Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A phase II study of VP-16, a semisynthetic Podophyllotoxin, was performed in patients with solid tumors. VP-16 was administered orally at a dose of 200mg/day for 5 consecutive days at 3 to 4-week intervals. Out of 41 patients who were entered into the study, 35 patients comprising 17 lung cancer, 10 hepatoma and 8 other tumors were evaluable. There were 4 partial responses (23.5%) for lung cancer, 1 (10.0%) for hepatoma and 1 for rhabdomyosarcoma. Overall response rate was 18.2% for patients with prior chemotherapy and 15.4% for those given no prior chemotherapy respectively. Thus the results indicated VP-16 has no cross-resistance to other antitumor agents. Leukopenia (less than 4,000/mm3) and thrombocytopenia (less than 10 X 10(4)/mm3) were observed in 72.7% and 29.4% of the patients, respectively. Other toxicities were alopecia (59.5%) and gastrointestinal disturbances such as nausea (46.2%), vomiting (20.5%) and anorexia (20.5%), but these were all well tolerated.
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PMID:[Phase II study of VP-16 (capsule) in solid tumors. A cooperative study]. 298 32

Primary liver sarcoma is rare and especially its coexistence with hepatocellular carcinoma is extremely rare. We have collected eight cases of their coexistence in the literatures. The patient was a 62-year-old male complaining of right hypochondralgia and general malaise for about one month. CT scanning revealed the liver tumor and right hepatic lobectomy was performed. The tumor was sized in 14 by 9 by 9 cm and composed of hepatocellular carcinoma and rhabdomyosarcoma, which were were collided. Apparent striations in the rhabdomyosarcoma cells was observed under light-microscope. Alphafetoprotein, of which serum level was extraordinarily high, was detected only in hepatocellular carcinoma by special stains. He discharged one month after operation. He was readmitted due to recurrence and received trans-arterial embolisation therapy and systemic chemotherapy. Though transient effect was obtained. He died forty-five days after operation. Autopsy revealed that recurrent liver tumors consisted of only hepatocellular carcinoma and that no other tumorous lesion was found in the other parts of the body. Rhabdomyosarcoma was proved to be primary tumor the liver.
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PMID:[A resected case of collision tumor of hepatocellular carcinoma and primary liver rhabdomyosarcoma]. 301 14

Twenty children with recurrent or unresponsive tumours (10 Wilms', 3 rhabdomyosarcoma, 4 Ewings's, 1 osteosarcoma, 1 hepatoblastoma, 1 hepatoma) and one untreated patient with renal carcinoma were given ifosfamide as a 24-h infusion (5 mg/m2), with mesna as uroprotective. The number of courses ranged from 1 to 13 (median 3), and the interval between them was 2-3 weeks. Sixteen of these patients had previously received cyclophosphamide. Complete clinical responses were seen in 3 cases (2 Wilms' and 1 Ewing's) and lasted 5, 7, and 9 months. Partial responses were seen in 3 instances, mixed response or stable disease in 4, and progressive disease in 11. Treatment was well tolerated in most patients, with no cystitis or severe myelosuppression, but 2 children developed transient neurological symptoms and 1 became hypertensive. Nausea and vomiting were controlled by high-dose dexamethasone in most children. Plasma ifosfamide levels were estimated by means of gas-liquid chromatography in 10 patients. Peak concentrations ranged from 38 to 125 micrograms/ml (median 80). The elimination half-life, at 2.5-5.2 h (median 3.2) was shorter than previously reported in adults. Future studies should test the possibility that ifosfamide-containing combination chemotherapy may be more effective than the regimens, usually including cyclophosphamide, that are currently used as front-line treatment of embryonal and Ewing's sarcoma.
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PMID:A phase II study of ifosfamide in children with recurrent solid tumours. 405 69

While magnetic resonance imaging (MRI) is not a screening examination in the search for metastatic disease, it has already demonstrated its value when performed as a carefully directed study to detect focal hepatic lesions. In the past 18 months we have encountered nine patients (six men, three women--ages 14-66) with a variety of primary tumors (renal cell carcinoma, two; colon carcinoma, two; hepatocellular carcinoma, two; pancreatic carcinoma, one; pheochromocytoma, one; rhabdomyosarcoma, one) whose MR scans revealed hepatic metastases after normal or nondiagnostic computed tomographic (CT) scans. The lesions were most clearly demonstrated using spin echo (SE) technique with recovery times (TR) of 2.0 seconds and delay times (TE) of 56 msec; metastases usually imaged with greater signal intensity than surrounding liver parenchyma. Lesions were solitary in three patients, multiple in six, and were found in all hepatic lobes without any specific location predominating. Pathologic confirmations of MR diagnoses were available in six of nine patients. In two patients, CT scans were of poor technical quality because streak artifacts from surgical clips obscured portions of the liver. In one patient iodinated contrast medium could not be given. In the remaining six patients CT scan quality was acceptable. This report is not a comparison study of the two modalities. We simply present nine patients in whom metastases were not detected by CT for various reasons but were found by MRI using SE technique.
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PMID:Magnetic resonance imaging diagnosis of hepatic metastases in the presence of negative CT studies. 408 52

