Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute acalculous cholecystitis (AAC) is a rare and dangerous complication of various medical and surgical conditions. We report on a male patient with bile panperitonitis caused by gangrenous AAC, which developed while he was on total parenteral nutrition (TPN) for ileus related to obstructive colon cancer. We also review the relevant Japanese literature on AAC associated with TPN. Our patient suddenly developed right hypochondrial pain after 3 days of TPN while waiting for colon cancer surgery. We diagnosed acute AAC by ultrasonography, and salvaged the patient by cholecystectomy plus left colectomy. Early diagnosis by ultrasound is important for this critical condition. Knowledge of the risk of acute gangrenous cholecystitis during TPN may allow the physician to provide an appropriate diagnosis and treatment.
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PMID:Acute acalculous cholecystitis in a patient on total parenteral nutrition: case report and review of the Japanese literature. 1052 69

Angiogenesis, the formation of new capillary blood vessels, is essential not only for the growth and metastasis of solid tumors, but also for wound and ulcer healing, because without the restoration of blood flow, oxygen and nutrients cannot be delivered to the healing site. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, indomethacin and ibuprofen are the most widely used drugs for pain, arthritis, cardiovascular diseases and, more recently, the prevention of colon cancer and Alzheimer disease. However, NSAIDs produce gastroduodenal ulcers in about 25% of users (often with bleeding and/or perforations) and delay ulcer healing, presumably by blocking prostaglandin synthesis from cyclooxygenase (COX)-1 and COX-2 (ref. 10). The hypothesis that the gastrointestinal side effects of NSAIDs result from inhibition of COX-1, but not COX-2 (ref. 11), prompted the development of NSAIDs that selectively inhibit only COX-2 (such as celecoxib and rofecoxib). Our study demonstrates that both selective and nonselective NSAIDs inhibit angiogenesis through direct effects on endothelial cells. We also show that this action involves inhibition of mitogen-activated protein (MAP) kinase (ERK2) activity, interference with ERK nuclear translocation, is independent of protein kinase C and has prostaglandin-dependent and prostaglandin-independent components. Finally, we show that both COX-1 and COX-2 are important for the regulation of angiogenesis. These findings challenge the premise that selective COX-2 inhibitors will not affect the gastrointestinal tract and ulcer/wound healing.
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PMID:Inhibition of angiogenesis by nonsteroidal anti-inflammatory drugs: insight into mechanisms and implications for cancer growth and ulcer healing. 1058 Oct 68

Two recent studies reported that many patients with colorectal carcinoma have elevated serum prolactin (PRL) concentrations and have suggested ectopic PRL secretion as the cause. In the present study, serum PRL was minimally elevated in 16 of 116 colon cancer patients and 2 of 25 control subjects; medications or chemotherapy appeared to be responsible for the PRL elevations in 11 of 16 cancer patients. Serum PRL was not correlated with either plasma carcinoembryonic antigen or disease stage. Preoperative and postoperative serum PRL concentrations were similar in 26 evaluated patients. None of 19 colorectal tumors was positive for PRL staining by immunohistochemistry. Thus, we could not confirm previous reports of frequent hyperprolactinemia in patients with colorectal cancer; factors such as medications, anxiety, pain, and nausea may have raised serum PRL in these earlier studies. Serum PRL is not a useful marker for colon carcinoma, at least in patients in the United States.
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PMID:Lack of association between hyperprolactinemia and colon carcinoma. 1070 75

