Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In scheduling chemotherapy and radiotherapy for locally advanced non-small cell lung cancer (NSCLC), chemotherapy can be given pre-radiotherapy or concurrently as a single agent or in combination. Optimal scheduling has yet to be established. Optimal pre-radiotherapy for NSCLC requires further development but cisplatin with vinblastine, vindesine, etoposide or navelbine appear the best currently available. A number of new drugs show potential for enhancing radiation effects. Concurrent chemotherapy and radiotherapy has been tested in a number of experimental tumours in cell culture. In these systems cisplatin, carboplatin, 5-fluorouracil, mitomycin-C and other agents appear to improve cell kill compared to chemotherapy alone. Mouse xenograft models allow the study of various concurrent drug and radiation schedules including the effect of radiation with cisplatin, carboplatin, paclitaxel and gemcitabine. In these systems, cisplatin in divided doses shows optimal enhancement with fractionated radiotherapy. There are a number of drug candidates for concurrent chemotherapy and radiotherapy programs. Clinical studies in head and neck cancer, esophageal cancer, small cell lung cancer and NSCLC show promising results with concurrent chemotherapy and radiotherapy. Cisplatin given daily with radiotherapy improved survival in NSCLC compared to cisplatin given weekly with radiotherapy or to radiotherapy alone. To study the toxicity of radiation and concurrent carboplatin, we have studied 170 patients with unresectable locally advanced NSCLC in a 4-arm randomized trial. An analysis of the first 100 patients entered revealed significantly more neutropenia (P < 0.0001) and thrombocytopenia (P < 0.004) with the combined modality arms. Esophagitis was worse on all three experimental arms but was significantly more prolonged with accelerated radiotherapy arms.(ABSTRACT TRUNCATED AT 250 WORDS)
Lung Cancer 1995 Jun
PMID:Scheduling of chemotherapy and radiotherapy in locally advanced non-small cell lung cancer. 755 50

The role of prophylactic cranial irradiation (PCI) in the management of patients with small cell lung cancer is reviewed, with emphasis on 11 randomised trials. Several interpretive and methodological problems related to PCI investigations are identified, and it is argued that given the current data PCI should be considered as an optional treatment component in CR patients, that these authors do not recommend, while other investigators do.
Lung Cancer 1995 Jun
PMID:Prophylactic cranial irradiation in small cell lung cancer--an update. 755 54

The bombesin-like peptides can function as autocrine growth factors in lung cancer and candidate tumor suppressor genes on chromosomes 3 and 9 play important roles in lung cancer. Bombesin-like peptides can function as mitogens for normal bronchial epithelial cells and lung cancer cell lines. The monoclonal antibody directed against gastrin releasing peptide and bombesin, 2A11, can inhibit the growth of small cell lung cancer in vitro and in vivo and intravenous administration has induced a clinical remission in a patient with relapsed small cell lung cancer. The loss of a portion of one of the two short arms of chromosome 3 (3p) is identified in nearly 100% of tumor cell lines and tumors from patients with small cell lung cancer. Introduction of chromosome 3 into tumor cell lines suppresses their tumorigenicity in athymic nude mice, one of the characteristics of the cancer phenotype. Both copies of the candidate tumor suppressor gene on chromosome 9, CDKN2, are deleted in approximately one-fourth of lung cancer cell lines examined and the protein product of CDKN2, p16 is undetectable in one-third of the lung cancer cell lines studied. The CDKN2 gene is inactivated more commonly in non-small cell lung cancer than small cell lung cancer while the retinoblastoma gene is inactivated more commonly in small cell lung cancer than non-small cell lung cancer. It appears that a single defect in this cell cycle pathway is necessary for unregulated growth in lung cancer and current evidence suggests these defects differ between small cell and non-small cell lung cancer.
Lung Cancer 1995 Jun
PMID:Biology of small cell lung cancer. 755 56

Recently there has been a number of new active drugs which have been identified for treating patients with SCLC. These drugs include paclitaxel, docetaxel, CPT-11, topotecan and gemcitabine. The range of response rates are as follows for each of the drugs given: (1) to previously untreated patients: paclitaxel (34-41%), topotecan (39%) and gemcitabine (30%), and (2) to previously treated patients: docetaxel (28%), CPT-11 (47%) and topotecan (35%). Further studies with these new drugs utilized in combination chemotherapeutic regimens are needed to define the role of these agents in the treatment of patients with SCLC.
Lung Cancer 1995 Jun
PMID:New drugs for treating small cell lung cancer. 755 57

After a remarkable improvement of the very poor prognosis of small cell lung cancer with very simple therapy such as iv and oral cyclophosphamide the role of oral therapy has become minimal. However, since more than a decade results of combination chemotherapy are at a plateau and it is necessary to reconsider the role of simple therapy in patients without the prospect of cure. Oral therapy might be worthwhile because it is probably less effecting the quality of life of the patient and makes it unnecessary to visit the hospital frequently. All drugs available for oral use with known activity against small cell lung cancer are reviewed. The best example of the success of oral therapy is etoposide, other candidates that need to be tested in a modern way are oral cyclophosphamide and hexamethylmelamine. New concepts of prolonged chemotherapy and dose-intensity are easier evaluated by using oral drugs. The discovery of the activity of prolonged oral etoposide is an excellent example how to test a new concept in a very simple way.
Lung Cancer 1995 Jun
PMID:Oral therapy for small cell lung cancer. 755 58

