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At least 19 recordsLinked to original sources
PubMed1990

Mutations in the p53 gene are frequent in primary, resected non-small cell lung cancer. Lung Cancer Study Group.

The p53 gene has been implicated as a tumor suppressor gene with mutations found in common human cancers. We examined 51 early stage, primary, resected non-small cell lung cancer specimens using an RNAase protection assay and cDNA sequencing. Mutations changing the p53 coding sequence were found in 23/51 (45%) tumor specimens, but not in the corresponding normal lung, were distributed between codons 132 to 283, and included tumors with and without 17p allele loss. Fifteen of the 23 mutations lay in the predicted binding regions for SV40 large T antigen, and 14 were located in regions highly conserved between species. G to T transversions were a common result of p53 mutations in lung cancer compared to other cancers suggesting exposure to different mutagens. In univariate and multivariate analysis the presence of p53 mutations was associated with younger age and squamous histology. However, the presence of p53 mutations was not significantly associated with tumor stage, nodal status or sex and was found in all histologic types of lung cancer. We conclude that somatic mutations in the p53 gene play an important role in the pathogenesis of early stage non-small cell lung cancer.

Aged↗
PubMed1989

Combined modality treatment for non-small cell lung cancer. Lung Cancer Study Group.

A total of 265 patients with non-small cell lung cancer at stages 1 and 2 by preoperative clinical staging were divided into 4 stages after exploratory thoracotomy. Patients at each stage were further divided into subgroups to receive different adjuvant therapies. The cumulative 5-year survival rate showed to be 44.4% for stage 1, 35.5% for stage 2, 7.4% for stage 3 and 0% for stage 4. Histologically, the rate was 28.8% for squamous cell carcinoma, 23.4% for adenocarcinoma, and 29.8% for large cell carcinoma and carcinoma poorly differentiated. For patients at stage 1, it made no significant difference whether they underwent surgical resection only or combined with postoperative intrapleural BCG injection. For patients at stage 2, there was no significant difference between surgical resection only and resection combined with postoperative radiotherapy. For patients at stage 3, who underwent surgical resection combined with chemotherapy and/or radiotherapy, it seemed that combined chemotherapy and radiotherapy presented better results than radiotherapy or chemotherapy alone.

Carcinoma, Non-Small-Cell Lung↗
PubMed1990

A randomized trial of two platinum combinations in patients with advanced non-small cell lung cancer: a preliminary report. European Organization for the Research and Treatment of Cancer--Lung Cancer Working Party.

A randomized study with cisplatin (120 mg/m2) or carboplatin (325 mg/m2) plus etoposide (100 mg/m2, days 1 to 3) in 162 evaluable patients with advanced non-small cell lung cancer (NSCLC) compared response and survival after treatment. No statistically significant difference in survival rates was detected; median survival was 25 weeks for patients receiving cisplatin and 24 weeks for those receiving carboplatin. The objective response rate was 25% for cisplatin plus etoposide and 20% for carboplatin plus etoposide. Granulocytopenia, diarrhea, and nephrotoxicity were significantly more frequent with cisplatin plus etoposide than with carboplatin plus etoposide. Severe nausea and/or vomiting occurred during 59 of 77 courses (77%) with cisplatin and 48 of 75 (64%) with carboplatin (P = .13). Unlike cisplatin plus etoposide, carboplatin plus etoposide was administered on an outpatient basis. At the dose used in the present study, carboplatin plus etoposide was as effective as but less toxic than cisplatin plus etoposide for NSCLC and could be given more easily.

Adenocarcinoma↗
PubMed1989

Cisplatin versus cisplatin plus etoposide in the treatment of advanced non-small-cell lung cancer. Lung Cancer Working Party, Belgium.

We conducted a randomized study comparing the survival after treatment with cisplatin (120 mg/m2) or cisplatin plus etoposide (100 mg/m2 on days 1, 2, and 3) in 162 evaluable patients with advanced non-small-cell lung cancer (NSCLC). No statistically significant difference in survival was detected; the median survival was 26 and 22 weeks, respectively, for patients receiving cisplatin and for those receiving cisplatin plus etoposide. The objective response rate was 19% for cisplatin and 26% for the combination; the corresponding response rates were 17% and 43% in patients with limited disease. No significant differences were detected between the two study arms as far as toxicity was concerned, except for alopecia and granulocytopenia, which occurred more frequently in patients treated with cisplatin plus etoposide.

