Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antitumor activity (increase in lifespan and cure) was greater for ifosfamide (IFO) in several experimental tumors, some of which were primarily resistant to cyclophosphamide (CYC). IFO has been shown to be active in anthracycline-resistant and in adriamycin/cisplatin-resistant sublines of an Ehrlich ascites tumor, as well as in tumor cells primarily resistant to CYC. The few comparative controlled clinical trials available suggest superior single-agent activity of IFO compared with CYC in soft tissue sarcoma and ovarian cancer. Combination chemotherapy with IFO has been effective in second-line treatment of sarcomas, malignant lymphomas, lung cancer, and testicular cancer, most of them pretreated with or refractory to CYC. Although it is difficult to obtain clinical proof that there is no cross-resistance between IFO and CYC, IFO has been shown to be active in multirefractory malignant lymphomas, in small cell lung cancer not responding to adriamycin, vincristine, and etoposide, and in soft tissue and bone sarcomas. Testicular cancer and pancreatic cancer are some of the tumors in which IFO activity is currently being evaluated and in which CYC has so far failed to show sufficient clinical activity. More comparative controlled clinical trials are needed in ovarian cancer, breast cancer, malignant lymphomas, sarcomas and cervical cancer, in which IFO has already shown sufficient single-agent activity. Due to its lower level of cross-resistance with a variety of heterocyclic products, but also with other alkylating agents, in addition to its use in induction chemotherapy, IFO is an important second-line agent in many clinical situations.
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PMID:Comparative activity of ifosfamide and cyclophosphamide. 354 22

Eleven population-based cancer registries tabulated second cancers among 133,411 patients diagnosed with testicular cancer, ovarian cancer or Hodgkin's disease between 1945 and 1984. Overall, 3,157 second cancers were observed, as compared with 2,420 expected at least one year after the first cancer. Survivors of testicular and ovarian cancer experienced 30% and 20% more cancers respectively than the general population comparison group, and patients previously diagnosed with Hodgkin's disease had an 80% excess of cancer. No information was available either on treatment for the first cancer, or other risk factors. However, temporal patterns in the risk of specific second cancers were analysed, with particular reference to the possible role of therapy for the first cancer. Leukaemia of the acute or non-lymphatic type, which has been previously linked to alkylating agent therapy, occurred in excess following all 3 first cancers, as did non-Hodgkin's lymphoma (overall relative risks of 6.1 and 1.8 respectively, with considerably higher relative risks following Hodgkin's disease). Other cancers for which important and plausibly therapy-induced excesses occurred were lung cancer following Hodgkin's disease (relative risk 1.9), breast cancer following Hodgkin's disease (relative risk 1.4) and bladder cancer following ovarian cancer and Hodgkin's disease (relative risks 1.7 and 2.2 in women, respectively). Rarer sites at which striking excesses occurred were the salivary gland, thyroid, bone and connective tissue. There were smaller, but clear excesses for cancers of the rectum and colon following ovarian cancer and testicular cancer, skin cancer following Hodgkin's disease, and kidney cancer following ovarian cancer. Overdiagnosis, misclassification of metastases and confounding by other risk factors were all considered as explanations of observed excesses. Nonetheless, it appeared that there are clear excess risks for cancers other than acute leukaemia which must be ascribed to therapy for the first cancer, especially in view of the possible under-reporting in registry material. Case-control studies are under way to provide information on the role of specific aspects of therapy.
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PMID:Second malignancies following testicular cancer, ovarian cancer and Hodgkin's disease: an international collaborative study among cancer registries. 357 May 50

