Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two adenocarcinoma cell lines were established from metastatic lymph node of lung cancer patients. The cell lines were named NUTLC-1 and NUTLC-3. They were found to have the following biological characterization and sensitivity to anticancer agents by comparison with clinical effect of the drugs on each donor patient: 1) By chromosomal analysis, the tumor cells of two cell lines were human-origin cells. Number of chromosomes of these cell lines ranged from 67 to 77 in NUTLC-1 cells and from 61 to 66 in NUTLC-3 cells, with the modal numbers of 73 and 64, respectively. 2) The tumor cells of the two cell lines were heterotransplanted subcutaneously into nude mice, but, no natural distant metastasis was observed 2 months after transplantation. 3) Sensitivity to anticancer agents on NUTLC-1 and NUTLC-3 cells differed individually according to methylthiazol tetrazorium (bromide) (MTT) colorimetric assay. NUTLC-1 cells were sensitive to Mitomycin C (MMC) and Adriamycin (ADM), and insensitive to Cisplatinum (CDDP), 5-Fluorouracil (5-FU) and Etoposide (VP-16). Antitumor effect of CDDP and 5-FU on recurrent tumor of donor patient was not observed clinically. NUTLC-3 cells were sensitive to CDDP, MMC and ADM, and insensitive to 5-FU and VP-16. Sensitivity to CDDP and MMC on NUTLC-3 cells also correlated to clinical effect of the drugs on the donor patient. From these results, it appears that these new cell lines are useful materials for studies on lung cancer.
 ...
PMID:Characteristics of the two newly established cell lines of human pulmonary adenocarcinoma and their sensitivity to anticancer agents. 802 20

Etoposide is a schedule-dependent cytotoxic drug with high single agent activity in small-cell lung cancer and lymphoma. Despite its clear dose-dependent myelosuppressive activity, dose-dependent evidence of its anti-tumour activity is harder to demonstrate. A number of reports have correlated haematological toxicity with pharmacokinetic and physiological parameters, which explains some of the variability in dynamic effects that exists between patients. Recent reports have also suggested that anti-tumour response may be related to plasma etoposide concentration. In our own studies we have investigated factors that influence the pharmacodynamic effects of etoposide, principally with regard to haematological toxicity, and these studies have highlighted a number of patient groups who are at risk. Impaired renal function causes a reduction in clearance of etoposide, resulting in increased systemic exposure and more profound myelotoxicity. A 30% dose reduction in this group is recommended to normalise the area under the plasma concentration-time curve (AUC). Patients with low serum albumin concentrations (< 35 g/l) also showed significantly worse haematological toxicity, but with no apparent change in total drug pharmacokinetics. There was, however, an increase in the free drug fraction in this group due to decreased protein binding, such that the free drug AUC was similar to that found in patients with renal dysfunction. This would also indicate that a dose reduction of around 30%-40% is required in this patient group. Patients with normal albumin levels but liver enzyme values (aspartate transaminase or gamma-glutamyl transpeptidase) more than 3 times the upper limit of normal also had a less marked but significant increase in neutropenia. In patients with normal organ function, age was the only significant factor in predicting the degree of leukopenia/neutropenia, and increasing age was also associated with decreasing drug clearance and an increase in drug AUC. A small dose reduction and/or careful monitoring is required in this patient group. Further studies are required to elucidate further the relationship between the pharmacokinetics of etoposide and its pharmacodynamics, particularly with regard to anti-tumor activity, and to determine the role of individualised therapy, based on a pharmacokinetic parameter, in reducing the dynamic variability and optimising the use of this drug.
 ...
PMID:Etoposide dosage and pharmacodynamics. 807 31

A 24-year-old man presented with right scrotal swelling and was diagnosed as having a testicular cancer. A high inguinal orchiectomy was carried out. Histological examination revealed immature teratoma and yolk sac tumor of the testis. Eight months later, 2 separate metastatic lesions appeared in the lungs, both of which were removed by operation after a course of combination chemotherapy with Etoposide and Cisplatin. The histology showed one to be composed of immature teratoma, and the another of yolk sac tumor.
 ...
PMID:[A case of immature teratoma and yolk sac tumor of the testis associated with pulmonary metastases of 2 distinct histological types]. 812 Nov 20

