Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1140680 (ovarian cancer)
 28,141 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum is known to be required for invasion or phagokinesis of certain tumor cells, although the mechanism of its action is not well understood yet. In the in vitro invasion assay system we have developed, MM1 cells exhibiting extensive invasiveness against cultured mesothelial cell monolayers in the presence of 10% fetal calf serum did not invade them without serum. Human small cell lung cancer (OC10) cells also required serum in invasion. Serum could be completely substituted by oleoyl-lysophosphatidic acid (LPA) or bacterial phospholipase D (PLD). Phosphatidic acid also had an invasion-inducing activity, though to a lesser degree. Since human ovarian cancer (RMUG-S) cells require neither serum, LPA nor the PLD for invasion of mesothelial cell monolayers, the production of phospholipid like LPA, a candidate for intracellular second messenger, in tumor cells seems critical for the invasion by MM1 cells or OC10 cells. This result suggests a possible participation of particular signaling cascade, PLD-LPA(PA) system, in the invasion of certain tumor cells.
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PMID:Induction of in vitro tumor cell invasion of cellular monolayers by lysophosphatidic acid or phospholipase D. 839 Feb 42

One hundred four consecutive patients with newly diagnosed small cell lung cancer, metastatic breast cancer, and ovarian cancer in good physical functional condition (performance rating 0-1 on Eastern Cooperative Oncology Group scale) were divided into a weight-losing group (> or = 5% unintentional weight loss within 3 mo; n = 48) and a weight-stable group (n = 56). Dietary intakes in relation to fat-free mass were not different in the two groups. According to the Quality of Life index and the General Health Questionnaire, weight-losing patients had significantly lower quality of life than weight-stable patients. In patients with weight loss, daily intakes of energy and protein correlated significantly with scores on the General Health Questionnaire. This study has shown that many ambulatory cancer patients do not eat enough to maintain weight and that even a moderate weight loss is associated with psychological distress and lower quality of life.
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PMID:The interrelationship of weight loss, dietary intake, and quality of life in ambulatory patients with cancer of the lung, breast, and ovary. 850 86

Prolonged oral etoposide monotherapy is an effective treatment in patients with small cell lung cancer (SCLC) and refractory malignant lymphoma. It shows remarkable activity in relapsed or refractory breast and ovarian cancer (response rates up to 35% and 26%), and was also active in refractory germ cell tumours. Results in small numbers of patients with haematological malignancies merit further investigation. There is considerable pharmacokinetic variability after oral etoposide administration and further investigations are needed to establish optimal dose. Side effects (in particular leucopenia and universal alopecia) should not be underestimated, especially in elderly bad risk patients.
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PMID:Review of current clinical experience with prolonged (oral) etoposide in cancer treatment. 857 46

Using an 'intelligent' tablet bottle which, unknown to the patient, electronically records the times of opening, we have assessed the compliance of patients with prescribed oral altretamine for ovarian cancer. During the periods of compliance monitoring the physical and mental state of the patients was also monitored by means of self-assessed diary cards. 11 patients were assessed over 21 monitoring periods, each of 14 days, representing a total of 294 days. The Overall Compliance (OC), which we define as the number of bottle openings in a monitoring period as a percentage of that number expected on the assumption of perfect compliance, had a mean (SD) of 97.4 (6.9)% over the 21 periods. The OC was not related to any of the diary card measures, or to the cycle number (range 1-5) of the treatment. The high level of compliance is encouraging and is in line with our previous reports in patients with lymphoma and with small cell lung cancer.
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PMID:Patient compliance with prolonged oral altretamine treatment in relapsed ovarian cancer. 865 77

From June 1993 to April 1994, a multi-centre prospective clinical trial was conducted to evaluate efficacy of domestic oral etoposide in the treatment of malignancies. One hundred and ten evaluable patients were assessed for both response and toxicity. Oral etoposide was given as single agent in 50 patients, including 18 patients with small cell lung cancer (SCLC), 18 with malignant lymphoma (ML), 8 with gastric cancer and 6 with ovarian cancer. The response rate was 50% in SCLC, 83.3% in ML, 16.7% in ovarian cancer and 0 in gastric cancer. Sixty patients were treated with combination chemotherapy containing oral etoposide. There were 45 patients in the control group. The response rates in the treated and control groups were 57.1% and 55.6% in SCLC, 95% and 87.5% in ML, 20% and 0 in gastric cancer, respectively. Oral etoposide was well tolerated by the majority of patients. In conclusion, oral etoposide has definite antitumor activity in SCLC, ML and ovarian cancer.
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PMID:[Clinical trial of oral etoposide in the treatment of malignancies]. 869 2