In spite of the numerous reports indicating the presence of humoral immunosuppressive factors in cancer patients, only a few of these factors have been biochemically identified. Furthermore, their role as effective immunosuppressors in vivo remains to be established. Our laboratory has attempted to isolate and identify the major immunosuppressive factor in the malignant effusions derived from ovarian and lung cancer patients. We have previously demonstrated that the Mr 52,000 immunosuppressive factor isolated from the ascites fluid of an ovarian cancer patient inhibited T-dependent immune responses in vivo and in vitro including the inhibition of E-rosetting. Thus, this immunosuppressive factor was named "suppressive E-receptor" (SER). Our current study demonstrates that this SER factor purified from malignant effusions derived from ovarian, lung, or head and neck cancer patients had a common component which dissociated equally into Mr 38,000-42,000 and 17,000-19,000 moieties on sodium dodecyl sulfate-polyacrylamide gel electrophoresis under vigorous reducing conditions. Electroelution of these two components followed by a limited amino acid sequence determination revealed these two components to have N-terminal amino acid sequences identical to the beta and alpha 2 subunits of normal adult haptoglobin. Immunoelectrophoresis of SER using a polyclonal antiserum to neonatal cord blood demonstrated that SER, unlike normal haptoglobin, has slower electrophoretic mobility than the normal adult haptoglobin. Western blotting analysis of SER separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis under denaturing conditions failed to recognize a monoclonal antibody directed specifically to SER. However, this monoclonal antibody exclusively reacted with the SER separated by an analytical polyacrylamide gel electrophoresis gel under nondenaturing conditions while normal adult haptoglobins or purified but denatured haptoglobin obtained from the same malignant fluid as SER all failed to react with this antibody. Thus, SER appears to bear an additional epitope(s) that is absent in normal adult haptoglobin. Since the SER as well as the neonatal haptoglobin have at least 100 to 1000-fold more potent immunosuppressive activity than the normal adult haptoglobin, this additional epitope(s) present in SER may be responsible for the potent immunosuppressive property of SER.
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PMID:An analogy between fetal haptoglobin and a potent immunosuppressant in cancer. 362 Nov 98

In previous work the authors observed that platinum (free and bound) does not seem to accumulate in the peripheral compartment following the administration of two courses of cisplatin (cis-DDP) therapy (65 mg/m2) in patients with mammary and ovarian cancer. The aim of the present work was to study the disposition of platinum (Pt) after a higher dose of cis-DDP, to verify the rate of free drug penetration into the tissue and to observe changes in protein binding relative to the dose. cis-DDP, at the dose of 100 mg/m2, was administered i.v. over 60 min to patients with lung cancer. Serum and urine were collected before infusion and at various intervals afterwards. The plasma and urine levels of Pt were determined by flameless atomic absorption spectrophotometry, using a Varian model AAS 1475-GTA 95. Serum levels were analysed by a two-compartment open pharmacokinetic model. After the higher dose there was a substantial increase in central volume Pt and slight increase in peripheral volume Pt as compared with levels observed previously at the lower dose. In some subjects receiving high doses elimination half-life decreased and total body clearance increased, while in others these kinetic parameters were unchanged in comparison with those observed after a low dose. Protein binding seems to influence the persistence of platinum in the vascular space, modifying to a minor degree tissue penetration of the drug.
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PMID:Kinetics of platinum in cancer patients treated with cisplatin at different doses. 365 26

