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 38-year-old man was admitted to Nara Medical University Hospital on Feb.7,1983, because of swelling of the scrotal contents on the right side and elevated serum AFP, beta-HCG and LDH suggestive of testicular tumor. Right orchiectomy was carried out and a pathological diagnosis of embryonal cell carcinoma of the right testis (pT3N0M1) was made. The patient, upon evidence of multiple pulmonary metastases, was treated with a combination chemotherapy of cis-Diamminedichloroplatinum, vincristine and peplomycin. After three courses of combination chemotherapy, pulmonary metastases were decreased, but their foci persisted. The patient was then treated with Etoposide 62 mg/m2 daily for 5 days every three weeks, and after this course, complete remission of pulmonary metastases was obtained. The patient recieved 3 courses of Etoposide and retroperitoneal lymph node dissection, and has since shown no evidence of disease for 2 years and 4 months after surgery.
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PMID:[Complete remission obtained in advanced testicular cancer treated by etoposide (NK-171)]. 242 Feb 82

A 33 months old girl and a 5 months old boy presented with unresectable hepatoblastoma (group III) and were treated with combination chemotherapy using Adriamycin, Cyclophosphamide, Cisplatinum (regimen I) and Adriamycin, Etoposide, Cisplatinum (regimen II). In both patients tumor size and alpha-fetoprotein levels decreased remarkably. Tumor regression was considerably enhanced by selective chemoembolization (Ethibloc, Adriamycin) of the right hepatic artery in one patient. After preoperative chemotherapy hepatoblastomas could be removed surgically. Local recurrence in the older patient was treated again successfully by surgery and chemotherapy. The patients are surviving disease-free 17 and 28 months from diagnosis. The efficacy of the treatment warrants prospective clinical trials in patients with unresectable hepatoblastoma.
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PMID:[Combination chemotherapy and chemoembolization in the treatment of primary inoperable hepatoblastoma]. 242 23

It is very common for intraarterial infusion therapy of some anticancer agent to be effective against hepatocellular carcinoma. In this case, the patient was a 74-year-old man who suffered from very advanced hepatocellular carcinoma with tumor thrombus of the intrahepatic portal vein and IVC. He was treated with intraarterial infusion of CDDP, Etoposide, 5-FU, through a catheter placed in the proper hepatic artery. CDDP (30 mg/day) and Etoposide (60 mg/day) were given once every 5 days, and then 5-FU(250 mg/day) was infused daily for 26 days. The patient underwent this protocol study twice in 3 months. After the intraarterial infusion, transarterial embolization using CDDP (100 mg) powder added to lipiodol and aluminum stearate as suspension was done a month later. The tumor regression rate was 84% after intraarterial infusion of CDDP, Etoposide and 5-FU. The tumor thrombus in the intrahepatic portal vein and IVC had completely disappeared. We could not find lipiodol accumulated in the tumor after TAE. Thus, we assumed that the remaining tumor was a necrotic scar and that a complete response was obtained in the patient. There were some side effects, such as nausea, vomiting, pancytopenia and gastritis but no severe complication occurred.
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PMID:[A case of hepatocellular carcinoma effectively treated by intraarterial infusion of CDDP and other agents]. 255 Dec 53

The sequence dependency of the antitumor effect of etoposide and ara-C was investigated against the L1210 ascites tumor in BDF1 mice. Etoposide (7.5 mg/kg or 15 mg/kg) and ara-C (25 mg/kg or 500 mg/kg) were administered intraperitoneally on days 1, 4 and 7 after inoculation of L1210 with or without time interval of 3 or 6 h. Antitumor effect was decided for cure rate and post inoculation survival time of the mice died of tumor. Six hours pretreatment with 15 mg/kg of etoposide followed by 500 mg/kg of ara-C yielded 100% of cure rate, but only 20% of cure rate was obtained with the reverse sequence. Simultaneous administration of etoposide and ara-C produced 70% of cure rate. At every dosage examined, pretreatment with etoposide given 6 hr before ara-C was the most effective antitumor schedule in L1210 leukemia.
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PMID:[Studies on the relationship between therapeutic schedule and antitumor effect of etoposide and cytosine arabinoside in murine L1210 leukemia]. 261 69