Topotecan (Hycamtin), a semisynthetic water-soluble derivative of camptothecin, is a potent inhibitor of DNA topoisomerase I in vitro and has demonstrated encouraging antitumour activity in a wide variety of tumours, including ovarian cancer and small cell lung cancer. Now approved in the US, topotecan has completed single-agent phase I testing; phase II/III trials are ongoing. Under physiological conditions the lactone moiety of topotecan undergoes a rapid and reversible pH-dependent conversion to a carboxylated open-ring form, which lacks topoisomerase I inhibiting activity. At equilibrium at pH 7.4 the open-ring form predominates. Topotecan is stable in infusion fluids in the presence of tartaric acid (pH < 4.0), but is unstable in plasma, requiring immediate deproteinisation with cold methanol after blood sampling and storage of the extract at -30 degrees C to preserve the lactone form. Topotecan has been administered in phase I trials in several infusion schedules ranging from 30 minutes to 21 days. The plasma decay of topotecan concentrations usually fits a 2-compartment model. Rapid hydrolysis of topotecan lactone results in plasma carboxylate levels exceeding lactone levels as early as 45 minutes after the start of a 30-minute infusion. The peak plasma concentrations and the area under the plasma concentration-versus-time curves (AUC) show linear relationship with increasing dosages. No evidence of drug accumulation is seen with daily 30-minute infusions for 5 consecutive days. Topotecan lactone is widely distributed into the peripheral space, with a mean volume of distribution (Vd) at steady-state of 75 L/m2. The mean total body clearance of the lactone form is 30 L/h/m2, with a mean elimination half-life (t1/2 beta) of 3 hours; renal clearance accounts for approximately 40% of the administered dose with a large interindividual variability. The oral bioavailablity of topotecan is approximately 35%. The low bioavailability may be caused by hydrolysis of topotecan lactone in the gut, yielding substantial amounts of the open-ring form, which is poorly absorbed. Renal dysfunction may decrease topotecan plasma clearance. Creatinine clearance is significantly, but poorly, correlated with topotecan clearance. Hepatic impairment does not influence topotecan disposition. Indices of systemic exposure (steady-state concentrations and AUC) are correlated with the extent of myelotoxicity. Sigmoidal functions adequately describe the relationships between systemic exposure and the percentage decrease in neutrophils.
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PMID:Clinical pharmacokinetics of topotecan. 885 31

Sera from 23 patients with paraneoplastic disease of the central nervous system (PNS) were examined for the presence of anti-neuronal (anti-Hu, anti-Yo/PCA) and anti-Ri) and systemic auto-antibodies, including antibodies against DNA, centromeres, nRNP, Sm antigen, Scl-70, Ro(SS-A), La(SS-B), mitochondria, thyroid antigens, parietal calls, brush border antigen and rheumatoid factor. As controls, sera from 33 patients with small cell lung cancer, 33 with ovarian cancer and 7 with breast cancer and from 107 aged-matched healthy persons were used. Systemic auto-antibodies were found in 52% of patients with paraneoplastic neurological syndromes compared with only 16% (P = 0.001) in the control group with cancer only and 15% in the group of healthy controls. The relatively high percentage of systemic auto-antibodies in patients with PNS indicates that there is a genetic susceptibility to the development of auto-immune phenomena. This may provide an explanation for the relatively rare occurrence of PNS in patients with cancer.
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PMID:Systemic and anti-neuronal auto-antibodies in patients with paraneoplastic neurological disease. 886 87

