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PubMed1987

Teniposide in the treatment of non-small cell lung carcinoma.

Forty-two evaluable patients with advanced non-small cell lung cancer were treated with teniposide at doses ranging from 120 to 180 mg/m2 on Days 1, 3, and 5 every 3 weeks. Thirty-four patients had received no prior chemotherapy. Seven partial responses (16.6%) were obtained (21% in chemotherapy-unexposed patients). Marrow toxicity was the main side effect: life-threatening thrombocytopenia occurred in 9% of patients, and 54.5% experienced severe leukopenia. Teniposide, at the doses and schedule employed, has moderate activity in non-small cell lung cancer.

Adult↗
PubMed1987

Total-body irradiation and high-dose teniposide: a pilot study in bone marrow transplantation for patients with relapsed acute lymphoblastic leukemia.

Inadequate leukemic ablative therapy ending in leukemic relapse is the source of most failures following bone marrow transplantation. Attempting to improve pretransplant leukemic ablative therapy, we report on a pilot regimen that includes teniposide, the principal chemotherapy, and total-body irradiation. Ten patients with acute lymphoblastic leukemia in relapse underwent allogeneic bone marrow transplantation. All patients engrafted. Toxicity, primarily mucositis, was manageable. Two patients have survived for 1547 and 1988 days in continued remission. Eight patients have died: three from sepsis in the immediate posttransplant period, four with recurrent leukemia, and one with chronic graft-versus-host disease and pneumonia. We believe that these results support further trials with teniposide in pretransplant leukemic ablative therapies.

Adolescent↗
PubMed1985

A novel treatment of childhood lymphoblastic non-Hodgkin's lymphoma: early and intermittent use of teniposide plus cytarabine.

We treated 24 children and adolescents with stage III or IV lymphoblastic non-Hodgkin's lymphoma, using a protocol designed for patients with poor-prognosis acute lymphoblastic leukemia (ALL). Early therapy consisted of teniposide plus cytarabine administered before and immediately after prednisone, vincristine, and asparaginase. The two-drug combination was also given intermittently with continuous 6-mercaptopurine and methotrexate during the first year of continuation chemotherapy. Periodic intrathecal methotrexate and delayed cranial irradiation were used to prevent central nervous system involvement. Anthracycline compounds, alkylating agents, high-dose methotrexate, and involved-field irradiation were not used in any phase of treatment. Twenty-two (96%) of the 23 evaluable patients achieved complete remission. With a median follow-up of 2 1/2 years, only four patients have relapsed; the remainder have been disease-free for eight months to more than five years. The projected four-year continuous complete remission rate is 73% for all patients and 79% for the 19 with mediastinal involvement at diagnosis. These results demonstrate that use of teniposide plus cytarabine with an otherwise conventional plan of ALL therapy is an effective approach to the treatment of childhood lymphoblastic lymphoma.

Adolescent↗
PubMed1984

Phase II study of teniposide in small cell carcinoma of the lung.

Fifty-one patients with small cell bronchogenic carcinoma received 60 mg/m2 of teniposide iv on Days 1-5 every 3 weeks. All patients had received previous combination chemotherapy. Twenty patients with prior etoposide treatment and 20 without such prior treatment were evaluable. A partial response was observed in one of 20 and in five of 20 patients, respectively. The duration of responses was short (28-50 days). Sixty-one percent of patients experienced grade 3 or 4 toxicity on the World Health Organization scale. The activity in previously treated patients not exposed to etoposide was considerable, justifying further evaluation of teniposide in the treatment of small cell carcinoma of the lung.

Adult↗
PubMed1982

Comparison of the use of teniposide and vincristine in combination chemotherapy for non-Hodgkin's lymphoma.