We have experienced eight patients with advanced bronchogenic carcinomas who underwent resectional surgery after receiving preoperative adjuvant chemotherapy and radiotherapy during the period March, 1990, to February, 1992. Four patients were in stage IIIA and four in stage IIIB, of which six had epidermoid carcinomas and two small cell carcinomas. All patients were male with ages ranging from 48 to 73 (mean 56.7) years. The induction chemotherapy for six patients consisted of cisplatin and VP-16 (Etoposide) only, and two patients were given fluorouracil/cyclophosphamide and cyclophosphamide/adriamycin/cisplatin in addition to cisplatin/VP-16, respectively. All patients also received four to six weeks of radiotherapy following chemotherapy and were re-evaluated for the possibility of surgery after four weeks of observation. All patients underwent pneumonectomies. Postoperative histological staging revealed complete responses in two patients, partial responses in three and no response in three. Patients were followed-up for seven to 33 (mean 21.5) months after the diagnosis of lung cancer. Six patients died 1, 2, 3, 10, 14 and 26 months postoperatively and two patients are alive, revealing no evidence of tumor recurrence 24 months postoperatively. Induction therapy may induce a better resectability by the conversion of the lung cancer to a lower clinical stage by the time of surgery.
 ...
PMID:Surgical treatment of stage III lung cancer after chemotherapy and radiotherapy. 815 56

A peritoneal dialysis patient was reported who had ultrafiltration loss due to a marked increase in lymphatic absorption and peritoneal membrane permeability. A 33-year-old male was transferred from hemodialysis to peritoneal dialysis because of acute subdural hematoma. His complicated history included left testicular tumor with retroperitoneal lymph node metastasis in 1982. He was treated with CDDP, Etoposide, Bleomycin, Vinblastine sulfate and Vincristine and received operation of retroperitoneal lymph node dissection in 1982. He had been on hemodialysis since 1983 due to cisplatinum nephropaty. Ultrafiltration failure was found immediately following the insertion of Tenckhoff catheter without malfunction of peritoneal catheter. Peritoneal equilibrate test and lymphatic absorption measurement showed a high permeability peritoneum with a marked increase in lymphatic absorption rate (3.7 ml/min). These two factors were thought to result in ultrafiltration loss. CAPD with 4-6 times exchange daily did not maintain ultrafiltration, because it gave approximately 2000 ml negative water balance every day. He was well maintained on a short time exchange intermittent peritoneal dialysis (IPD) with cycler using 18 L for 8 hours. We concluded that increased lymphatic absorption is one of the important factors for ultrafiltration fafilure and IPD with frequent exchange by cycler is suitable for the patient with ultrafiltration loss.
 ...
PMID:[Ultrafiltration failure in a peritoneal dialysis patient due to a marked increase in lymphatic absorption a case report]. 818 65

Etoposide is an important anti-neoplastic drug, but the best dose and schedule for its administration remain unknown. The schedule-dependency of etoposide for small cell lung cancer (SCLC) is now proven and it is probably true for other sensitive neoplasms as well (e.g., lymphoma and germ cell tumors). Recent data suggest that an extended schedule of administration (i.e., 14 to 21 days) may be more effective than the standard 3- to 5-day schedule. Several phase II studies with etoposide have demonstrated its activity against several neoplasms. Some have assessed the relationship of etoposide plasma levels to dose, schedule, and tumor responsiveness. Preliminary data suggest that high peak plasma levels (i.e., > 5 to 10 micrograms/ml) are associated with more severe myelosuppression than lower peak plasma levels (i.e., 1 to 3 micrograms/ml). Response and survival rates in previously untreated SCLC patients given low daily doses of etoposide for 14 to 21 days are at least comparable with results achieved with standard etoposide doses given for 3 to 5 days, and the extended etoposide schedule is less toxic than the 3- to 5-day schedule. Preliminary data from several studies suggest that administering low, daily etoposide doses over a prolonged schedule is a superior method of administration. Other studies, including randomized comparisons, are necessary to confirm these observations.
 ...
PMID:Chronic etoposide administration: overview of clinical experience. 822 15

We investigated the antitumor effect of oral administration of etoposide and arabinofuranosylcytosine-5'-stearylphosphate (C18PCA) against P388 ascites tumors in B6D2F1 mice. Etoposide (25 mg/kg) and C18PCA (5 mg/kg) were given orally on days 1-5 after tumor inoculation. The median life span of the mice treated with etoposide or C18PCA alone was 19.5 and 18 days, respectively. The combination of both drugs significantly extended the median life span to 33 days. To clarify this enhancement of the increase in median life span, we examined intracellular deoxyribonucleoside triphosphate (dNTP) pools, cell-cycle distribution, DNA fragmentation, and the time course of the plasma drug concentration. Etoposide had no effect on intracellular dNTP pools in this experimental system, whereas treatment of cells with C18PCA or with the combination of both drugs resulted in a significant increase in dTTP pools to values ranging from 1.8- to 2.0-fold higher than the control levels. There was a significant increase in cells in the S + G2/M phase when cells had been treated with both etoposide and C18PCA. Agarose-gel electrophoresis of the extracted DNA revealed that C18PCA enhanced the fragmentation of DNA, with a length of about 180 bp being induced by etoposide. The plasma peak levels of etoposide (1000 nM) and ara-C (50 nM) were observed at 20 and 30 min after the simultaneous administration of both drugs, respectively. The plasma etoposide level gradually decreased to 10% of the peak level at 240 min after administration. On the other hand, the plasma concentration of ara-C was maintained at above 20 nM at 240 min. These observations suggest that C18PCA and etoposide act on P388 murine leukemic cells by accumulating cells in the S + G2/M phase. Even if the plasma concentration of ara-C is low, the repair of DNA damage by etoposide may be hindered in the presence of ara-C following an increase in DNA fragmentation.
 ...
PMID:Combined oral administration of etoposide and arabinofuranosylcytosine-5'-stearylphosphate enhances the antitumor effect against P388 ascites tumors. 828 19