An autopsy case of primary rhabdomyosarcoma of the liver in a 70-year-old man is described. The case could not be clinically differentiated from hepatocellular carcinoma. The tumor showed typical features of rhabdomyosarcoma; phosphotungstic acid hematoxylin (PTAH)-positive myofibrils and cross-striations were observed in the cytoplasm of highly plemorphic tumor cells.
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PMID:An adult case with rhabdomyosarcoma of the liver. 631 44

A total of 114 children with solid tumors refractory to conventional therapy were evaluated for response and/or toxic effects after receiving cisplatin at doses of 3.0-4.5 mg/kg with aggressive hydration and mannitol diuresis every 3 weeks; a minimum of two courses was required for evaluation of response (110 patients). Objective responses were noted in 18 patients: rhabdomyosarcoma (three), Wilm's tumor (three), osteogenic sarcoma (three). Ewing's sarcoma (two), neuroblastoma (one), undifferentiated sarcoma (one), hepatoblastoma (one), ovarian teratoma (one), hepatocellular carcinoma (one), embryonal carcinoma of the mediastinum (one), and thymoma (one). Twenty-six patients had some evidence of renal toxicity. Asymptomatic hearing loss was commonly found when audiometry was performed (eight of 18 patients tested). Eight additional patients had symptomatic hearing problems--tinnitus or hearing loss. Myelosuppression was mild. Hypomagnesemia and/or hypocalcemia were common but only one patient had symptoms. Cisplatin, administered at a dose of 3.0 mg/kg with aggressive hydration and mannitol diuresis, is reasonably well-tolerated. Its role in the therapy for those tumors against which it shows activity remains to be determined.
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PMID:Phase II trail cisplatin in refractory childhood cancer: Children's Cancer Study Group Report. 694 56

We have studied the induction of a granulocyte-associated leukocytosis (leukemoid reaction) in C3HA, C57B1/6, and DBA/2 mice by a number of transplantable tumors of different origin. Leukemia L1210, Hepatoma 22, a transplantable mammary carcinoma of spontaneous C3HA origin, and a L929 culture fibroblasts-derived rhabdomyosarcoma, all induced a leukemoid reaction in their specific mouse strain. Melanoma B16 and Lewis lung carcinoma gave no reaction; Adenocarcinoma 755 and Harding-Passey melanoma evoked a leukocytosis but not due to an increase in neutrophils. Some extratumoral factors can influence the hematological response; the intensity of final leukemoid reaction was higher in female mice than in males bearing the same tumor. On the other hand, Ehrlich ascites tumor transplanted in all three inbred mouse strains rendered different levels of leukemoid reaction; response was higher in DBA/2, intermediate in C3HA and lower in C57B1/6.
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PMID:Leukemoid reaction induced by different transplantable tumors in three inbred mouse strains. 707 May 57

A dose-intensive regimen of cyclophosphamide (140 mg/kg over 2 days), doxorubicin (Adriamycin, 75 mg/m2 over 3 days), and vincristine (1 mg/m2 on days 1, 2, and 3 and 1.5 mg/m2 on day 9) was tested in 18 children and adolescents with poor-prognosis recurrent or refractory solid tumors. Nine were affected by neuroblastoma, 3 by Ewing's tumors, 2 by rhabdomyosarcoma, 2 by synovial sarcoma, 1 by hepatocellular carcinoma, and 1 by osteogenic sarcoma. All enrolled patients were heavily pretreated, including 2 patients after bone marrow transplantation. Forty courses were applied (median, 2). The overall response rate was 33% (2 complete remissions and 4 partial remissions). Responses were obtained in children with neuroblastoma, Ewing's tumors, and hepatocellular carcinoma. Myelosuppression [World Health Organization (WHO) grade IV after all courses] and cardiac toxicity (3 WHO grade I, 5 WHO grade III, and 3 WHO grade IV) were the main side effects. Nephrotoxicity and hepatoxicity were not observed. With further therapy consisting of surgery, radiotherapy, and high-dose chemotherapy [cisplatin, carboplatin/etoposide (VP16), or ifosfamide/VP16 with or without autologous stem cell reinfusion after conditioning with melphalan/VP16/carboplatin], 3 complete remissions and 5 very good partial remissions were obtained. Ten of 18 patients are alive after a median follow-up of 16 months.
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PMID:High-dose cyclophosphamide, adriamycin, and vincristine (HD-CAV) in children with recurrent solid tumor. 785 84