To assess the usefulness of 4-hydroperoxycyclophosphamide (4-HC) and Etoposide (VP-16) as a purging agent for myeloma cells in bone marrow ex-vivo, myeloma cell lines (SK-RCS-1, RPMI-8226), lymphoma cell line (SK-DHL-2) and normal bone marrow (BM) cells were treated at different concentrations of 4-HC, VP-16. In separate experiments, LAK cells or antibodies were also used to treat the above cell lines. Clonogenic tumor cells from all three cell lines could be reduced by more than 4 logs, when treated alone or as a mixture with irradiated normal bone marrow cells at a 4-HC concentration of 60 mumol/l. Under similar conditions, approximately 1% of normal BM myeloid progenitor granulocyte-macrophage colony forming cells (CFU-GM) survived. The results with LAK cells and antibodies were also encouraging. These observations support the use of various purging methods for myeloma cells for autologous bone marrow transplantation.
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PMID:Ex vivo treatment of myeloma cells by 4-HC, VP-16, LAK cells and antibodies. 262 87

Tumor-promoting phorbol esters such as phorbol 12-myristate 13-acetate (PMA) induce the monocytoid differentiation of HL-60 human leukemia cells. The cellular receptor for PMA is protein kinase C. However, cellular events distal to protein kinase C phosphorylation are also critical steps toward differentiation. These events may include specific programs of oncogene transcription that have been associated with phorbol ester-induced leukemic cell differentiation. Recently, it has been found that topoisomerase II could be activated by protein kinase C-mediated serine phosphorylation and that PMA treatment of HL-60 cells enhanced extractable topoisomerase II from these cells. Additionally, topoisomerase II-reactive antineoplastic drugs could block PMA-induced differentiation of HL-60. This enzyme has been implicated in gene regulation, and drug-induced, topoisomerase II-mediated DNA cleavage sites have been identified within cellular oncogenes. Thus, topoisomerase II could play a critical role in the signal transduction cascade leading from PMA-protein kinase interaction to monocytoid differentiation. We have examined this relationship between topoisomerase II and PMA-induced differentiation through measurements of drug-induced, topoisomerase II-mediated DNA cleavage (via alkaline elution) in PMA-treated HL-60 cells. Etoposide-induced DNA cleavage was reduced 10-fold in HL-60 cells treated with 10 nM PMA for 24 h. Neither dimethyl sulfoxide (which produces granulocytoid differentiation) nor non-differentiation-inducing phorbol esters could produce this effect. The decreased cleavage was not due to a PMA-induced inhibition of cell-associated etoposide and was demonstrable in nuclei isolated from PMA-treated cells. The decrease was not simply related to decreased cellular proliferation rate as reflected in the inhibition of DNA synthesis because conditions leading to marked inhibition of DNA synthesis did not necessarily inhibit etoposide-induced DNA cleavage. By contrast, lower concentrations of PMA inhibited etoposide-mediated DNA cleavage disproportionately compared with PMA effects on DNA synthesis. Interestingly, PMA reduced cleavage induced by the topoisomerase II-reactive DNA intercalator 4'-(9-acridinylamino)methanesulfon-m-anisidide by 2-fold, suggesting that specific drug-DNA interactions could partially overcome the PMA-induced effect that resulted in decreased etoposide-induced, topoisomerase II-mediated DNA cleavage. Nuclear proteins in 0.35 M NaCl extracts from untreated or PMA-treated HL-60 cells were virtually identical in topoisomerase II activity and in topoisomerase II-associated drug sensitivity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of phorbol ester treatment on drug-induced, topoisomerase II-mediated DNA cleavage in human leukemia cells. 284 55

A 47-year-old male was diagnosed as having gastric cancer with metastases to liver, para-aorta node and Virchow node. He was treated with EAP (Etoposide, Adriamycin, Cisplatin) therapy, as a result of which a partial response was obtained according to the criteria of the Jpn. Soc. Cancer. Ther. The response was disappearance of subjective symptoms and Virchow's metastasis and reduction of chief tumor and liver metastases. However, this therapy was accompanied by severe side effects such as leucopenia and thrombocytopenia, but in this case, these side effects improved within 20 days.
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PMID:[A case of gastric carcinoma remarkably responding to etoposide, adriamycin and cisplatin (EAP) therapy]. 317 44

