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)

A 53-year-old man who suffered from advanced hepatocellular carcinoma (HCC) was treated with hepatic arterial infusion (HAI) of Etoposide, Epirubicin and CDDP. Treatment consisted of a continuous HAI of Epirubicin (50 mg/body, day 1.7), CDDP (75 mg/body, day 2.8) and Etoposide (80 mg/body, day 4-6). He had two series of infusions and was treated by transarterial embolization using CDDP powder (100 mg) added to lipiodol and aluminum stearate as suspension following HAI. The tumor regression rate was about 60% after HAI, but the remaining tumor seemed to be almost necrotic. AFP and PIVKA-II reached the normal range after TAE. We could not find lipiodol accumulated in tumor on CT carried out eight weeks after TAE. No recurrence has been noticed in the following 8 months. Toxicity was not so severe and was well tolerated.
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PMID:[A case with hepatocellular carcinoma effectively treated by continuous hepatic arterial infusion of etoposide, epirubicin and CDDP]. 131 15

A 29-year-old-woman with recurrent cancer of rectum was treated with Etoposide, cis-platinum and external irradiation. Previous postoperative chemotherapies consisted of MMC, CPA, VCR and HCFU. Histologically, the tumor invaded in sheets and nests, and consisted of round to ovoid malignant cells with high nuclear/cytoplasmic and hyperchromatic nuclei with a coarse, clumped, or stippled chromatin pattern. Most cells demonstrated a positive reaction by Grimelius and NSE staining. Eight months after surgery, we switched to Etoposide cis-platinum and external irradiation, because of local recurrence. Etoposide (total 725 mg) and cis-platinum (total 100 mg) were injected into bilateral iliac artery and 60 Gy radiotherapy was performed. The patient showed a good response, and a complete response (CR) was evident for the following 42 months. Thus, Etoposide, Cis-platinum and radiotherapy are considered an effective combination therapy for a patient with small cell undifferentiated carcinoma.
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PMID:[A case of small cell undifferentiated carcinoma (SCUC) of the rectum treated with etoposide, cis-platinum and radiotherapy]. 133 27

Etoposide and teniposide are closely related derivatives of podophyllotoxin, and both have a phase-specific action in the late S and early G2 phases of the cell cycle. Etoposide has attracted more widespread use and study, although no evidence suggests a differing mode of action or spectrum of anticancer activity. The drugs have significant differences in their clinical pharmacology, however. Teniposide exhibits greater protein-binding affinity, has a longer plasma terminal elimination half-life, and has reduced plasma and renal clearances. Little is accurately known about the metabolism of either drug, but the fact that 40% to 60% of administered etoposide is accounted for by excretion or metabolism, whereas the range is only 10% to 25% for teniposide, reflects a further difference between the drugs. Renal dysfunction impairs etoposide excretion, but the effect of hepatic impairment on drug clearance is unclear. A specific oral formulation exists only for etoposide, although the unpalatable intravenous preparations of both drugs can be taken orally. The bioavailability of oral etoposide is about 50% at doses of 200 mg or less and decreases as drug doses increase. There is considerable intrapatient and interpatient variation in etoposide absorption, but the reasons for this are unknown. In vitro, the efficacy of etoposide is highly dependent on the schedule of administration. The superior efficacy without increased toxicity of more prolonged schedules of etoposide administration has been demonstrated recently in patients with small cell lung cancer (SCLC). Although the optimal schedule in any specific tumor is not known, current pharmacodynamic evidence suggests that the efficacy of etoposide, at least in SCLC, is related to the maintenance of prolonged low blood concentrations of drug.
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PMID:Clinical pharmacology and schedule dependency of the podophyllotoxin derivatives. 141 35

