Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021843 (bowel obstruction)
9,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1974-1990, 23 women with stage I and five with stage II epithelial ovarian carcinoma received intraperitoneal chromic phosphate (32P) as the only form of adjuvant therapy after complete debulking and comprehensive surgical staging laparotomy. Surgery consisted of total abdominal hysterectomy with bilateral salpingo-oophorectomy, omentectomy, peritoneal washings for cytology, multiple biopsies of pelvic and abdominal peritoneum, and selective pelvic and para-aortic lymphadenectomy. Intraperitoneal 32P therapy was administered a median of 7 days after laparotomy. Significant toxicity was minimal; none of these patients required surgery for bowel obstruction. Overall 5-year survival was 90 and 100%, but disease-free survival was only 65% (95% confidence interval [CI] 36-86%) and 60% (95% CI 12-81%) for patients with stage I and II disease, respectively. Two patients developed intraperitoneal and six systemic relapses; all patients received cisplatin regimens after relapse. Univariate analysis of age, stage, histology, Ovarian Cancer Study/Gynecologic Oncology Group risk status, lesion size, and presence or absence of capsular adhesions revealed that only an age of 50 or more years had an adverse effect on disease-free survival (P less than .03). This study suggests that determination of early-stage disease and host-tumor biology may be the most important factors in determining the survival of women with early ovarian cancer defined by comprehensive surgical staging. Intraperitoneal 32P does not appear to be effective adjuvant therapy in these women.
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PMID:Adjuvant therapy with intraperitoneal chromic phosphate (32P) in women with early ovarian carcinoma after comprehensive surgical staging. 157 29

Bowel obstruction may be a mode of presentation of intra-abdominal and pelvic malignancy or a feature of recurrent disease following anticancer therapy. Malignant bowel obstruction is well-recognized in gynecologic patients with advanced cancer. Retrospective and autopsy studies found the frequency at approximately 5-51% of patients with gynecological malignancy(1-7). Malignant bowel obstruction (MBO) is particularly frequent in patients with ovarian cancer where it is the most frequent cause of death(7). Patients with stage III and IV ovarian cancer and those with high-grade lesions are at higher risk for MBO as compared to patients with lower stage or low-grade tumors(1,8). Ovarian carcinoma accounted for 50% of small bowel obstruction and 37% of large bowel obstruction treated in a large gynecological oncology service(8-11).
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PMID:Palliative management of malignant bowel obstruction. 1197 72

The biology of ovarian carcinoma differs from that of hematogenously metastasizing tumors because ovarian cancer cells primarily disseminate within the peritoneal cavity and are only superficially invasive. However, since the rapidly proliferating tumors compress visceral organs and are only temporarily chemosensitive, ovarian carcinoma is a deadly disease, with a cure rate of only 30%. There are a number of genetic and epigenetic changes that lead to ovarian carcinoma cell transformation. Ovarian carcinoma could originate from any of three potential sites: the surfaces of the ovary, the fallopian tube, or the mesothelium-lined peritoneal cavity. Ovarian cacinoma tumorigenesis then either progresses along a stepwise mutation process from a slow growing borderline tumor to a well-differentiated carcinoma (type I) or involves a genetically unstable high-grade serous carcinoma that metastasizes rapidly (type II). During initial tumorigenesis, ovarian carcinoma cells undergo an epithelial-to-mesenchymal transition, which involves a change in cadherin and integrin expression and up-regulation of proteolytic pathways. Carried by the peritoneal fluid, cancer cell spheroids overcome anoikis and attach preferentially on the abdominal peritoneum or omentum, where the cancer cells revert to their epithelial phenotype. The initial steps of metastasis are regulated by a controlled interaction of adhesion receptors and proteases, and late metastasis is characterized by the oncogene-driven fast growth of tumor nodules on mesothelium covered surfaces, causing ascites, bowel obstruction, and tumor cachexia.
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PMID:Ovarian cancer development and metastasis. 2518 1