groups (4%-5%). CONCLUSIONS: These results suggest that peptic ulcer outside the EGC contributes to the development of the intestinal type of EGC, with the background of more severe intestinal metaplasia during the peptic ulcer healing processes, whereas peptic ulcer inside the EGC develops secondary to EGC and favors cancer extension and metastasis. Peptic ulcer associated with EGC can be considered to exert different biological roles in the carcinogenesis or extension of ECG according to the location of the peptic ulcer.
Disease Progression↗
Prospectively performed modified D1 lymphadenectomy for clinically diagnosed mucosal, node negative gastric cancer: findings over the past decade.
Based on retrospective analyses demonstrating the low probabilities of both lymph node metastasis and recurrence of curatively resected mucosal gastric cancer, we have established criteria for modified D1 lymphadenectomy (lymphadenectomy in the perigastric region as well as along the left gastric artery) and performed this in a prospective manner. In this study, we evaluate our treatment strategy by reviewing the patients prospectively undergoing modified D1 lymphadenectomy. The clinicopathological characteristics and survival data of 138 patients who underwent modified D1 lymphadenectomy between 1987--when we first introduced endoscopic ultrasonography--and 1996 were analyzed. The criteria for modified D1 lymphadenectomy were mucosal, node negative gastric cancer by pre-operative and intra-operative examinations. Depth of invasion was correctly diagnosed in 80% of the patients. Among the resultant submucosal gastric cancer patients, the incidence of slight submucosal invasion was increased in the second half-period (78%) as compared with that in the first half-period (44%). Nodal involvement was observed in 4 patients (2.9%); all of them exhibited the depressed type with ulceration and a histologically high grade of gastric cancer. Because their metastasized lymph nodes were all confined to the perigastric region, surgical treatment resulted in no residual cancer macroscopically. No patients succumbed to gastric cancer within the median and mean follow-up periods of over 6 years. These results suggest that our modified D1 lymphadenectomy is an effective option for the pre-operatively and intra-operatively diagnosed mucosal, node negative gastric cancer which meets our criteria.
Female↗