Adenocarcinoma↗
PubMed1985

The sarcoma, breast cancer, lung cancer, and adrenocortical carcinoma syndrome revisited. Childhood cancer.

We studied two children who had rhabdomyosarcoma and glioblastoma and who were from a family with a hereditary cancer syndrome that was characterized by sarcoma, breast cancer, brain tumors, lung cancer, laryngeal carcinoma, leukemia, and adrenocortical carcinoma. The deleterious genotype has now been expressed through the fourth generation of this large kindred. The pedigree emphasizes the need for an extended history of several generations to arrive at a hereditary-syndrome diagnosis. A limited pedigree may result in nonappreciation of the genetic component. The pedigree illustrates that, in certain circumstances, the highly specific varieties of cancer may occur in children before it is expressed in the parent who carries the putative gene. Pediatricians, in evaluating the causes of childhood cancer, must be cognizant of cancer among adult relatives, since this recognition may aid in the diagnosis of those hereditary cancer syndromes that are characterized by cancer occurrence in children as well as adults.

Adrenal Cortex Neoplasms↗
PubMed1986

Excess mortality from stomach cancer, lung cancer, and asbestosis and/or mesothelioma in crocidolite mining districts in South Africa.

To determine whether exposure to crocidolite is associated with excess mortality, the authors calculated standardized mortality ratios based on deaths in South African crocidolite mining districts from 1968 to 1980 for selected causes of death. Contiguous districts were used as controls. To take account of background geographic variability, they divided the control districts into groups of population size similar to those of the crocidolite mining districts. Standardized mortality ratios in crocidolite mining districts were elevated for asbestosis and/or mesothelioma, and cancer of the lung and stomach. These findings could not be explained by background geographic variability in mortality and are likely to be due to exposure to South African crocidolite during mining and milling or to environmental contamination. The increased standardized mortality ratios for stomach cancer are of particular interest, since excess deaths have not previously been shown in individuals exposed to crocidolite alone.

Adolescent↗
PubMed1992

Epirubicin in malignant mesothelioma: a phase II study of the European Organization for Research and Treatment of Cancer Lung Cancer Cooperative Group.

PURPOSE: The doxorubicin analog, epirubicin (EPI), was tested in patients with malignant mesothelioma. PATIENTS AND METHODS: Sixty-three patients with malignant mesothelioma were given EPI 110 mg/m2 every 3 weeks. Histology was reviewed and confirmed by a pathology panel. On the basis of unconvincing or wrong histology, insufficient material or cytology only, nine cases were considered ineligible for the study. None of the patients had received prior chemotherapy. RESULTS: The main side effects were myelosuppression, alopecia, and gastrointestinal toxicity. Tumor response, assessed by computed tomographic (CT) scans, was assessable in 48 patients. Seven patients (15%) achieved a partial response that lasted a median of 37 weeks; 19 patients had stable disease, and 22 patients progressed on treatment. Median survival time was 40 weeks from the start of chemotherapy, and the median survival of responding patients was 87 weeks. One responding patient is still alive and free of relapse 4 years from the start of chemotherapy. CONCLUSION: We conclude that further testing of EPI in malignant mesothelioma is warranted.

Adult↗
PubMed1987

Immunohistochemical and histochemical markers of primary lung cancer, lung metastases, and pleural mesotheliomas.

Sections of primary lung carcinomas, lung metastases, mesotheliomas, and lung metastases of some rare mesenchymal tumors were incubated with different cytokeratin (CK), vimentin, desmin, and tissue polypeptide antigen (TPA) antibodies and with antibodies reactive with different hormones (ACTH, PTH, alpha-HCG, Calcitonin CT), CEA, carcinoma-associated antigen (CA1), secretory component (SC), neuron-specific enolase (NSE), alpha-1-antitrypsin (alpha-1-AT), lysozyme (lyso), and S-100 protein (S 100). CK antibodies derived from a 49 kD (reactive with simple epithelia [SE]) and a 67 kD CK polypeptide fraction (reaction with complex epithelia [CE] were useful differentiation markers for the four major groups of lung carcinomas. In one half of small cell carcinomas a positive reaction with NSE antibodies was found. S 100 and SC were good markers for papillary and bronchioloalveolar adenocarcinomas, whereas CEA was less important because of its reactivity with different types of lung carcinomas. To discern clear cell carcinomas of lung and renal origin a positive reaction with vimentin antibodies (some renal but not lung types) and with CA1 (no renal but all lung types) seemed to be useful. All hormone antibodies were of no importance as markers for difficult differential diagnosis, because positive reactivities were found in cases from every major carcinoma group. In addition, a Ca2+-activated adenosine triphosphatase (ATPase) was found in mesotheliomas but not in papillary adenocarcinomas.