A total of 164 patients with non-Hodgkin's lymphoma (NHL) were randomized to receive cycles of treatment every 3 weeks with either CTP, ie, cyclophosphamide (400 mg/m2/day orally X 5), teniposide (VM-26) (100 mg/m2 iv X 1), and prednisolone (60 mg/m2/day orally X 5), or COP, ie, vincristine (1.4 mg/m2 iv X 1; maximum, 2 mg) with the same cyclophosphamide and prednisolone doses listed above. Results were analyzed according to whether the patients' NHL histology was favorable (47 patients) or unfavorable (117). The great majority of patients in each group had advanced disease (stage IV in 70% and stage III in 20%). For each histologic group, the results with the two regimens were similar with respect to remission incidence and survival. In favorable-histology NHL, CTP produced 57% complete remissions (CR) and 29% partial remissions (PR), compared with 54% CR and 19% PR for COP. Survival in these patients was also similar for the two regimens, the relative death rates being 1.13 for CTP-treated patients and 0.88 for COP-treated patients (P = 0.75). In patients with unfavorable-histology NHL, CTP produced 38% CR and 28% PR, compared with 43% CR and 35% PR for COP, the relative death rates being 1.10 for CTP-treated patients and 0.90 for COP-treated patients (P = 0.49). Neurotoxicity was virtually absent in patients treated with CTP, whereas in COP-treated patients it was severe in 12% and moderate in 36%. Other toxic effects occurred with equivalent frequency in the two regimens. These results show that teniposide can replace vincristine in combination with cyclophosphamide and prednisolone in the treatment of NHL, with freedom from neurotoxicity and comparable survival and response rates.

Antineoplastic Agents↗
PubMedDate not supplied

Radiotherapy plus carboplatin and teniposide in patients with brain metastases from non small cell lung cancer.

BACKGROUND: The role of chemotherapy alone or added to radiation treatment for the palliation of multiple, unresectable brain metastases from non small cell lung cancer (NSCLC), is not yet well defined. Carboplatin and teniposide, however, are an interesting combination in this setting since they are active in NSCLC and because of encouraging results against brain metastases in other tumor types. METHODS: Twenty patients with brain metastases from NSCLC were treated with whole brain irradiation (total dose of 45 Gy) and chemotherapy (carboplatin, 300 mg/sm on day 1 and teniposide, 60 mg/sm on days 1, 2 and 3). RESULTS: Nine patients (45%) showed a complete remission of neurologic symptoms, and 7 (35%) an improvement. Neurologic signs disappeared in 8 patients (40%) and improved in 7 (35%). Three patients (15%) had partial (50%) regression of brain metastases at CT scan, and also showed response in other tumor sites. One other patient had a response of chest and liver lesions, while the cerebral metastases remained stable. Median survival was 7 months with a range of 1-9 months. Toxicity was mild, with no toxic deaths. CONCLUSIONS: Aggressive treatment can be taken into consideration also in the case of NSCLC patients with brain metastases and negative prognostic features. Their participation in clinical trials should be encouraged, since this will allow definition of the contribution of combined radiotherapy, chemotherapy and supportive care to the quality and duration of the patient's life.

Aged↗
PubMed1994

[Chemotherapy of small-cell lung cancer by a combination of teniposide, ifosfamide and carboplatin].

Thirty six SLC patients have been treated with a combination therapy of ifosfamide 2 g/m2, D1 and D2, carboplatin 300 mg/m2 D1 and teniposide 100 mg/m2 D1 to D3. All patients were younger than 70 years, 31 males, five females, ten limited diseases, 26 extended diseases (without brain metastasis) Performance status 0, 1 or 2, mean weight loss 3.7 kg. Thirty six patients were evaluable for response. We have noted three complete response and 28 partial response (objective response rate 86%). The main toxicity of this combination therapy was myelo-suppression (86% of grade 3 and 4). Twenty seven patients have relapsed, the median relapse free survival time is 310 days. The median survival of the 36 patients is 340 days, one patient is alive more than 30 months after the diagnosis. The ifosfamide-carboplatin-teniposide combination is an effective treatment in small cell lung cancer, its toxicity remains tolerable.

Adult↗
PubMed1993

[In vitro comparison of podophyllotoxin analogues; etoposide, teniposide and NK 611 using human lung cancer cell lines].