Intrathecal administration of 5-fluoro-2'-deoxyuridine (FdUrd) was performed in patients with meningeal dissemination of malignant tumors during the period from January 1996 to September 1998, and they were followed up until February 1999. The study population consisted of 23 patients: 12 with lung cancer, 4 with breast cancer, 2 with colon cancer, 1 with malignant lymphoma, 2 with glioblastoma and 2 with metastatic brain tumors of unknown origin. FdUrd was administered intrathecally through an Ommaya reservoir placed in the lateral ventricle initially at a dose of 1 microg twice per week, and the dose was increased to 10 microg and administration schedule was also increased every day. Headache and nuchal pain were relieved in all patients regardless of responsiveness to intrathecal FdUrd therapy as determined from the findings in the cerebrospinal fluid (CSF). Patients showed no side effects during the course of intrathecal chemotherapy except for slight nausea in two patients and dull headache in one. Sixteen of the 23 patients showed decreased cell number in the cerebrospinal fluid (CSF). Positive cytological findings in CSF became negative in 6 of the 23 patients, and the levels of CSF tumor markers were decreased in 14. Responsiveness to intrathecal administration of FdUrd was defined as 'response' when both the cell number and tumor markers were decreased in both ventricular and spinal CSF or when the cell number was decreased in cases in which the tumor markers were not detected. Overall, 16 of the 23 patients (70%) showed complete or partial responses to intrathecal FdUrd therapy as determined from CSF findings. These results demonstrated the efficacy of intrathecal FdUrd chemotherapy without apparent neurotoxicity for treatment of meningeal dissemination of malignant tumors.
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PMID:Clinical trial of intrathecal administration of 5-fluoro-2'-deoxyuridine for treatment of meningeal dissemination of malignant tumors. 1077 33

The prostaglandin endoperoxide H synthases-1 and 2 (PGHS-1 and PGHS-2; also cyclooxygenases-1 and 2, COX-1 and COX-2) catalyze the committed step in prostaglandin synthesis. PGHS-1 and 2 are of particular interest because they are the major targets of nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin, ibuprofen, and the new COX-2 inhibitors. Inhibition of the PGHSs with NSAIDs acutely reduces inflammation, pain, and fever, and long-term use of these drugs reduces fatal thrombotic events, as well as the development of colon cancer and Alzheimer's disease. In this review, we examine how the structures of these enzymes relate mechanistically to cyclooxygenase and peroxidase catalysis, and how differences in the structure of PGHS-2 confer on this isozyme differential sensitivity to COX-2 inhibitors. We further examine the evidence for independent signaling by PGHS-1 and PGHS-2, and the complex mechanisms for regulation of PGHS-2 gene expression.
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PMID:Cyclooxygenases: structural, cellular, and molecular biology. 1096 56

Locoregional administration using OK-432 was evaluated in treating malignant effusion. Positive clinical responses were seen in 19 (52%) of 36 gastric cancer patients, and in 9 (90%) of 10 colon cancer patients (p < 0.05), indicating its clinical benefit in treating malignant effusion of colon cancer. Fever elevation was observed in 43 (93%) patients and local pain occurred with 9 (20%) of 46 administrations. Immunological analysis for responder patients with rectal cancer revealed that OK-432 induced autologous tumor-reactive CD 3+ CD 4+ TCRV beta 20+ killer lymphocytes. The TCR gene analysis permitted us to clone a V beta 20 CDR 3 sequence, by which positive bands were shown in 3 (75%) of 4 responders and negative bands in 3 (100%) of 3 non-responders. It is suggested that cross-antigenicity exists between OK-432 and colon cancer, and that genetic analysis using the TCRCDR 3 sequence makes it possible to predict responder patients to OK-432 immunotherapy.
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PMID:[Locoregional immunotherapy of malignant effusions for colorectal cancer using OK-432 and its acting mechanisms--possibility of molecular diagnosis using TCRCDR 3 sequence]. 1108 33

Prostaglandins are formed from arachidonic acid by the action of cyclooxygenase and subsequent downstream synthetases. Two closely related forms of the cyclooxygenase have been identified which are now known as COX-1 and COX-2. Both isoenzymes transform arachidonic acid to prostaglandins, but differ in their distribution and their physiological roles. Meanwhile, the responsible genes and their regulation have been clarified. COX-1, the pre-dominantly constitutive form of the enzyme, is expressed throughout the body and performs a number of homeostatic functions such as maintaining normal gastric mucosa and influencing renal blood flow and platelet aggregation. In contrast, the inducible form is expressed in response to inflammatory and other physiological stimuli and growth factors, and is involved in the production of the prostaglandins that mediate pain and support the inflammatory process. All the classic NSAIDs inhibit both COX-1 and COX-2 at standard anti-inflammatory doses. The beneficial anti-inflammatory and analgesic effects are based on the inhibition of COX-2, but the gastrointestinal toxicity and the mild bleeding diathesis are a result of the concurrent inhibition of COX-1. Agents that inhibit COX-2 while sparing COX-1 represent a new attractive therapeutic development and could represent a major advance in the treatment of rheumatoid arthritis and osteoarthritis. Apart from its involvement in inflammatory processes, COX-2 seems to play a role in angiogenesis, colon cancer and Alzheimer's disease, based on the fact that it is expressed during these diseases. The benefits of specific and selective COX-2 inhibitors are currently under discussion and offer a new perspective for a further use of COX-2 inhibitors.
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PMID:Cyclooxygenase inhibitors--current status and future prospects. 1131 43

