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 podophyllotoxin derivative VP 16-213 was used as monotherapy in 6 patients and combined with 5-fluorouracil in another 6. Of the 12 patients treated, 11 had measurable tumor criteria and 5 of these responded to treatment. These responses were attributed mainly to the effects of VP 16-213. Patients responding to chemotherapy lived significantly longer than non-responders. Each case of objective tumor response was accompanied by subjective improvement. In view of these results, a more active approach to the treatment of hepatocellular carcinoma would seem to be justified.
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PMID:[Therapeutic results using VP 16-213 alone or in combination with 5-fluorouracil in liver cancer (hepatoma)]. 20 20

cis-Dichlorodiammineplatinum(II) (cis-platinum) has no more than additive, and often much less than additive, lethal toxicity for mice when given in combination with other anticancer agents representing several of the major functional classes of clinically useful anticancer drugs. The previously reported broad spectrum of anticancer activity of cis-platinum against tumors in laboratory animals has now been extended to promisingly useful therapeutic synergism in combination with other active anticancer drugs, including advanced-staged tumors in mice; eg, cis-platinum plus cyclophosphamide against advanced Ridgway osteogenic sarcoma and advanced P388 leukemia, and as surgical adjuvant chemotherapy against advanced colon tumor 26; cis-platinum plus Adriamycin against advanced P388; and cis-platinum plus VP-16-213 against advanced P388. Therapeutic synergism was also seen with cis-platinum plus carminomycin (an Adriamycin analog) against early colon tumor 26. Resistance and cross-resistance studies using sublines of L1210 and P388 selected for resistance to various alkylating agents (cyclophosphamide, melphalan, BCNU, or cis-platinum) indicate a variety of resistance and cross-resistance patterns which further support the growing body of evidence that wide differences in mechanism of cytotoxic activity exist among alkylating agents having experimentally and clinically useful anticancer activity. These data support the observed therapeutic synergisms with combinations of alkylating agents seen against a broad spectrum of murine tumors, and they suggest other drug combinations that might be considered for experimental and clinical trial based on a growing number of logical differences in biochemical mechanism of action of alkylating agent anticancer drugs that have been reported.
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PMID:cis-Dichlorodiammineplatinum(II): combination chemotherapy and cross-resistance studies with tumors of mice. 29 80

In an attempt to improve upon the 42% regression rate of the CAP-I regimen in patients with advanced adenocarcinoma of the lung, VP-16 was added to that regimen. VP-16, as a single agent, had a response rate of 12.5% (3/24) In a similar group of patients. The new regimen, V:CAP-I, had a tumor regression rate of 35% (7/20) and an estimated median survival of 171 days. Hence, we were unable to conclude that the addition of VP-16 to the CAP-I regimen statistically improved the regression rate of the CAP-I regimen.
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PMID:VP-16, cyclophosphamide, adriamycin and cis-platinum (V:CAP-I) in patients with metastatic adenocarcinoma of the lung. 44 15

Comparison of a water-soluble (27-487) with a water-insoluble (VP-16-213) podophyllotoxin derivative in seven murine neoplasms revealed slight therapeutic superiortiy of VP-16-213 but also slightly greater toxicity when compared with 27-487. A strikingly good response of the Taper liver tumor to both compounds was observed, providing further incentive to the use of podophyllotoxin derivatives in human hepatomas.
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PMID:Comparison of a water-soluble and a water-insoluble podophyllotoxin derivative in murine neoplasms. 52 64

The teratogenic effects of three new plant-derived antitumor agents, maytansine, VP-16-213 and VM-26, were compared to the effects of vincristine and colchicine in pregnant Swiss albino mice that received a single ip injection of drug on day 6, 7 or 8 of gestation. Cytogenetic studies were also performed using maternal bone marrow and embryos obtained 48 hours after injection of maytansine, vincristine, VP-16-213, VM-26 and colchicine on day 6, 7 or 8 of gestation. A close correlation between teratogenic and cytogenetic effects was not noted among the compounds tested. Vincristine had greater embryotoxic and teratogenic activity than maytansine at equimolar doses (0.36 mu moles/kg), with the peak effects appearing after injection on day 7 of gestation. Colchicine, VP-16-213 and VM-26 were comparatively less potent than maytansine and vincristine, since doses of 2.5 mu moles/kg (colchicine and VP-16-213) and 1.5 mu moles/kg (VM-26) were required to elicit embryotoxic effects. At their teratogenic doses, all compounds induced various cranial abnormalities including exencephaly, hydrocephalus, anophthalmia and microtia, as well as major skeletal malformations. The teratogenic dose of vincristine is comparable to its effective antitumor dose in transplantable rodent tumor systems; in contrast, the teratogenic dose of maytansine in approximately 10-fold higher than its antitumor dose. Of the compounds studied, VP-16-213 and VM-26 exerted the most consistent cytogenetic effects in embryonic tissue. Alarge proportion of the structural chromosome aberrations induced in embryonic cells by VM-26 were stable and are most likely capable of surviving at least one cell division.
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PMID:Teratogenic and cytogenetic effects of some plant-derived antitumor agents (vincristine, colchicine, maytansine, VP-16-213 and VM-26) in mice. 69 77

