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Squamous cell carcinoma presenting 10 years after cystectomy for leukoplakia.

Leukoplakia of the bladder is widely accepted as a precancerous lesion. We describe a patient in whom squamous cell carcinoma presented as an enterourethral fistula 10 years after cystectomy for leukoplakia of the bladder. During cystectomy we left most of the prostate and posterior urethra intact to preserve potency. In view of this case we recommend that in patients with bladder leukoplakia in whom ablative surgery is being contemplated a complete cystoprostatectomy be performed and a urethrectomy be considered seriously.

Adult↗

Gastric and small bowel lymphoma.

Despite the vague presentation of gastric and small bowel lymphoma, survival can be achieved by adequate surgical resection of stage I disease. A role still exists for debulking of advanced stage disease by surgical excision. Debulking enhances potential for complete response with chemotherapy, decreases the risk of gastric and small bowel perforation with large exophytic tumors as they necrose with chemotherapy, and prevents gastrointestinal obstruction from limiting patients' ability to receive chemotherapy. All attempts should be made to maintain nutritional support of these patients to allow them an adequate chance of receiving chemotherapy. The increasing frequency of immunodeficiency disorders will continue to produce higher numbers of patients with non-Hodgkin's lymphoma. Awareness of our surgical limitations is important because surgical exploration is frequently the first step. Multimodality therapy of gastric and small bowel lymphoma offers the best chance for successful outcome. Surgical resection should not prevent patients from receiving a complete trial of chemotherapy and radiation if appropriate.

Humans↗

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. III. Changes in kinetics of enterocyte populations in the course of experimental intestinal tumour induction in rats.

A stage-by-stage study of disturbances in enterocyte proliferation in the ileum and descending colon in the course of tumour induction by treatment with 1,2-dimethylhydrazine was performed. Even at early stages, an expansion of the zone of epithelial cell proliferation in the crypts and migration of dividing cells as far as to the crypt mouth, which is a manifestation of enterocyte differentiation disturbances, were observed. Enterocytes of the crypts chiefly proliferated through a short cycle, the mean duration of which was slightly greater than in normal intestinal tissue. The reduced cell loss in the epithelium and resultant disturbances of its steady state led to the accumulation of great numbers of atypical cells in the superficial layers of the crypts and formation of carcinomas in situ in the descending colon. The microscopically unaltered sections of the mucosa, prior to development of overt neoplastic changes carcinomas in situ, superficial cancers and small-size adenocarcinomas revealed a simplified structure of enterocyte population, as compared with normal epithelium. As tumours progressed, the heterogeneity of its component cell subpopulations increased, and several subpopulations, differing in mean duration of the mitotic cycle, were formed. Pathologic mitoses made up a greater portion (50-60 per cent) of the dividing cells of the descending colon, as compared with ordinary 4 per cent at all stages of experimental tumour induction.

1,2-Dimethylhydrazine↗

The effects of different MNNG (N-methyl-N'-nitro-N-nitrosoguanidine) doses on the stomach and the upper small intestine of the rat. I. The frequency and histopathology of the induced tumours.

N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was given to 3 groups of rats with the drinking water for 32 weeks in different doses: 25, 50 and 100 micrograms/ml. After 50 weeks the induced tumours of the stomach and the upper small intestine were investigated. Most tumours were well differentiated adenocarcinomas or adenomatous-hyperplastic lesions with focal adenocarcinoma. After low MNNG-concentration (25 micrograms/ml) only adenomatous hyperplastic lesions with focal adenocarcinoma were found. A tumour development in connection with intestinal metaplasia was detectable exclusively in two rats of the group receiving 50 micrograms MNNG/ml. The frequency of gastric tumours shows a relatively low peak (3.3 tumours/10 animals) after administering a medium MNNG-concentration (50 micrograms/ml) and a little decrease of the frequency after higher MNNG-concentration, as opposed to the approximately linear dose-related increase of the tumour frequency in the upper small intestine. The highest tumour induction rate was found in the upper small intestine after 100 micrograms MNNG/ml (5.6 tumours/10 rats). It can be concluded that the mucosa of the upper small intestine possesses a greater susceptibility to the carcinogenic effect of MNNG than the glandular stomach of the rat.