In an attempt to predict the antitumor activity of a new podophyllotoxin analogue, NK 611, in the treatment of lung cancer, we compared the drug with etoposide and teniposide using four human small cell lung cancer (SCLC) cell lines, SBC-2, -3, -4, -7, and two non-small cell lung cancer cell lines, ABC-1, EBC-1. In terms of the fifty percent tumor growth inhibitory concentration (IC 50) determined by MTT assay, teniposide was most potent among the drugs. The degree of cross-resistance of each drug was investigated using an etoposide-resistant SCLC subline (SBC-3/ETP), an adriamycin-resistant subline (SBC-3/ADM 100), and a cisplatin-resistant subline (SBC-3/CDDP). As for relative resistant (the ratio of IC 50 for resistant subline to that for the parent subline), NK 611 was least cross-resistant to etoposide, adriamycin, and cisplatin among drugs tested. These results indicate that NK 611 may play a role in a salvage chemotherapy for patients with resistant SCLC.

Adenocarcinoma↗
PubMedDate not supplied

Neo-adjuvant chemotherapy with carboplatin, 4-epiadriamycin and teniposide (CET) in locally advanced cancer of the cardia and the lower oesophagus: a phase II study.

Disappointing results after surgery alone for locally advanced adenocarcinoma of the cardia and the distal oesophagus (stage IIIB/IV) prompted us to combine surgery with neo-adjuvant chemotherapy. With a remission rate of about 70% the combination of etoposide, adriamycin and cisplatin (EAP) has been considered to be the superior treatment, but it has inherent severe toxicity. The authors conducted a phase II study of combined treatment with Carboplatin, 4-Epiadriamycin and Teniposide (CET) to ameliorate this toxicity and to evaluate the effectivity of this regimen in patients with these unresectable tumours. A regimen of 4 cycles of Carboplatin 300mg/m2, 4-Epiadriamycin 80mg/m2 and Teniposide 100mg/m2 was administered intravenously. Treatment cycles were repeated every 3 weeks in patients with initially unresectable adenocarcinoma of the gastro-oesophageal junction proven at laparotomy and/or CT scanning. Nineteen patients were studied and 17 underwent a second laparotomy in an attempt to resect the tumour radically. Eleven patients (65%) of the re-explored group achieved tumour reduction, enabling resection with curative intent. Recurrences, however occurred in 9 patients after a median of 9.5 (4-42) months. One patient died postoperatively as a result of pulmonary embolism. Only one patient remained free of disease after 42+ months. Leucopenia and thrombocytopenia of WHO grade 23 occurred in 58% and 37% of the patients, respectively. This regimen appears to be effective in patients with locally advanced adenocarcinoma of the cardia and the distal oesophagus. Although it can be used in an outpatient setting, the overall toxicity is relatively high and the results are comparable with other less toxic regimens.

Adult↗
PubMed1984

A phase II trial of teniposide (VM 26) in advanced non-Hodgkin's lymphoma, with emphasis on the treatment of elderly patients.

Fifty-four patients entered a phase II trial of teniposide (VM 26) in Stage III (35 patients) and stage IV (19 patients) non-Hodgkin's lymphoma (NHL) classified according to modified Rappaport system. The median age was 71 years (range, 19-85). Thirty-two patients were previously treated at least with combination chemotherapy and radiotherapy, whereas 22 were elderly (range, 70-85 years) untreated patients with a median Karnofsky score of 70. VM 26 was given by IV infusion at 100 mg/m2 weekly for at least 3 doses in "unfavorable" histologic subtypes, and for at least 6 to 9 doses in "favorable" subtypes, prior to the evaluation of response. The overall objective response rate was 43% in the 51 evaluable patients. The median duration of the 12 complete responses (CRs) was 7+ months (26+ to 2). According to the histology, VM 26 was very effective in the six patients with diffuse "histiocytic" (DH) subtype (four CRs, one partial response [PR]), and in the 8 patients with mycosis fungoides (MF) (two CRs, two PRs). Diffuse lymphocytic poorly differentiated and lymphoblastic NHL were less sensitive subtypes to VM 26. Among the 20 evaluable elderly patients a 50% objective response rate was obtained with five CRs. Four CRs and one PR were obtained in the five patients with DH subtype; no response was obtained in the only patient with MF. Toxicity, usually hematologic, was mild, even in elderly patients; neurotoxicity occurred in four instances. VM 26 seemed to be an effective and well-tolerated drug in advanced NHL; this drug should be further evaluated as first line chemotherapy in elderly (greater than or equal to 70 years) previously untreated patients with poor general conditions and DH histology.