CPT-11 was synthesized in 1984 at the laboratory of Yakult Honsha. Phase I study of CPT-11 was begun in 1986. The appropriate doses for phase II studies were decided to be 100 mg/m2 weekly or 150 mg/m2 every 2 weeks. Phase II study was conducted and this drug was approved for NSCLC, SCLC, uterine cancer and ovarian cancer by MHW in 1994. It obtained approval for stomach cancer, colorectal cancer, breast cancer, skin cancer and non-Hodgkin's lymphoma in 1995. The combination chemotherapies including CPT-11 have been conducted by using various regimens such as CPT-11 + CDDP, CPT-11 + VP-16, CPT-11 + 5-FU and CBDCA + CPT-11. In stage IV SCLC two prospective randomized controlled trials are on going comparing CPT-11 vs. CPT-11 + CDDP vs. VDS + CDDP and CPT-11 + CDDP vs. VDS + CDDP. In advanced SCLC Japanese Clinical Oncology Group (JCOG) started a randomized controlled trial comparing CPT-11 + CDDP vs. VP-16 + CDDP. In stage III NSCLC the dose escalation studies of CPT-11 (CPT-11) in the combination with TRT are ongoing by JCOG. The problem of CPT-11 in the combination chemotherapy and combined modality is that it is quite difficult to increase the dose of CPT-11 to full dose to obtain the maximum effect.
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PMID:Clinical trials of irinotecan hydrochloride (CPT, campto injection, topotecin injection) in Japan. 899 23

Cisplatin (CDDP) has a curative effect in approximately 80%, of patients with testicular cancer, in contrast to the frequent development of resistance in patients with small cell lung cancer and ovarian cancer, and to the natural resistance of colon cancer. At present it is unknown which factors explain the unique curability of testicular cancer. Since it is very likely that the absence or presence of specific proteins plays an important role in cellular sensitivity towards CDDP, we have screened the protein patterns of various human CDDP-sensitive cell lines and cell lines with acquired or intrinsic resistance to CDDP of testicular, lung and colon origin. The expression of several proteins appeared to correlate with in vitro CDDP sensitivity. The most striking difference found was a relative increase in expression lactate dehydrogenase (LDH) H-subunit expression in the germ cell lines. In testis and colon tumour samples some of these proteins, LDH-H included, also appeared to correlate with in vivo CDDP sensitivity. In the analysis of the mechanisms of drug-resistance, screening of the protein patterns of intrinsic sensitive and resistant cell lines could be a valuable approach.
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PMID:Expression of proteins correlated with the unique cisplatin-sensitivity of testicular cancer. 906 79

Oxaliplatin is a new platinum analog of the DACH family. Recent preclinical data have confirmed its non overlapping spectrum of activity with cisplatin, including acquired and intrinsic platinum resistant cell lines (as KB-CP, A 2780, HT29, CaCo2 colon cancer). When combined with other cytotoxic agents (5FU, SN38, CDDP, carboplatin), oxaliplatin has additive and/or synergistic antitumoral effects on various in vitro and in vivo models (colon, breast, ovarian and epidermoid tumors). Phase II trials have confirmed a sensorial peripherical neuropathy as its limiting toxicity while neither ototoxicity nor renal toxicities and only limited myelotoxicity were noted. Available phase II studies have established its antitumoral activity as single agent in 5FU refractory colon carcinoma while preliminary results suggest efficacy in cisplatin resistant ovarian cancer, in non small cell lung cancer, non Hodgkin lymphoma. Antitumoral activity has been observed during phases 1 in melanoma, glioma, breast and oesophageal cancers. A high response rate (28-65%) with the triple association (FU/folinic acid/oxaliplatin) has been reported in advanced colon cancer treated in first and second line settings. The results of two randomized phase III studies (FU/folinic acid +/- oxaliplatin) are expected. The oxaliplatin/cisplatin combination as salvage regimen had produced significant antitumoral activity (response rate: 45%) in resistant/refractory ovarian cancer. Finally, recent experimental and clinical data have outlined the potential interest in the development of this new original platinum compound. New single agent phases II are expected in other tumor types as well as new oxaliplatin combinations are ongoing (phase I trials of oxaliplatin/CPT-11 and of oxaliplatin/carboplatin, phase II study of oxaliplatin-vinorelbine in lung cancer.
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PMID:[Oxaliplatin: the first DACH platinum in clinical practice]. 929 71


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