The characteristic of malignant pleural mesothelioma is a tumor that grows by plate-like extension over the pleura, and invades adjacent tissues and organs. Radical surgical removal of the tumor is generally not possible, and most treatment regimens involve combined chemotherapy and radiotherapy, as well as debulking surgery. We have prospectively evaluated five locally-aggressive multi-modality treatment programs, using different hemithorax irradiation schedules and chemotherapy regimens. One hundred patients with confirmed malignant pleural mesothelioma entered the study between 1977 and 1989. The treatment programs, which can consecutively, were: I, 20 Gy (10 x 2 Gy) to the hemithorax + CYVADIC (cyclophosphamide 500 mg/m2 d 1, vincristine 1 mg/m2 d 1 and 5, adriamycin 40 mg/m2 d 1 and dacarbazine 200 mg/m2 d 1 and 5, several cycles before and after irradiation); II, 55 Gy (25 x 2.2 Gy) to the hemithorax + 15 Gy (6 x 2.5 Gy) to the tumor + CYVADIC (2 cycles before, 1 cycle during, and 2 cycles after irradiation); III, Mitoxantrone (14 mg/m2 q 28 d, < or = 6 cycles) followed by 70 Gy (56 x 1.25 Gy, twice a day); IV, 4-Epirubicin (110-130 mg/m2 q 28 d, < or = 6 cycles) followed by 35 Gy (28 x 1.25 Gy twice a day) to the hemithorax + 36 Gy (9 x 4 Gy every 2 days) to the tumor; V, Etoposide (150 mg/m2 1, 3, 5 q 28 d) followed by 38.5 Gy (11 x 3.5 Gy) to the hemithorax. A new system for evaluating tumor response in pleural mesothelioma was applied. None of the combined treatment programs prevented local invasive growth or the spread of mesothelioma outside the hemithorax. The median survival time was slightly increased from 8 to 12 months for those patients who completed the protocol treatments, but progressive disease was the invariable outcome. Radiation pneumonitis and fibrosis were severe and compatible with results of total loss of lung function on the irradiated side. We conclude that data relating to therapeutic responses and treatment programs in malignant mesothelioma should be better correlated internationally, if the problems associated with the evaluation of treatment and the management of patients with mesothelioma are to be improved.
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PMID:Multimodality treatment programs for malignant pleural mesothelioma using high-dose hemithorax irradiation. 142 86

Etoposide is an important antineoplastic drug. Despite the use of several combination chemotherapy regimens that include etoposide, the best dose and schedule for etoposide remains unknown. The schedule dependency for small cell lung cancer is now known, and it is likely the same for other sensitive neoplasms (ie, lymphoma, germ cell tumors). Recent data suggest that even a more extended schedule of administration (ie, 14 to 21 days) may be more effective than the standard 3- to 5-day schedule. Several studies have assessed plasma levels in reference to dose, schedule, and tumor responsiveness. Preliminary data suggest that high peak levels (ie, > 5 to 10 micrograms/mL) are associated with more severe myelosuppression than lower peak plasma levels (ie, 1 to 3 micrograms/mL). Response rates and survival in small cell lung cancer patients given low daily doses for 14 to 21 days are comparable with results achieved with standard doses given for 3 to 5 days. Preliminary data from several studies suggest that administering low doses for a prolonged schedule is a superior method of etoposide administration. Other studies including randomized comparisons are necessary to confirm these observations.
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PMID:Etoposide: seeking the best dose and schedule. 148 56

An advanced gastric cancer with liver metastasis was treated with the combination MMC, Etoposide and UFT. Etoposide was administered orally at 25-50 mg/day to the gastric cancer patient with liver metastasis. In operative findings, there was no liver and lymphoid node metastasis. The gastric tumor diminished in size and changed its characteristics due to the chemotherapy. In 19 months, no liver nor LN metastasis was observed by CT scan. Presently, the patient feels well and receives outpatient treatment.
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PMID:[A resected case of advanced gastric cancer with complete remission of liver metastasis by chronic daily administration of oral etoposide and UFT]. 162 43