Adult↗
PubMed1990

Teniposide (VM-26) and continuous infusion cytosine arabinoside for initial induction failure in childhood acute lymphoblastic leukemia. A Pediatric Oncology Group pilot study.

Twenty-six evaluable children with newly diagnosed acute lymphoblastic leukemia (ALL) who failed to achieve initial remission after receiving two to seven drugs for at least a 4-week period were given teniposide (VM-26) and continuous infusion cytosine arabinoside (Ara-C). Twenty-two received 150 mg/m2 of VM-26 on days 1 and 2 with 100 mg/2 of Ara-C as a continuous infusion on days 1 through 5; a second shortened course was given on day 14 to eight patients who had evidence of some antileukemic effect or were clinically judged able to tolerate a second course. The last four patients received three daily doses of VM-26 and a 7-day infusion of Ara-C at the same daily dosages. Twelve (48%) achieved complete remission (CR) of ALL. There was a trend toward decreasing response rates with an increasing number of drugs used in the initial induction regimen, i.e., five CR among seven patients with a prior two-drug induction attempt, six CR among 14 patients with a prior three- to four-drug induction attempt, and one CR among four patients with a prior five- to seven-drug induction attempt (P = 0.14). Ten of 17 non-T-cell patients and two of nine T-cell patients achieved remission (P = 0.10). The median time required to achieve a complete remission from the initiation of treatment was 26 days (range, 14-72 days). This period was shorter in those who required one course compared with those who required two induction courses, i.e., 25 days median vs. 44 days median. Toxicity was significant and due mainly to marrow aplasia and infection; one patient had severe prolonged VM-26-induced hypotension. Of the 12 patients entering remission, two were removed for marrow transplant and one was removed due to parental request. In the remaining nine patients, median remission duration was only 2 months (range, 1-18 months). All nine patients relapsed in the marrow. Among the entire group of 26 patients, only one patient is alive and a long-term event-free survivor (after allogeneic marrow transplant). Due to the current use of more aggressive initial induction regimens and the extremely poor prognosis in children who fail to achieve initial remission, more intensive regimens of continuation therapy or alternative therapies, such as bone marrow transplant, should be considered.

Adolescent↗
PubMed1992

Potentiation by novobiocin of the cytotoxic activity of etoposide (VP-16) and teniposide (VM-26).

The coumermycin antibiotic novobiocin, which interacts with the nuclear enzyme topoisomerase II, produced supra-additive toxicity to WEHI-3B D+ leukemia cells at clinically achievable concentrations, when combined with teniposide (VM-26) or etoposide (VP-16). Simultaneous exposure of cells to both agents was required for maximum efficacy of the combination. Novobiocin also produced supra-additive toxicity to A549 human lung carcinoma cells when combined with VM-26 or VP-16. At concentrations above the peak plasma levels achievable in patients, novobiocin lost its potentiating activity. Exposure of WEHI-3B D+ cells to novobiocin did not modify the cytotoxicity produced by the topoisomerase II inhibitor m-AMSA, whereas, in contrast, novobiocin antagonized the cytotoxicity of m-AMSA in A549 cells. Although it has been suggested that inhibitors of the syntheses of DNA and RNA interfere with the cytotoxic activity of the epipodophyllotoxins, maximum potentiation of the cytotoxicities of VP-16 and VM-26 occurred at novobiocin concentrations that decreased the rates of synthesis of both DNA and RNA in WEHI-3B D+ cells by about 50%. The number of DNA-topoisomerase-II covalent complexes stabilized by VM-26 in WEHI-3B D+ cells was greatly increased when cells were exposed simultaneously to VM-26 and novobiocin for 1 hr, but not when cells were treated with m-AMSA and novobiocin for the same period of time. Novobiocin did not affect the amount of covalent complexes produced by VM-26 in isolated nuclei, suggesting that the potentiating activity of novobiocin was not due to its direct interaction with the nuclear topoisomerase II enzyme. Our findings suggest that therapeutic levels of novobiocin may be capable of enhancing the clinical activities of VP-16 and VM-26.