Adenocarcinoma↗

Is laparotomy for staging early ovarian cancer an absolute necessity?

STUDY OBJECTIVE: To demonstrate that palpation of the omentum, mesentery, and intestine can be omitted from the laparoscopic staging of stage I carcinoma of the ovary. DESIGN: Retrospective analysis of 223 women with stages III and IV ovarian cancer treated by laparotomy. SETTING: Gynecological Oncology Clinic, M. Sklodowska-Curie Memorial Cancer Institute of Oncology, Warsaw, Poland. INTERVENTIONS: Observation of macroscopic spread of tumor to areas accessible to laparoscopic inspection versus spread to areas inaccessible to laparoscopic evaluation. MEASUREMENTS AND MAIN RESULTS: Macroscopically detectable disease in the areas easily accessible to laparoscopic inspection was present in all cases of metastases to the mesentery, omentum, or intestine. CONCLUSION: The diagnosis of FIGO stage I ovarian cancer can be made with confidence if laparoscopic inspection of certain areas reveals no evidence of metastases.

Adnexa Uteri↗

Effects in rats of sodium chloride on experimental gastric cancers induced by N-methyl-N-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide.

The effects were studied of NaCl on the production of gastric carcinomas by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and by 4-nitroquinoline-1-oxide (NQO) in male Wistar rats. Nine groups of rats were treated as follows: Group 1 was given 50 mg MNNG/liter and 6 g NaCl solution/liter to drink and was fed a stock diet supplemented with 10% NaCl. Group 2 received 1 ml saturated NaCl once a week and 50 mg MNNG/liter to drink. Group 3 was treated with MNNG alone. Group 4 was given a solution of 1 mg NQO once a week and fed a stock diet supplemented with 10% NaCl. Group 5 received a solution of 1 mg NQO saturated with NaCl. Group 6 was given NQO alone. Groups 7 and 8 were given NaCl alone. Group 9 was untreated. Adenocarcinomas developed in the glandular stomach in group 2 at a significantly higher incidence than in group 3. Poorly differentiated adenocarcinomas of the glandular stomach were detected in only groups 1 and 2. One poorly differentiated adenocarcinoma metastasized to the lymph nodes. A high incidence of squamous cell carcinomas of the forestomach was found in groups 4 and 5. No malignant tumors were seen in groups 6-9. NaCl given alone had no apparent carcinogenicity in rats but, when administered with MNNG or NQO, it enhanced the carcinogenic effects of MNNG and NQO in the stomach.

4-Nitroquinoline-1-oxide↗

Glucocorticoid hormone effect on transplacental carcinogenesis and lung differentiation: influence of histocompatibility-2 complex.

In the mouse, the histocompatibility-2 (H-2) haplotype influences induction of lung and intestinal tumors by N-ethyl-N-nitrosourea (ENU) treatment of fetuses or infant mice. The differentiation of lung and intestinal epithelium is known to be regulated by glucocorticoids. We show that glucocorticoid-induced development of alveolar lung volume is H-2 influenced and that glucocorticoid treatment of fetuses also influences prenatal ENU induction of lung and intestinal tumors. These glucocorticoid effects on tumorigenesis are also H-2 influenced. The number of papillary lung tumors increased in B10 (H-2b) and decreased in B10.A (H-2a) mice. In the intestine, the number of tumors increased in H-2b females and decreased in H-2b males. In H-2a mice, the number of intestinal tumors was unchanged but their location was altered. We propose that the H-2 complex influences tumorigenesis in lung and small intestine by affecting the hormonal regulation of differentiation of target epithelial cells.

Adenocarcinoma, Papillary↗