A mammary adenocarcinoma (16/C) was isolated and maintained in serial passage by transplantation of metastatic lung foci. This tumor originated as a spontaneous mammary adenocarcinoma in a C3H/He female mouse. It was selected as a model from greater than 50 mammary tumors studied because it was highly metastatic and because it responded to most of the agents reported to be active against breast cancer in women. Sc implanted 16/C tumors (in the 300--1000-mg range) metastasized to the lungs in greater than 75% of the mice and to the axillary lymph nodes in greater than 30%. This tumor has been tested for sensitivity to greater than 40 clinically used agents. Adriamycin was the most active single agent. Other active agents included cyclophosphamide, 5-fluorouracil, vincristine, melphalan, dibromodulcitol, maytansine, neocarzinostatin, palmO-ara-C, vinblastine, and VP-16-213. Agents most active against 40--1000-mg tumours were also most active against micrometastatic disease (eg, adriamycin). The converse was also true; agents inactive or marginally active against 40--1000-mg tumors were at best marginally active against micrometastatic disease (eg, BCNU). Tumors greater than 20 mg were not curable by chemotherapy alone, although adriamycin treatment caused complete regressions of 100--400-mg tumors in greater than 80% of the mice. Surgical removal of 300--1000-mg tumors plus therapy with adriamycin resulted in 40%--72% cures as compared to 0--26% cures with surgery only. Data resulting from treatment with other agents, singly and in combination, are presented.
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PMID:Biology and therapeutic response of a mouse mammary adenocarcinoma (16/C) and its potential as a model for surgical adjuvant chemotherapy. 70 50

Forty-two patients with advanced malignant lymphomas, all of whom had failed at least one prior course of chemotherapy, were treated with one of two new combination chemotherapy regimens to determine patient tolerability. Twenty-seven patients received regimen 1, after which this study was discontinued, and subsequently 15 additional patients were treated with regimen 2. Regimen 1 (BAP) consisted of BCNU and adriamycin administered iv on Day 1 and prednisone administered orally on Days 1--5 with cycles repeated at 21-day intervals. Regimen 2 (VAP) consisted of VP-16-213 given iv on Days 1 and 2, adriamycin given iv on Day 3, and prednisone given on Days 3--7 in a schedule designed to produce cell cycle synchronization; cycles were repeated at 21--28-day intervals. Both regimens were, in general, well tolerated. Reversible bone marrow depression was the major toxic reaction observed. Nine of 27 patients treated with regimen 1 and five of 15 patients treated with regimen 2 experienced objective tumor regressions. Tolerable dosage levels of both regimens have been defined for future clincial trials.
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PMID:Pilot study of two adriamycin-based regimens in patients with advanced malignant lymphomas. 86 63

Thirty patients with bronchogenic carcinoma underwent an 8 week course of induction therapy consisting of cyclophosphamide, methotrexate, vincristine, and VP 16-213 (NSC 141 540). Those who achieved objective remission or tumor stabilization were then placed on an intermittent treatment schedule with the same drugs. Of the 30 patients, 17 had an objective response, 5 were unchanged and 8 progressed. Responses were more frequent in anaplastic carcinoma (13/19) than epidermoid or adenocarcinoma (4/11). The toxicity mainly consisted of leukopenia, thrombopenia, alopecia, nausea and vomiting. The implications of these findings in the planning of further chemotherapeutic programs are discussed.
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PMID:[VP 16-213 in combination with endoxan, methotrexate and oncovin as polychemotherapy for bronchogenic carcinoma]. 87 37

Thirty patients with bronchogenic carcinoma were treated with an 8-week induction therapy consisting of cyclophosphamide, methotrexate, vincristine and VP 16-213 (NSC 141 540). Those who achieved objective remission of tumor stabilization were then placed on an intermittent treatment schedule with the same drugs. Of the 30 patients, 17 had an objective response, 5 remained without change, and 8 progressed. Responses were more frequent among anaplastic (13/19) than epidermoid or adenocarcinoma (4/11). The toxicity consisted mainly of leucopenia, thrombopenia, alopecia, nausea and vomiting. The implications of these findings in the planning of further chemotherapeutic programs are discussed.
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PMID:A combination of cyclophosphamide, methotrexate, vincristine and VP 16-213 (NSC 141 540) in the treatment of bronchogenic carcinoma. 89 87

Described are primary treatment protocols for 1) those patients with gorssly unresectable stage III or IV ovarian carcinoma, considered reasonable candidates for therapeutic trials aimed at the identification of antitumor activity as determined by the regression of objectively evaluable lesions; and 2) those patients with stage II or III ovarian carcinoma, with little or no visible tumor remaining after surgery, considered reasonable candidates for therapeutic trials involving regimens that may delay or prevent the recurrence of clinically apparent disease. Both protocol involve initially a comparison of cyclophosphamide alone with cyclophosphamide plus adriamycin. A third protocol--an activity-seeking study of two new cytotoxic agents, developed to provide secondary treatment opportunities for patients who have failed on one of the primary chemotherapy protocols--is designed to seek evidence of any cross-resistance between cytembena (beta-4-methoxybenzoyl beta-cis-bromacrylate) and VP-16 (4'-demethyl-epipodophyllotoxin-beta-D-ethylidene glucoside). Data from all three protocols are so far insufficient to allow meaningful analysis of their results.
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PMID:Status report of Mayo Clinic studies. 124 94


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