The treatment of small cell lung cancer (SCLC) has continued to evolve over the past 20 years and now consists primarily of combination chemotherapy with or without thoracic radiotherapy depending on stage at presentation. However, despite marked improvement in overall survival, a majority of patients continue to die of their disease. It is not likely that conventional chemotherapy agents will substantially alter this dismal fact but new agents are available with novel mechanisms of action some of which yield excellent response rates. The agents with greatest promise include the taxanes and drugs that target topoisomerase I. Real progress in the management of SCLC will come with the identification of methods for overcoming drug resistance, exploration of new treatment strategies including gene therapy and possibly through the use of biological agents. Chemoprevention trials are of the utmost importance given the high incidence of second primary tumors that arise in the few long term survivors of this disease. All these areas are fertile grounds for future investigation in the management of SCLC.
Lung Cancer 1995 Jun
PMID:Future directions in the management of small cell lung cancer. 755 59

Advances in the treatment of SCLC have been slow but sure over the past decade. It is now recognized that a small subset of patients may be cured of this disease, particularly with combined modality treatment with radiation therapy and systemic chemotherapy. However, perhaps only 25% of all patients will be candidates for this intensive/combined modality approach. Therefore, there is a need to identify effective combination chemotherapy regimens that can be easily administered to the remaining 75% of poor prognosis SCLC patients. Our studies and those of others would suggest that the combination of carboplatin and oral etoposide is a highly effective regimen for the treatment of these patients with results equal to and comparable with more intensive schedules. The ease of administration of this combination with acceptable toxicity would suggest that for such a subset of patients it may be the treatment of choice against which other combination schedules should be compared.
Lung Cancer 1995 Jun
PMID:Carboplatin/etoposide combination chemotherapy in the treatment of poor prognosis patients with small cell lung cancer. 755 60

Etoposide phosphate, a water soluble prodrug of etoposide, has several potential advantages including easier and more rapid administration, avoidance of large fluid loads, and elimination of hypersensitivity reactions and other problems related to the solubilizer. This randomized Phase II study was done to evaluate the efficacy and toxicity of etoposide phosphate and etoposide, when used in combination with cisplatin in the treatment of patients with small cell lung cancer. Previously untreated small cell lung cancer patients were randomized to receive cisplatin in combination with molar equivalent does of either etoposide or etoposide phosphate. The patients were evaluated with respect to response rate, time to progression, survival, and toxicity. Response rates with etoposide phosphate and etoposide were 61% (95% confidence interval 55-67%) and 58% (95% confidence interval 52-64%), respectively (P = 0.85). Median time to progression was 6.9 months for patients who received etoposide phosphate and 7.0 months for those with etoposide (P = 0.50). For extensive stage disease patients, median survival with etoposide phosphate was 9.5 months versus 10 months for etoposide (P = 0.93). The corresponding median survivals for patients with limited stage disease were > 16 months and 17 months, respectively (P = 0.62). Myelosuppression was the most common toxicity; Grade 3 and 4 leukopenia occurred in 63% of patients receiving etoposide phosphate compared with 77% receiving etoposide (P = 0.16). The combination of etoposide phosphate and cisplatin is effective in the treatment of small cell lung cancer, and can be administered with acceptable toxicity. This study was not designed to be a formal Phase III comparative trial, but the efficacy and toxicity observed with this regimen were found to be similar to a standard etoposide/cisplatin regimen, using molar equivalent etoposide doses. Etoposide phosphate is preferable to etoposide because it is easier to use.
Lung Cancer 1995 Jun
PMID:Etoposide phosphate or etoposide with cisplatin in the treatment of small cell lung cancer: randomized phase II trial. 755 61

In a previous registry-based survey of 999 patients injected with alpha-emitting 232ThO2 (Thorotrast), we identified elevated risks for lung carcinoma and malignant mesothelioma. Since injected Thorotrast is retained lifelong mostly in liver, spleen and lymph nodes, the mesothelial surfaces of these organs are constantly irradiated. Thorotrast-administered patients also perpetually exhale 220Rn, a 232Th-daughter. Study of Thorotrast-exposed patients may, therefore, provide data with regard to carcinogenicity of radon exposure, a current public health concern, as well as the pathogenesis of malignant mesothelioma. The incidence and histologic types of lung carcinoma and malignant mesothelioma within the cohort were examined by review of available histopathologic material and medical records. Further, mutations of the p53 gene were analyzed whenever possible as it has previously been suggested that radon-associated lung carcinomas exhibit specific mutational patterns. The cumulative risk for lung carcinoma reached 11.0% based on 20 confirmed cases. Nine were small cell lung cancer (SCLC), whereas the expected frequency was 18%. The risk for malignant mesothelioma reached 2.5% based on 7 cases. The actuarial risk of malignant mesothelioma for patients given more than 20 ml Thorotrast was 7.8% compared to 1.4% for patients administered smaller amounts. Seven lung carcinomas and 5 malignant mesotheliomas were analyzed for p53 mutations; only 1 (in a lung adenocarcinoma) was detected. A possible association between Thorotrast and SCLC is suggested. In addition, a possible dose-response gradient exists for Thorotrast and malignant mesothelioma.
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PMID:Lung carcinoma and malignant mesothelioma in patients exposed to Thorotrast: incidence, histology and p53 status. 759 Dec 26

Oral etoposide has considerable activity in small cell lung cancer and the low risk of toxicity has resulted in the frequent prescription of this agent in elderly or infirmed patients. We describe a case of fatal pulmonary toxicity following the administration of oral etoposide. This is the first report of biopsy-proven pulmonary toxicity associated with this agent.
Lung Cancer 1995 Mar
PMID:Fatal pulmonary toxicity following oral etoposide therapy. 760 34


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