Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a 49-year-old female with a left parietal convexity meningioma associated with an acute subdural hematoma is described. She was admitted because of sudden onset of severe headache accompanied by nausea and vomiting. She was also confused, and 6 hours after admission she developed lethargy, right hemiplegia, and left mydriasis with no pupillary reaction to light. Computed tomography disclosed a round, extra-axial mass in the left parietal region; it was heterogeneously enhanced. Emergency craniotomy, performed after carotid angiography, revealed a tumor with a massive underlying subdural hematoma. The histological diagnosis was meningotheliomatous meningioma, and there were many meningothelial cells within the hematoma.
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PMID:Meningioma associated with subdural hematoma--case report. 169 43

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

The authors treated 14 patients with advanced squamous cell carcinoma (SCC) of the skin or lip with one to four cycles of combination chemotherapy consisting of cisplatin by bolus injection, and 5-fluorouracil (5-FU) and bleomycin by continuous 5-day infusion. Objective responses were seen in 11 of the 13 evaluable patients (84%). Four patients had a complete remission (30%) and seven patients, a partial remission (54%). Local control after definitive complementary radiation and/or surgical treatment was achieved in seven patients. Toxic side effects was acceptable; they consisted of nausea and vomiting in all patients, transient skin changes, hematologic (Grade 3/4) abnormalities in four patients, and pulmonary fibrosis in one elderly patient. These results show that this chemotherapy combination could play a role in reducing the tumor mass and in facilitating definitive treatment to obtain better functional and cosmetic results in advanced SCC of the skin.
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PMID:Treatment of advanced squamous cell carcinoma of the skin with cisplatin, 5-fluorouracil, and bleomycin. 169 29

We investigated the clinical effects and toxicity of chemotherapy with Cisplatin (CDDP) for head and neck cancer as the third joint research project of the Tokai Meeting for Head and Neck Tumors. The cases were examined at the cooperating institutions from September 1986 to March 1988. The subjects were 93 cases consisting of 66 patients (intravenous infusion: 47 cases; intraarterial infusion: 19 cases) of PP therapy (CDDP + PEP), 16 cases of PF therapy (CDDP + 5-FU) and 11 cases of PPV therapy (CDDP + PEP + VCR). The regimens of PP therapy were: CDDP 50-100 mg/body x 1 day, PEP 5 mg/body x 5 days (i.v.), and CDDP 10-20 mg/body x 5 days, PEP 5-10 mg/body x 5 days (i.a.). In the regimen of PF therapy, CDDP 80-100 mg/body x 1 day and 5-FU 750-1,000 mg/body x 5 days were administered. In the regimen of PPV therapy, CDDP 80-100 mg/body x 1 day, PEP 5 mg/body x 5 days and VCR 1 mg/body x 1 day were administered. As a rule, two courses of each of the regimens were performed. The total dose of CDDP in intraarterial infusion of PP therapy was significantly less than in intravenous infusion. The major results were as follows: 1) Total response rate was 57.0% on the average, and this was not significantly different among the regimens. 2) The response rate of intraarterial infusion of PP therapy was as high as that for intravenous infusion in spite of the lower CDDP dose. 3) The response rate of oral cavity was significantly higher than that of nasal cavity and paranasal sinuses. 4) In the squamous cell carcinoma, the response rate of the well differentiated type was significantly higher than that of the poorly differentiated type. 5) The leukocyte counts significantly decreased with the intravenous infusion of PP therapy, PF therapy and PPV therapy. 6) The platelet counts significantly decreased with PPV therapy. 7) There were no significant changes with time with Ccr and PaO2 of PP therapy. 8) The frequency of toxicities such as nausea and vomiting was high in the intravenous infusion of PP therapy, PF therapy and PPV therapy. However, the frequency of toxicity was low in the intraarterial infusion of PP therapy.
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PMID:[Clinical effects and toxicity of chemotherapy with cisplatin for head and neck cancer--the multi-institutional joint research in Tokai district]. 170 33