The pilot protocol of the German Society of Pediatric Oncology for treatment of non testicular germ cell tumors was initiated in November 1987. The final protocol was started at 1. 1. 89. Different therapy was administered depending on histology, primary localisation or stage of tumors. Patients with malignant germ cell tumors such as dysgerminomas, embryonal carcinomas, yolk sac tumors or chorio carcinomas received BEP (Bleomycin 15 mg/m2/days 1-3, Etoposide 100 mg/m2/days 4-8, Cisplatinum 20 mg/m2/days 4-8), followed by VIP (Vinblastine 3 mg/m2/days 1 + 2, Ifosfamide 1500 mg/m2/days 1-5 including Mesna uroprotection and Cisplatinum 20 mg/m2/days 1-5). Patients with ovary tumors of stage 1 were treated with 3 courses of BEP, patients with ovary tumors stage II and extragonadal localisation received 3 courses of VIP in addition to 3 courses of BEP. In cases of extended tumors 4 courses of BEP were followed by delayed resection of tumors and 4 courses of VIP. Patients with intracranial germinomas were treated with 30 Gy of craniospinal radiation therapy and additional 15 Gy as a tumor boost. Since some cases of spinal extension were reported a spinal radiation therapy seems to be indispensable. Patients with intracranial embryonal carcinomas, yolk sac tumors or chorio carcinomas tumors were given 2 courses of BEP and VIP followed by 30 Gy of craniospinal radiation therapy and additional 20 Gy as a tumor boost. Patients with immature teratomas of the ovary grade 1-3 and grade 3 of tumors with extragonadal localisation were treated with 3 courses of BEP after resection of tumors. Until 1. 1. 1991 92 patients were reported to the study--27 with intracranial and 65 with extracranial primary localisation of tumors. 43 patients suffered from teratomas (including 20 immature teratomas grade 1-3), 18 from germinomas (seminomas/dysgerminomas) and 31 from malignant non-seminomatous germ cell tumors. After an observation period of 29 months disease-free survival rate was 80% (79/92 patients, Kaplan-Meier Statistics). Outcome of intracranial tumors was death or relapse in 2/9 patients with malignant non-seminomatous germ cell tumors, in 2/14 patients with intracranial germinomas, in 2/4 patients with teratomas. Patients with extracranial localisation of tumors suffered from death or relapse in 1/21 cases with non-seminomatous tumors, in 0/4 cases with dysgerminomas and 5/39 cases with teratomas. During pilot study one infant with a malignant non-seminomatous germ cell tumor died of a pneumopathia. Therefore infants treated according to the final protocol did not receive Bleomycin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Treatment of non-testicular germ cell tumors in children and adolescents with BEP and VIP: initial results of the MAKEI 89 therapy study]. 171 67

The activity of Etoposide (VP16) in combination chemotherapy against four human transitional cell carcinoma cell lines of bladder (TCCaB) was determined by in vitro colony formation assay. Four anti-tumor agents (methotrexate: MTX, vinblastine: VBL, adriamycin: ADM, cisplatin: DDP) were used for combination chemotherapy with VP16. The ADM + VP16 combination exhibited a strong synergistic antitumor effect against the human TCCaBs compared with other combinations in this study. The combination chemotherapy of ADM + VP16 may be useful as a new chemotherapeutic regimen for advanced bladder cancer.
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PMID:[The activity of etoposide (VP16) in combination chemotherapy against human bladder cancer cells in vitro]. 178 27

Etoposide is one of the few cancer chemotherapy agents that is schedule-dependent in both preclinical and clinical studies. A randomized trial of etoposide as initial therapy in extensive small cell lung cancer (SCLC) demonstrated the superiority of a 5-day course versus the same total dose administered over 24 hours. The recent availability of oral etoposide capsules has led to further exploration of etoposide's schedule-dependency through the use of daily oral etoposide. Initially, studies at Indiana University and the Hoosier Oncology Group concentrated on refractory germ cell tumors and refractory SCLC. Although both of these tumor types are sensitive to etoposide combination chemotherapy as initial treatment, it is rare to see a response with any single agent in refractory disease. In 25 patients with refractory germ cell tumors, we observed 5 objective responses (20%). In addition, 3 other patients (12%) clearly achieved antitumor effect with a greater than 90% reduction in tumor markers, although radiographic findings remained stable. In refractory SCLC, 1 complete and 5 partial responses were observed in 26 patients, for a 23% response rate. Twenty-five of the 26 had received prior cisplatin/etoposide and 14 also had received prior cyclophosphamide/doxorubicin/vincristine. Daily oral etoposide is capable of producing palliation and objective responses in heavily pretreated patients and may be a preferable method of administration. Future trials are planned using daily oral etoposide as a component of combination chemotherapy as first- and second-line therapy in patients with SCLC.
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PMID:Daily oral etoposide in the treatment of cancer. 184 80

Etoposide (VP-16) resistance is expressed following in vitro exposure of HN-1 and MCF-7 human tumor cells to the drug itself or to fractionated X irradiation. VP-16-selected sublines prove cross-resistant to Adriamycin, amsacrine and actinomycin D, whilst X-ray-pretreated sublines show cross-resistance to only actinomycin D. These differential responses, in the HN-1 series, are not associated with significant differences in amounts of immunoreactive topoisomerase (topo) II, altered topo-II catalytic activity of nuclear extracts or changes in susceptibility of the topo II to VP-16- or amsacrine-induced DNA-protein cross-link formation. Therefore significant modifications in topo II appear not to be implicated in VP-16 resistance in these HN-1 sublines.
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PMID:A lack of detectable modification of topoisomerase II activity in a series of human tumor cell lines expressing only low levels of etoposide resistance. 184 24


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