Multiple cytotoxic drug administration is the generally accepted treatment of patients with a high-risk stage of choriocarcinoma. Based on this principle a 27-year old woman, classified as being in the high-risk group (Goldstein and Berkowitz score: 11), was treated with multiple cytotoxic drugs. The multiple drug schema consisted of: Etoposide 16.213, Methotrexate, Cyclophosphamide, Actomycin-D, and Cisplatin. On the first day of the schedule, moderate high doses of Methotrexate, Etoposide and Cyclophosphamide were administered. Within 8 hours after initiation of therapy the patient died with a clinical picture resembling massive pulmonary obstruction due to choriocarcinomic tissue plugs, probably originating from the uterus. Formation of these plugs was probably due to extensive tumor necrosis at the level of the walls of the major uterine veins, which resulted in an open exchange of tumor plugs to the vascular spaces; decrease in tumor tissue coherence secondary to chemotherapy may have further contributed to the formation of tumor emboli. In view of the close time association between the start of chemotherapy and the acute onset of massive embolism other explanations, such as spontaneous necrosis, must be considered less likely. Patients with large pelvic tumor loads are, according to existing classifications, at high risk to die and to develop drug resistance. Notwithstanding these facts our findings suggest that these patients might benefit from relatively mild initial treatment, especially true for patients not previously exposed to this drug. Close observation of the response status both clinically and with beta-hCG values may indicate whether and when more agressive combination chemotherapy should be started.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Death from chemotherapy in gestational trophoblastic disease. 319 36

Etoposide (VP-16-213) has been used in the treatment of many solid tumors and hematologic malignancies. When used in high doses and in conjunction with autologous bone marrow transplantation, this agent has activity against several treatment-resistant cancers including malignant glioma. In six of eight patients (75%) who we treated for recurrent or resistant glioma, sudden severe neurologic deterioration occurred. This developed a median of 9 days after initiation of high-dose etoposide therapy. Significant clinical manifestations have included confusion, papilledema, somnolence, exacerbation of motor deficits, and sharp increase in seizure activity. These abnormalities resolved rapidly after initiation of high-dose intravenous dexamethasone therapy. In all patients, computerized tomographic (CT) brain scans demonstrated stability in tumor size and peritumor edema when compared with pretransplant scans. This complication appears to represent a significant new toxicity of high-dose etoposide therapy for malignant glioma.
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PMID:Acute neurologic dysfunction after high-dose etoposide therapy for malignant glioma. 328 26

We examined the effects of various concentrations of etoposide (20-125 microM, 2-h incubation) on normal bone marrow and seven malignant cell lines: HL-60, K562, Namalva, MOLT-3, CEM-7, and the Hodgkin's cell lines L428KS and L428KSA. Tumor cell log-kill was dose dependent and greater than 4 for all cell lines but L428KSA (log-kill, 3.73). Median recovery of CFU-GM after purging with 75, 100, and 125 microM etoposide was 3.6%, 1.3%, and 1% of the controls, respectively. After one week of long-term marrow culture (LTMC), recovery increased 10-20 times/10(5) cells plated, reaching median values of 33.6%, 23.5%, and 20.7% of the controls in samples purged with 75, 100, and 125 microM etoposide, respectively. Flow cytometry for cell-cycle analysis and RNA content, and chromosomal studies of one-week-old LTMC from healthy donors detected no significant abnormalities in purged as compared to control cultures. After 3-4 weeks of LTMC, both control and etoposide-treated cells formed confluent monolayers. Using a panel of seven monoclonal antibodies (S3.13, S16.144, S4.7, S8.6, RIB-19, anti-HLA-DR, and VIL-A1), we investigated the expression of early and late differentiation antigens on LTMC after various culture times (0, 1, 2, 3, and 4 weeks). None of the early antigens S3.13, S16.144, and S8.6 was significantly reduced following etoposide treatment, either in nonadherent cells collected from the supernatant or in the adherent cell population obtained from trypsinized monolayers. Etoposide treatment dose dependently delayed the expression of RIB-19 (a late myeloid antigen) and, to a lesser extent, of S4.7 (an "intermediate" myelomonocytic marker). VIL-A1 expression was not affected by etoposide treatment. We conclude that etoposide purging of bone marrow in the 75-125 microM range spares a sufficient number of functionally intact stem cells to allow adequate in vivo reconstitution following autologous transplantation.
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PMID:Etoposide as an in vitro purging agent for the treatment of acute leukemias and lymphomas in conjunction with autologous bone marrow transplantation. 352 2


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