Gallbladder cancer afflicts predominantly women, the elderly, and persons with gallstones. Despite its producing symptoms of abdominal pain, nausea and vomiting, weight loss, jaundice, and anorexia, this disease remains difficult to detect. Even with contemporary imaging techniques, most gallbladder cancers escape diagnosis until the time of laparotomy. The aggressive character of this malignancy permits an overall 5-year survival rate of 3-5%. Although cures occur, the majority of operations performed for gallbladder cancer are for palliation. The objects of palliation include relief of pain, relief of jaundice, relief of intestinal obstruction, and the restoration of normal food intake. Resection of the tumor should be performed whenever possible; however, extensive operations including large liver resections and pancreaticoduodenectomy should be avoided in the presence of distant metastases. In the presence of large unresectable hilar masses, internal biliary bypass may relieve jaundice. Biliary-enteric anastomosis using the segment III duct exposed via the umbilical fissure may offer satisfactory relief of jaundice in selected cases.
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PMID:Palliative operative procedures for carcinoma of the gallbladder. 137 59

A 61-year-old female with recurrent endometrial cancer (serous papillary adenocarcinoma) was treated with etoposide because the pelvic tumor progressively increased in size with external beam irradiation. The etoposide (25 mg/day) was given orally for 10 days; the tumor decreased in size. And after an additional two courses of etoposide for 8 and 4 days, respectively, the tumor disappeared and the serum CA 125 level came to within normal limits. Because of moderate nausea and vomiting the etoposide could not be given for 14 days in the first 3 courses. Myelosuppression was not evident. Ten courses of etoposide (for 14 consecutive days a month) were followed without gastro-intestinal side effects, and the patient is alive with no evidence of recurrence at this writing. This case suggests that oral administration of etoposide may be effective for a patient with recurrent endometrial cancer, and this treatment could be administered on an outpatient basis.
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PMID:[A case of recurrent endometrial cancer successfully treated with oral administration of etoposide]. 172 57

A 71-year-old woman with a remote history of esophagogastric resection for malignancy developed abdominal pain, nausea and vomiting. She died of shock 15 days after admission, during which time clinical investigation failed to reveal recurrent tumor or an ulcer. The autopsy revealed massive exsanguination secondary to a peptic-ulcer-induced aortoenteric fistula (AEF). The ulcer involved the third portion of the duodenum, was chronic, and complicated by growth of fungus. We review the literature on peptic-ulcer-related AEF.
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PMID:Peptic-ulcer-induced aortoenteric fistula. Report of a case and review of the literature. 176 41

Fifty-four patients with advanced malignancies were treated on this phase I trial of coumarin and cimetidine. The dose of coumarin was escalated, with three patients treated at each dose level, while the cimetidine dose was held constant at 300 mg four times daily. Patients received coumarin alone as a single daily oral dose for 14 days; on day 15, cimetidine was added and both drugs were continued until progression of disease. This trial was initiated with patients receiving coumarin at 400 mg daily and closed at 7 g daily with four of five patients on this dose experiencing nausea and vomiting. Treatment was generally well tolerated over a wide range of coumarin doses. Symptomatic side effects were few, mild, and usually self limited. Side effects included insomnia, nausea, vomiting, diarrhea, and dizziness. Two patients withdrew from therapy because of daily nausea and vomiting. Typically, nausea, vomiting, and dizziness occurred 2.5-3 hours after a dose of coumarin. In most patients, these side effects abated spontaneously with continuation of therapy. There was no significant hematologic or renal toxicity. Hepatotoxicity occurred in only one patient and was manifested by asymptomatic abnormal elevations of serum hepatic transaminases. This toxicity was reversible upon interruption of therapy. Objective tumor regressions were observed in six patients with renal cell carcinoma. Responses occurred at coumarin doses ranging from 600 mg to 5 g daily. Coumarin is a relatively nontoxic, oral, outpatient therapy that warrants further investigations for the treatment of human malignancies. Because of its low toxicity, there is potential for combining coumarin with chemotherapeutic and/or biological agents in an attempt to improve on efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I evaluation of coumarin (1,2-benzopyrone) and cimetidine in patients with advanced malignancies. 176 68