Adenocarcinoma↗
PubMed1989

A preliminary evaluation of calcitonin and PDN-21 as tumor markers for lung cancer. EORTC Lung Cancer Working Party.

Immunoreactive calcitonin (iCT) can be ectopically secreted by lung cancer cells and has been proposed as a tumor marker for bronchial neoplasms. Since PDN-21 (katacalcin or the carboxyl-terminal flanking peptide of the calcitonin gene) and CT are cosecreted in normal subjects and in patients with medullary thyroid carcinoma (MTC), we sought to determine the potential utility of PDN-21 as a tumor marker for lung cancer. We measured carcinoembryonic antigen (CEA), neurone-specific enolase (NSE), iCT, and PDN-21 in 119 to 378 healthy subjects, 88 to 91 patients with benign pulmonary disease, and 249 patients with advanced lung cancer (108 small cell lung cancers and 141 other forms). Tumor marker specificity was satisfactory: the percentage of increased values (greater than the 95th percentile of normal subjects) in patients with benign pulmonary diseases varied from 9% (NSE, PDN-21) to 12% (CEA). PDN-21 was a more sensitive marker for lung cancer than iCT: the percentage of increased values was 44% for PDN-21 versus 19% for iCT, and 51% versus 23% for the subgroup of patients with small cell lung cancer (SCLC). PDN-21 concentrations were increased in 69 (34%) of 202 patients with a normal iCT level, whereas iCT concentrations were increased in only six (4%) of 139 patients with a normal PDN-21 level. However, markedly elevated concentrations of the two markers generally occurred in the same patients and the correlation between the two markers was significant (rs = 0.60; P less than 0.01). PDN-21 provided complementary information to that from the classical markers NSE and CEA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Should subcarinal lymph nodes be routinely examined in patients with non-small cell lung cancer? The Lung Cancer Study Group.

This study is based on a retrospective analysis of 163 patients with stage III non-small cell lung cancer randomized to one of three Lung Cancer Study Group postoperative resection-adjuvant treatment protocols. All patients underwent rigorous surgical/pathologic staging including required removal and examination of bronchopulmonary, hilar, subcarinal, and paratracheal lymph nodes. Patients were grouped as follows: group I, only subcarinal nodes diseased (N = 40); group II, only high paratracheal nodes diseases (N = 32); group III, only mid-mediastinal nodes diseased (N = 48); and group IV, subcarinal nodes plus nodes from any other site diseased (N = 43). Patient deaths and tumor recurrences were recorded. The death rate was highest for patients with metastases to subcarinal nodes plus nodes in another site (group IV). Pairwise comparisons of the survival rates of patients in each group disclosed a significant difference between group III and IV (p less than 0.02). In view of this observation, the Lung Cancer Study Group recommends that all patients have rigorous mediastinal lymph node staging done at the time of pulmonary resection to establish prognosis and criteria for study of adjuvant treatment interventions.

Carcinoma, Non-Small-Cell Lung↗
PubMed1992

Phase II study of ACNU as second-line treatment in small-cell lung cancer. EORTC Lung Cancer Cooperative Group.

A total of 24 patients presenting with small-cell lung cancer either resistant to or relapsing within 3 months after first-line treatment were entered in a phase II study of 1-(4-amino-2-methyl-5-pyrimidinyl)-methyl-(2-chloroethyl)-3- nitrosourea hydrochloride (ACNU). ACNU was given i.v. at a dose of 75 mg/m2 every 6 weeks. We observed a partial response of 7 months' duration in one patient and one case of stable disease that lasted for 6 months; all other subjects exhibited progressive disease. Two patients developed brain metastases during treatment. The toxicity of ACNU consisted mainly of bone marrow suppression, especially thrombocytopenia. At this dose and on this schedule, ACNU shows minimal activity as second-line treatment in small-cell lung cancer.

Carcinoma, Small Cell↗
PubMedDate not supplied

Small cell lung cancer.