Carzelesin (U-80244), one of the synthetic DNA minor groove binding cyclopropylpyrroloindole analogues, was selected for clinical development because of its high potency, promising antitumor activity in murine solid tumors and leukemia, and significant therapeutic efficacy against colon and rhabdomyosarcoma xenografts. In this Phase I study, carzelesin was given daily for 5 consecutive days to (a) determine the maximum tolerable dose (MTD) and the pattern of toxicity of this schedule; (b) define the pharmacokinetic profile of the parent, as was done for the intermediate compound U-76073 and the DNA-reactive agent U-76074; and (c) document any antitumor activity observed. Carzelesin was given as a 10-min infusion with a constant-rate infusion pump. Treatment was repeated every 4 weeks or when blood counts had recovered to normal values. The starting dose of 12 microgram/m2/day was escalated by 20-30% increments until the MTD (defined as the dose leading to grade 4 hematological or grade 3 nonhematological toxicity in at least two of six patients) was reached. Pharmacokinetic studies were planned on days 1 and 5 of the first cycle in at least two patients per dose level. Plasma levels of carzelesin, U-76073, and U-76074 were determined by high-performance liquid chromatography with UV detection and a detection limit of 0.5 ng/ml. Twenty-five patients were entered in the study, and 56 cycles were evaluable for hematological toxicity. Subsequent dose levels evaluated were 24, 30, 35, and 40 microgram/m2. Both neutropenia and thrombocytopenia were dose limiting and cumulative, with a high interpatient variability. Neutropenia occurred earlier (median time to neutrophil nadir and recovery, 15 and 29 days, respectively) than thrombocytopenia (median time to platelet nadir and recovery, 25 and >/=26 days, respectively); there were delays of treatment because of persisting thrombocytopenia in all patients treated at the MTD. At the MTD, the peak plasma concentrations of carzelesin were achieved at the end of the infusion and were higher than those found cytotoxic in vitro against tumor cell lines. Carzelesin was detectable up to a maximum of 1 h after the infusion. Smaller amounts of U-76073 were detectable for a maximum of 30 min only at the MTD, whereas U-76074 was never found. An 8-month partial remission was reported in one previously untreated patient with hepatocellular carcinoma at 40 microgram/m2. The MTD was fixed at 40 microgram/m2 daily; 35 and 30 microgram/m2 are the daily doses recommended for Phase II studies in good- and poor-risk patients. The daily regimen for 5 days seems to offer no advantage over the single intermittent schedule that has been selected for the Phase II program in Europe.
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PMID:Phase I clinical and pharmacokinetic study of carzelesin (U-80244) given daily for five consecutive days. 981 22

An unusual case of a massive liver tumour composed of rhabdomyosarcoma with a small focus of hepatocellular carcinoma in a 52-year-old man is presented. He had hepatitis B virus (HBV) surface antigen in his serum. Macroscopically, a large tumour with satellite nodules occupied the right lobe of the cirrhotic liver. Microscopically, the tumours were composed of small and short spindle-shaped undifferentiated cells, mixed with desmin-positive round rhabdomyoblasts and elongated striated muscle cells, strongly suggestive of rhabdomyosarcoma of the liver. Elevated levels of alpha-fetoprotein in the serum led us to examine the liver tumour closely in multiple sections, which disclosed a hepatocellular carcinoma component measuring 2 cm in diameter within the massive tumour. Immunohistochemically, the hepatocellular carcinoma cells were alpha-fetoprotein positive. There was neither a tumour capsule, nor distinct demarcation, and cytokeratin-positive clusters of undifferentiated cells were intermingled with the hepatocellular carcinoma and rhabdomyosarcoma at the border. The invading tumour outside the liver and metastatic tumours were pure rhabdomyosarcomas. It is suggested that the present case should be diagnosed as rhabdomyosarcoma transformed from hepatocellular carcinoma.
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PMID:Sarcomatoid hepatocellular-carcinoma showing rhabdomyoblastic differentiation in the adult cirrhotic liver. 1039 85


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