Two hundred and eighty-six patients presenting with metastatic adenocarcinoma or undifferentiated carcinoma whose primary site was not identified by clinical history, physical examination and chest radiograph have been studied. Median survival from presentation was 22 weeks. Factors independently predicting improved survival were lymph node presentations, good performance status and body weight loss of less than 10 per cent. In 88 (31 per cent) patients the primary tumour site was subsequently identified, in 58 (20 per cent) during life. Lung cancer was the most frequently identified primary tumour, and in only 32 (11 per cent) of the patients was a 'treatable' primary tumour (i.e. germ cell, breast, ovarian, prostate, thyroid cancer or lymphoma) identified. Among the treatable primary tumours were those in eight out of 16 female patients presenting with axillary metastases who were subsequently shown to have primary breast cancer and four of 13 females presenting with ascites who were found to have primary ovarian cancer. Prostatic cancer was confirmed in five out of 13 men with raised serum acid phosphatase. Of 22 patients with elevated serum alphafoetoprotein (AFP) or beta-human chorionic gonadotrophin levels (beta HCG) 18 had some features of the 'atypical teratoma syndrome'. Of the total of 32 patients with treatable tumour types, 29 (90 per cent) were identified during life. Median survival for patients with treatable tumour types identified during life was 104 weeks, compared with 22 weeks for the group as a whole. Retrospective immunocytochemical staining of the original biopsy showed that prostatic specific antigen and antibodies to beta HCG and AFP were diagnostically useful, but a series of organ site non-specific markers of histogenesis or cellular differentiation (carcinoembryonic antigen, secretory component for IgA, peanut lectin binding, epithelial membrane antigen and keratin) showed no significant correlations with identified primary sites, responsiveness to empirical chemotherapy or survival. Metastatic undifferentiated carcinoma or adenocarcinoma from an unknown primary site represents 6.5 per cent of all referrals to the medical oncology unit, Royal Prince Alfred Hospital, Sydney. We offer guidelines for the rapid identification of the limited number of primary sites for which effective and specific forms of systemic treatment are available.
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PMID:Metastatic adeno or undifferentiated carcinoma from an unknown primary site--natural history and guidelines for identification of treatable subsets. 365 56

The antineoplastic activity of two ether lipid derivatives, the alkyl-lysophospholipid derivative (ALP) ET-18-OCH3 and the ether-linked lipoidal amine CP-46,665 was tested in a human tumor clonogenic assay (HTCA) in vitro. CP-46,665 suppressed the colony formation of various human tumors with a slight dose response relation after 1 hr incubation and with a clear optimum (85% response rate) after continuous exposure in the higher dose range tested (10 micrograms/ml). ET-18-OCH3 did not have substantial activity after 1 hr of incubation. However, when continuous exposure to the compound was used, ET-18-OCH3 seemed to have a modest dose response effect and yielded a response in about 60% of the tumor cell samples tested in the higher dose range (10 micrograms/ml). Thus, both compounds have in vitro antitumor activity in the HTCA within a dose range of 1-10 micrograms/ml, especially during continuous exposure. The tumor specific type activity was found in breast cancer, ovarian cancer, lung cancer and mesothelioma. Both compounds caused decreases in colony formation down to the 0%, 2% and 4% levels. In a comparison of specimens in which both compounds were used, only one of five times showed a discordance in sensitivity or resistance; therefore the compounds appear similar in their in vitro activity. In a second set of experiments we tested the structure-activity relationship among a variety of ALP in the [3H]thymidine incorporation assay after incubation with HL-60 leukemic blasts and other neoplastic cells from human origin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ether lipid derivatives: antineoplastic activity in vitro and the structure-activity relationship. 371 49

A human tumor cloning assay was utilized to evaluate the antineoplastic activity of the novel antitumor antibiotic fostriecin (CI-920). Initial screening with 10.0 mcg/ml continuous exposure against a variety of histologic tumor types resulted in 14/51 (27%) in vitro responses (defined as greater than 50% decrease in TCFUs). Further investigation of the compound was performed in 1-hr preincubation experiments. The in vitro response rate at a concentration of 1.0 mcg/ml (which was considered to correspond to a clinically achievable concentration) was 15/43 (35%). Response rates for specific tumor types included: 5/15 in ovarian cancer, 5/12 in breast, and 4/11 in human lung cancer. The impression of significant antitumor activity of the compound at this dose was further substantiated by comparing its in vitro activity with a variety of simultaneously tested standard anticancer agents. In addition, these data indicated the possibility of non-cross resistance of CI-920 to several established cytostatics. CI-920 is a compound with good in vitro activity which should be further developed for clinical trials.
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PMID:In vitro activity of the novel antitumor antibiotic fostriecin (CI-920) in a human tumor cloning assay. 377 49