Autopsy tissues were collected from ten patients who had received etoposide, 150-3480 mg, from 1 to 412 days antemortem and from five patients who had received teniposide, 234-1577 mg, from 3 to 52 days antemortem. Tissues were assayed for etoposide and teniposide using high-pressure liquid chromatography with electrochemical detection. Etoposide was detectable in tissues of three of four patients dying < 5 days after their last etoposide treatments to cumulative doses of 150-432 (median, 280) mg but was detectable in tissues of only one of six patients dying 7-412 (median, 37) days after their last etoposide treatment to a cumulative dose of 607-3600 (median, 1553) mg. The highest tissue concentrations were in the small bowel, prostate, thyroid, bladder, spleen, and testicle. Intermediate concentrations were found in the lymph node, skeletal muscle, adrenal gland, stomach, tumor, liver, lung, pancreas, and kidney, and the lowest concentrations were found in the heart, brain, diaphragm, vagina, and esophagus. Teniposide was detectable in one patient dying 3 days after a cumulative teniposide dose of 576 mg (spleen, prostate, heart > large bowel, liver, pancreas > thyroid, adrenal, stomach, small bowel, bladder, testicle, and skeletal muscle) but was not detectable in any tissue from four patients dying 5-52 (median, 8) days after their last treatment to a cumulative teniposide dose of 234-1577 (median, 520) mg. The very short tissue half-life contrasts with our previous observations for human autopsy tissue concentrations of mitoxantrone, doxorubicin, menogaril metabolites, diaziquone, and amsacrine. The short tissue half-life may help explain the schedule dependency of epipodophyllotoxin efficacy and may also help explain the lack of visceral toxicity of these compounds.
 ...
PMID:Human autopsy tissue distribution of the epipodophyllotoxins etoposide and teniposide. 833 87

For metastatic lung region, a 82-year-old woman with malignant fibrous histiocytoma was successfully treated with combination chemotherapy of Carboplatin and Etoposide. First, the tumor appeared on her right thigh, and we operated on August 1991. However, at the same time, a metastatic lung region was also noticed. Over a year, it worsened. We gave her 350 mg Carboplatin once a week and 100 mg Etoposide 3 times a week. After 3 weeks' treatment, we stopped treatment because of sudden granulocytopenia and thrombocytopenia. But to our surprise, the metastatic lung region almost disappeared 2 months after therapy. Considering the difficulty of medical treatment for malignant fibrous histiocytoma, this case suggests that combination chemotherapy of Carboplatin and Etoposide is valuable. However, due care must be taken for side effects such as granulocytopenia and thrombocytopenia.
 ...
PMID:[A combination chemotherapy of carboplatin and etoposide for malignant fibrous histiocytoma with marked effect on the metastatic lung region]. 839 28

12 patients: (7 males and 5 females) with recurrent brainstem gliomas were treated with the oral topoisomerase inhibitor VP-16 (Etoposide). Patients ranged in age from 3 to 49 years with a median age of 7 years. All patients had been previously treated with radiation therapy (conventional fractionation: 4; hyperfractionation: 8) and 5 had received prior nitrosourea-based chemotherapy at time of tumor recurrence. Tumor recurrence was documented by radiographic tumor enlargement utilizing brain MRI with gadolinium enhancement (12) and clinical neurologic deterioration (9). Two patients underwent biopsy pathologically documenting tumor recurrence. Each cycle of therapy consisted of 21 days of VP-16 (50 mg/m2/day) followed by a 14 day rest followed by an additional 21 days of VP-16 (50 mg/m2 day). Complete blood counts were followed bi-weekly and a neurologic examination and brain MRI scan with contrast were performed prior to initiation of each cycle of therapy. Treatment related complications included: partial alopecia (5); diarrhea (5); weight loss (4); neutropenia (2); and thrombocytopenia (4). No patient required transfusion or antibiotic treatment of neutropenic fever. There were no treatment related deaths. 12 patients were evaluable of whom 6 demonstrated a radiographic response (1 complete; 3 partial; 2 stable disease) with a median duration of response of 8 months. In summary; oral VP-16 is a well tolerated and relatively non-toxic chemotherapeutic agent with apparent activity in this small cohort of patients with recurrent brainstem gliomas.
 ...
PMID:Recurrent brainstem gliomas treated with oral VP-16. 850 18


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>