Tiludronate is a new bisphosphonate whose efficacy has already been reported for the prevention of postmenopausal bone loss. We have evaluated its efficacy and tolerance by a dose-finding study in 19 hypercalcemic cancer patients after adequate intravenous (iv) rehydration. Treatment consisted of 3 days of iv tiludronate given at doses of 3.0 mg/kg/day (n = 3), 4.5 mg/kg/day (n = 3), or 6.0 mg/kg/day (n = 13); this iv therapy was followed by 17 days of oral tiludronate, 400 mg (n = 13) or 800 mg (n = 6) daily. Treatment had to be discontinued in 9 patients, including 3 because of evident treatment failure and 1 because of severe toxicity. After iv tiludronate, 13/18 patients had a normal Ca level, including 10/12 who had received 6.0 mg/kg/day, but Ca2+ levels were fully normalized in only 4/18 and 3/12 patients, respectively. After 6.0 mg/kg/day, Ca levels had fallen from 12.1 +/- 0.3 to 10.0 +/- 0.4 mg/dl (P less than 0.0005), whereas fasting urinary calcium excretion went from 0.639 +/- 0.099 to 0.272 +/- 0.054 mg Ca/mg creatinine on d4 (P less than 0.001). On the other hand, oral tiludronate was unable to normalize Ca in patients who were still hypercalcemic after the iv course, although the daily administration of 800 mg appeared to be more efficient than the 400 mg daily dosage. The administration of tiludronate caused an increase in serum phosphate levels, from 2.9 +/- 0.2 to 3.7 +/- 0.2 mg/dl after the iv course, probably through an increase in the TmP/GFR index, which went from 2.3 +/- 0.2 to 3.6 +/- 0.4 mg/dl (P less than 0.05). Three patients had an increase in serum creatinine levels after the iv course, one obese patient developing an acute renal insufficiency; during oral tiludronate therapy, 5 other patients also presented an increase in serum creatinine levels. Oral tiludronate administration was also associated with occasional nausea and vomiting. In summary, compared with aminobisphosphonates, tiludronate is not indicated for the treatment of tumor-associated hypercalcemia because of the need for high iv doses which are potentially nephrotoxic.
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PMID:Efficacy and safety of the bisphosphonate tiludronate for the treatment of tumor-associated hypercalcemia. 177 38

The arylmethylaminopropanediols (AMAPs) are a new class of DNA intercalators. 773U82.HCl is the second of these compounds to enter clinical trial. Significant antitumor activity for 773U82.HCl was documented in a variety of murine and human tumor models. This phase I study examined a 1-, 2- and 6-hour infusion given every 28 days. Thirty-six patients received 58 courses of drug at doses ranging from 15 mg/m2 to 980 mg/m2. The dose-limiting toxicity of 773U82.HCl was hemolysis noted at 980 mg/m2. Change in color of the plasma and decreases in haptoglobin were correlated with drug concentrations of the infusate greater than or equal to 3 mg/ml. Clinically significant changes in hemoglobin levels requiring blood transfusions did not occur. Neurologic toxicity occurred at 720 mg/m2 with the most severe neurologic toxicity occurring in a patient with the highest peak plasma concentration (4.1 micrograms/ml). With an increase in duration of the infusion and amount of fluid administered, the neurologic toxicity resolved. Other toxicities included mild nausea and vomiting and a dose-related phlebitis. Pharmacokinetic studies were completed in 22 patients. The mean terminal t1/2 beta was 4.4 h with a mean apparent volume of distribution at steady state (Vdss) of 314 l/m2. The mean total body clearance was 72 l/h/m2. Peak plasma levels ranged from 0.04 to 4.14 micrograms/ml. Further studies with 773U82.HCl on this schedule at the doses studied are not recommended. Hematologic monitoring for evidence of intravascular hemolysis should be included in future studies with 773U82.HCl.
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PMID:Phase I evaluation of 773U82.HCl, a member of a new class of DNA intercalators. 179 91


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