In vitro phase II study of a new cyclic hexapeptide anticancer agent, RA-700 was studied on the human tumor clonogenic assay. From the results of the study using the human tumor cell line of lung cancer (PC-6), RA-700 appears to possess time-dependent antitumor activity. Therefore, against the 148 human specimens of various malignancies, the chemosensitivity of RA-700 was tested at the concentrations of 10 micrograms/ml, 1 microgram/ml and 0.1 microgram/ml in continuous exposure schedule for 2 weeks by using the human tumor clonogenic assay. If the criteria for in vitro sensitivity was based on greater than or equal to 70% inhibition of colony formation, out of 148 specimens 59 specimens (40%) were evaluable and the chemosensitivity rate of RA-700 were 67% (4/6), 22% (2/9), 17% (3/18) and 10% (1/10) for ovarian cancer, non-small cell lung cancer, breast cancer and colorectal cancer, respectively. An overall chemosensitivity rate against 13 different histologic types of cancers was 22% (13/59) (greater than or equal to 70% inhibition of colony formation) and 39% (23/59) (greater than or equal to 50% inhibition of colony formation). RA-700 showed almost same chemosensitivity compared to that of five standard anticancer drugs (adriamycin, mitomycin C, cisplatin, vinblastine and 5-FU), but the spectrum of RA-700 activity appears to be different from that of the standard drugs. Furthermore, the antitumor activity of RA-700 had no relationship with prior chemotherapy. These results indicated that RA-700 is a candidate for phase I study.
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PMID:Activity of RA-700, a cyclic hexapeptide from Rubiae Radix, in the human tumor clonogenic assay. 381 26

The relationship of cancer incidence to terrestrial radiation and population density was investigated. Cancer incidence was obtained using 40 years of age-standardized data from the Connecticut Tumor Registry, and environmental radiation was estimated using data from an airborne gamma radiation survey of the entire state. These variables were examined ecologically, using the 169 towns of the state as the analytic units in a weighted regression analysis. The study design involves a large population base in a state having relatively high terrestrial radiation exposure levels overall and reasonable variation in exposure between towns. For all cancer combined, only one of the eight sex-specific analyses by decade yielded a significant radiation regression coefficient, and this was negative. In the sex- and site-specific analyses, almost all the coefficients for radiation were not significantly different from zero. In contrast, significant positive relationships of cancer incidence with population density were found for all cancer, for cancer of the lung for both sexes, for stomach, colonic, and prostatic cancer for males, and for lymphomas, thyroid, breast, and ovarian cancer for females. Both the radiation and population density relationships were adjusted for socioeconomic status. Socioeconomic status was significantly negatively associated with stomach and lung cancer in males and with cervical cancer in females; it was also positively associated with lymphomas and breast cancer in females. A power calculation revealed that, despite the relatively large size of this study, there was only a small probability of detecting a radiation effect of the strength anticipated from previous estimates.
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PMID:The relationship of cancer incidence to terrestrial radiation and population density in Connecticut, 1935-1974. 394 Apr 29

Blood concentrations of total cholesterol, cholesterol of very high density lipoproteins (alpha-cholesterol), triglycerides, beta-lipoproteins and 11-hydroxycorticosteroids were studied in 560 patients with rectal, colon, lung, ovarian, breast and endometrial cancer as well as in 238 controls. Patients with breast and rectal cancer were examined before and repeatedly after operation (every 6-12 months within 4-5 years). The blood concentration of total cholesterol was found to be elevated in breast cancer patients and controls with fibroadenomatosis and decreased in females with ovarian cancer and males with lung cancer. The level of blood alpha-cholesterol was decreased in males with all tumor localizations under study and in females with ovarian and rectal cancer. The concentration of triglycerides was increased in women patients only. Three possible causes of dyslipidemia in cancer patients are discussed: its development before tumor manifestation, the effect of tumor on the metabolic status of the host and the role of emotional stress in the increase of triglycerides level in the blood of primary cancer patients.
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PMID:[Characteristics of dyslipidemia in cancer patients]. 394 86


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