Adenocarcinoma↗
PubMed1989

A pharmacokinetic model for intraperitoneal administration of drugs: application to teniposide in humans.

A pharmacokinetic study of teniposide after ip administration with a 4-h dwell time was performed in patients suffering from abdominal malignant ascites. A three-compartment open model was developed to fit together the data obtained in plasma and peritoneum. The pharmacokinetic parameters obtained by the model agreed with those obtained by model-independent analysis, and the fitting correctly depicted the plasma and peritoneal concentration decays. According to the results, such a model could be applied to ip administration of anticancerous drugs.

Adolescent↗
PubMed1988

Treatment of refractory lymphoma with methotrexate, VM-26 (teniposide), procarbazine, and dexamethasone: Cancer and Leukemia Group B study 7902.

Seventy-eight individuals previously treated with chemotherapy for non-Hodgkin's lymphoma were enrolled in a phase II pilot study employing methotrexate 100 mg/M2 iv (day 1), calcium leucovorin 10 mg/M2 iv and/or po q6h (days 2-4), VM-26 (teniposide) 100 mg/M2 iv (days 2 and 9), procarbazine 100 mg/M2 po (days 2-15), and dexamethasone 15 mg/M2po (days 2-8) (MV26PD). Thirty percent of the 78 patients treated had a response to therapy (8% complete, 22% partial). Twenty-four percent of patients with diffuse histiocytic (large cell) lymphoma had a response (12% complete, 12% partial). The estimated failure-free survival was 41% at 3 months and the median survival (death from any cause) was 4.5 months for the entire cohort. Two individuals, including one individual with diffuse histiocytic lymphoma, remain in a complete response for over 900 days. Significant hematologic toxicity and infectious complications were seen in this heavily pretreated group of patients. MV26PD represents an active combination of agents for the treatment of non-Hodgkin's lymphoma. The optimal dosing for MV26PD remains to be determined.

Adult↗
PubMed1992

Acute nonlymphoblastic leukemia in children treated for acute lymphoblastic leukemia with an intensive regimen including teniposide.

Some cases of conversion from acute lymphoblastic leukemia (ALL) to acute nonlymphoblastic leukemia (ANLL) at relapse have been reported recently. We report three cases initially diagnosed as having ALL and showing morphological, cytochemical, and immunophenotypic features of ANLL at relapse (lineage switch). Conversion was observed among 14 patients who developed bone marrow relapse while undergoing intensive treatment with our ALL protocol, which includes teniposide, and that had been administered to 62 patients. The three cases converted at first relapse, with a mean time of 20 months (13-29 months). Clinical and immunologic characteristics of T-cell leukemia were present in one patient. Changes documented in cytogenetic studies are discussed. The underlying mechanisms for the lineage switch remain unclear as does its relation with mixed lineage leukemias, but we believe that drugs employed in our therapy protocol could have had an influence on this conversion.

Child, Preschool↗
PubMed1982

Combination chemotherapy of the epipodophyllotoxin derivatives, teniposide and etoposide. A pharmacodynamic rationale?