The conventional and accepted treatment for curative resection of colon cancer is laparotomy with hemicolectomy for right or left sided lesions. The technique of colon resection through an open laparotomy incision is well known. Over the past several years, laparoscopically assisted colectomy has been developed and studied, following the explosion of laparoscopic technology from the cholecystectomy experience and with acquisition of advanced general laparoscopic techniques. The right, left or sigmoid colon can be mobilized and regional lymphadenectomy performed using laparoscopic instruments and video-imaging equipment. The advantage of laparoscopic colectomy is the use of small abdominal port site and wound incisions which translate to reduced postoperative pain and analgesic requirement, earlier return of bowel function and normal physical activities, and shorter hospital stay without increasing health care costs. Laparoscopic colectomy compares favorably with open colectomy in terms of surgical morbidity and mortality. The laparoscopic approach has been shown to be technically and oncologically feasible with equivalent lymph node harvest from mesenteric lymphadenectomy and achieves adequate proximal and distal margins of colonic resection. Despite initial early anecdotal reports of port site cancer recurrence in laparoscopically assisted colectomy, port site recurrence is rare and its incidence is similar to incisional recurrences in conventional open colectomy. Recent prospective comparative studies have demonstrated equivalent patient survival and equivalent local or distant colon cancer recurrences for open versus laparoscopic curative resection of colon cancer.
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PMID:Laparoscopic colectomy for cancer: an oncologic feasible option. 1135 41

Malignant-associated bowel obstruction remains a common and perplexing problem for patients with advanced gynecologic and gastrointestinal malignancies. The ability to locate and define its cause preoperatively has improved with the advent of computed tomography. Initial clinical experience with half-Fourier acquisition single-shot turbo spin-echo magnetic resonance imaging (HASTE MRI) and virtual colonoscopy is exciting. The surgical approach for primary obstructing colon cancer has become more aggressive, with experienced surgical groups doing one-stage procedures. Yet to be defined are guidelines for surgical management of obstructions occurring in the face of recurrent disease. Stent placement for upper and lower bowel obstructions is an option in nonoperable patients. Pharmacologic symptom management for intestinal obstructions consists of an opioid, an anticholinergic, and an antiemetic. Octreotide, either alone or added to the original regimen, will palliate symptoms that are resistant to the three-drug combination.
Curr Pain Headache Rep 2001 Jun
PMID:Modern management of cancer-related intestinal obstruction. 1140 Jun 96

We present an unusual case of a port site tumor from a colonic adenocarcinoma following laparoscopic cholecystectomy. A 66-year-old woman with a previous renal transplant underwent elective laparoscopic cholecystectomy for symptomatic cholelithiasis. Three months later, she re-presented with pain localized to the right lateral port wound. Subsequent investigation revealed an adenocarcinoma in the ascending colon with no evidence of local spread or liver metastases. The patient was enrolled in the ALCCAS trial (an Australasian multicenter prospective randomized clinical study comparing laparoscopic and conventional open surgical treatments of colon cancer in adults) and randomized to the laparoscopic arm. At laparoscopy, nodules of tumor were located at the sites of the previous right flank and umbilical trocar sites. The procedure was converted to an open hemicolectomy with excision of port sites. To our knowledge, only one other case of a colon carcinoma metastasizing to a port site following laparoscopic cholecystectomy has been reported. This case illustrates a number of points: (a) This was an advanced tumor at the time of diagnosis and was undoubtedly present at laparoscopic cholecystectomy. (b) This tumor was not manipulated at the time of laparoscopic cholecystectomy. (c) The patient was immunosuppressed at the time of laparoscopic cholecytstectomy. (d) The patient developed clinical recurrence in her laparotomy wound within 3 months of her open procedure. This case supports current arguments that the etiology of port site metastases is likely to be mulifactorial.
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PMID:An unusual case of port site seeding. 1144 29


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