Lung cancer is the most common cause of cancer death in the United States, with approximately 135,000 men and women dying each year. While much has been learned about the etiologic risk factors, less progress has been made in therapy. Five-year survival rates remain at less than 10%. However, there has been some progress in the therapy of one histological subtype of lung cancer, small cell lung cancer. Totaling around 20% of lung cancer cases, small cell lung cancer is distinct from the other histologic subtypes in its biologic behavior and responsiveness to therapy. In the 1960s, the median survival for patients with small cell lung cancer was approximately 3 months. With combination chemotherapy and radiotherapy median survivals now range from 1 to 2 years, and there is evidence for a curative potential since approximately 10% of patients who initially present with limited disease survive greater than 2 years. The unique clinical aspects of this histological subtype potentially relate to its underlying cell of origin. This behavior is reflected in the numerous paraneoplastic syndromes that frequently accompany small cell lung cancer. Its propensity for early dissemination have made staging the extent of disease an important part of the clinical evaluation. Since small cell lung cancer is sensitive to both chemotherapy and radiation therapy, there have been multiple clinical trials evaluating drug/radiotherapy combinations. This article will briefly describe the unique aspects of small cell lung cancer as opposed to other histological subtypes of lung cancer and give a overview of the current clinical approach and treatment of this disease.

Carcinoma, Small Cell↗
PubMed1989

Small cell lung cancer.

Lung cancer is the most common cause of cancer death in the United States, with approximately 135,000 men and women dying each year. While much has been learned about the etiologic risk factors, less progress has been made in therapy. Five-year survival rates remain at less than 10%. However, there has been some progress in the therapy of one histological subtype of lung cancer, small cell lung cancer. Totaling around 20% of lung cancer cases, small cell lung cancer is distinct from the other histologic subtypes in its biologic behavior and responsiveness to therapy. In the 1960s, the median survival for patients with small cell lung cancer was approximately 3 months. With combination chemotherapy and radiotherapy median survivals now range from 1 to 2 years, and there is evidence for a curative potential since approximately 10% of patients who initially present with limited disease survive greater than 2 years. The unique clinical aspects of this histological subtype potentially relate to its underlying cell of origin. This behavior is reflected in the numerous paraneoplastic syndromes that frequently accompany small cell lung cancer. Its propensity for early dissemination have made staging the extent of disease an important part of the clinical evaluation. Since small cell lung cancer is sensitive to both chemotherapy and radiation therapy, there have been multiple clinical trials evaluating drug/radiotherapy combinations. This article will briefly describe the unique aspects of small cell lung cancer as opposed to other histological subtypes of lung cancer and give an overview of the current clinical approach and treatment of this disease.

Antineoplastic Agents↗
PubMed1988

The benefit of adjuvant treatment for resected locally advanced non-small-cell lung cancer. The Lung Cancer Study Group.

The purpose of this trial was to investigate the impact of systemic combination chemotherapy on survival and recurrence patterns in incompletely resected non-small-cell lung cancer. Incomplete resection was defined as presence of residual tumor in the resection margin or by presence of metastasis in the highest paratracheal lymph node sampled during protocol-directed surgical staging of the mediastinum. One hundred seventy-two patients were randomized to receive either postoperative radiotherapy (RT) alone or postoperative RT plus chemotherapy with CAP (Cytoxan [cyclophosphamide; Bristol Myers, Evansville, IN], Adriamycin [doxorubicin; Adria Laboratories, Columbus, OH], and Platinol [cisplatin; Bristol Myers]) for 6 months. One hundred sixty-four patients were eligible for analysis at a mean time since randomization of 3.7 years. The chemotherapy arm showed significantly longer recurrence-free survival (two-sided Mantel-Haenszel log rank test, P = .004). This difference holds true for nonsquamous patients (P = .01), and approaches significance for squamous patients as well (P = .08). There was a 14% difference in survival rate favoring the chemotherapy arm 1 year after randomization. Analysis of sites of recurrence showed a significant decrease in distant metastases in the chemotherapy arm. Median survival for the entire group was approximately 17 months, and 35% are alive 2 years after resection. Toxicity of treatment consisted of esophagitis (mild-moderate by Eastern Cooperative Oncology Group [ECOG] criteria) and predictable hematologic, gastrointestinal (GI), and skin toxicity expected from CAP.

Antineoplastic Combined Chemotherapy Protocols↗