Previous studies in vitro on the influence of extracellular protein binding of Teniposide (VM26) and Etoposide (VP16-213) on subsequent cellular uptake by experimental murine tumor cells [Cancer Res 38:2549 (1978); Drug Metab Rev 8:119 (1978)] suggested that a timed-sequential combination of VM26 and VP16-213 may increase the bioavailability of VP16-213. This was studied clinically in six cancer patients with ascites (five ovarian, one rectal) whereby VM26 (20 mg/m2) was given i.p. 2 h prior to VP16-213 (100 mg/m2; i.p.) In some patients, this regimen was administered i.v. The i.v. regimen was found to be more toxic (myelosuppression, nausea, vomiting) than i.p. regimen at same doses of drugs. Several patients remained stable to disease during 1-2 courses of therapy (3 weeks per course), one patient had partial remission, and has been stable in her disease for more than 4 months. In two patients, plasma and ascites fluid was analyzed for VP16-213 and VM26 by a new reverse-phase high performance liquid chromatography method. Both VM26 and VP16-213 could be eluted isocratically (28% v/v acetonitrile in water) from a c18 column with retention times of 6.6 and 13.3 min, respectively. Subsequent pharmacokinetic analysis of one patient suggests that protein binding displacement of VP16-213 in plasma and perhaps ascites fluid increased the pharmacokinetic volume of distribution (28 l) and reduced the elimination half-life (12 h). The data suggests that VP16-213 is distributed more widely in the body and is represented by a single compartment pharmacokinetic model. Analysis of VM26 in ascites and plasma suggests that the so-called "deep pharmacokinetic compartment" represents ascites equivalent space and that the plasma concentration represents VM26 as free and protein-bound drug in kinetic distinguishable compartments. Determinants of drug action are potentially composed of a multiplicity of physiological, biochemical, and other factors. The potential for manipulating the pharmacodynamic properties of drugs to achieve greater therapeutic potential needs further study.

Adult↗
PubMed1987

Expressions of resistance and cross-resistance in teniposide-resistant L1210 cells.

Resistance to teniposide (VM-26) by VM-26 selected resistant L1210 cells in culture was attributed to alterations in the flux of VM-26 across the plasma membrane and to functions of homogeneously staining regions that appeared on one or more chromosomes. In the present study, electrophoresis of membrane-cytosol fractions of these resistant sublines demonstrated a protein band, Mr 22 kd, that was not evident in similar fractions of drug-sensitive L1210 cells or three revertant sublines. The distribution of this protein among various cellular fractions could be altered by manipulation of the concentration of calcium ions. A representative subline, LIa5 microM, was observed to have vesicles that reacted with Sudan black B stain, an indication of altered lipid metabolism. The LIa5 microM subline was cross-resistant to etoposide, vincristine, doxorubicin, amsacrine, and actinomycin D. Concentrations of VM-26 that inhibited cell division to the same extent caused an accumulation of fewer cells in the G2 stage of cell division in LIa5 microM cultures than in L1210 cultures. These observations indicate that the LIa5 microM subline expressed multiple drug resistance, as well as changes in the expression of cytotoxicity to VM-26.

Animals↗
PubMed1989

Effective reinduction therapy for childhood acute nonlymphoid leukemia using simultaneous continuous infusions of teniposide and amsacrine.

The combination of teniposide (VM-26) and amsacrine (AMSA) was evaluated in a dose-finding and efficacy study in 58 patients with relapsed or refractory acute leukemia. Both agents were given as simultaneous continuous infusions for 72 h through separate i.v. lines. All patients were evaluable for toxicity and 57 were evaluable for response; only 2 of 20 with acute lymphoblastic leukemia (ALL), acute mixed-lineage leukemia, or chronic myelogenous leukemia in blast crisis achieved a complete remission (CR). More encouraging was a second-remission rate of 43% (13 complete and 3 partial) in the 37 patients with acute nonlymphoid leukemia (ANLL). Responses occurred only in patients who received VM-26 doses of greater than or equal to 200 mg/m2 per day and AMSA doses of greater than or equal to 100 mg/m2 per day. Thus, the CR rate for relapsed ANLL patients who received the higher doses of both agents was 40% (13 of 33). All responders had previously received epipodophyllotoxin therapy and 40% had also received AMSA. All but one patient had severe leukopenia (less than 2.0 x 10(9) leukocytes/l) and thrombocytopenia (less than 50.0 x 10(9) platelets/l) as a results of therapy. Severe mucositis (grade 3 or 4) was the dose-limiting toxicity. Our results indicate that VM-26 plus AMSA, given by continuous infusion, is effective in the treatment of ANLL. Further phase II studies should consider using VM-26 at 200 mg/m2 per day and AMSA at 100 mg/m2 per day, but the best administration schedule remains unclear.

Adolescent↗