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)

Thirty-three patients with untreated small cell lung carcinoma received 6 cycles epirubicin 30 mg/m2 i.v. on days 1, 8, and 15, in combination with cyclophosphamide 1,000 mg/m2 on day 1 and vincristine 2 mg i.v. on day 1 every 3 weeks. Thirty-one patients were evaluable concerning state of remission. Four out of 13 patients with limited disease had a complete, and 6 a partial remission, while 2 out of 18 patients with extensive disease had a complete and 8 a partial remission. The toxicity of this therapy regimen was very low. The results of this treatment did not differ significantly in comparison to the standardized treatment of small cell lung cancer, but it was easier to tolerate.
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PMID:Epirubicin weekly in combination chemotherapy with cyclophosphamide and vincristine in untreated small cell lung cancer: a phase II trial. 216 28

The prognosis for carcinoma of the lung is influenced by the stage of the disease at presentation and by the potential for resectability. The five-year survival rate following resection of stage I carcinoma is as high as 83% for T1N0 lesions and about 65% for T2N0 tumors. Some stage III tumors are also amenable to surgery in the absence of distant metastases. N2 disease tends to be refractory to cure, despite a localized presentation; however, 20% of patients with N2 disease have resectable tumors despite the presence of lymph node metastases, with a 5-year survival rate of 30% following surgery and postoperative external radiation therapy. Surgery is not beneficial for patients with small cell lung cancer. Proper case selection and careful preoperative and perioperative management are necessary to minimize complications.
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PMID:Surgical treatment of lung cancer. 216 49

The EORTC Lung Cancer Working Party investigates various chemotherapeutic regimens in patients with bronchogenic cancer. Within 12 years our Group has conducted 8 international co-operative studies in patients with non small cell lung cancer. We have demonstrated that Cis-platin was an active agent and its activity increases in association with Etoposide, mainly in limited disease. Lastly, we tested regimens including Carboplatin. This agent does not improve results in terms of objective response. We are now testing regimens including radiotherapy after chemotherapy in limited disease.
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PMID:[Chemotherapy in non-small cell bronchial carcinoma. 12 years' experience in an international cooperative group: EORTC Lung Cancer Working Party]. 217 77

Cell lines derived from human squamous lung carcinoma release large amounts of a soluble glycoprotein into the culture media, having very high molecular weight (greater than 2 X 10(6] and mucin-like properties. A monoclonal antibody called 43-9F has been generated that recognizes a carbohydrate epitope on the glycoconjugate. The epitope is also present on a diverse set of smaller glycoproteins (Mr 50,000-200,000) distributed primarily on the surface of the squamous lung carcinoma cells. A sensitive assay using the 43-9F antibody in a dot blot procedure has been devised that is able to detect an amount of antigen less than that possessed by a single squamous lung carcinoma cell. This assay, and also conventional immunofluorescence and immunohistochemical assay procedures, have been used to screen different normal cells, normal tissues, cancer cells, and tumor biopsy specimens for the antigen. In the normal lung the 43-9F antigen is found only on cells of some of the seromucous glands. In the normal digestive system it is associated in certain organs only with a limited population of mucosal epithelial cells. Other organ systems lack any reactive cells. The cells of most human non-small cell lung carcinomas and their released glycoconjugates have large amounts of the 43-9F epitope, while small cell lung carcinomas and the glycoconjugates released by small cell lung cancer cells lack the epitope. The oligosaccharide recognized by the 43-9F antibody may therefore provide a useful marker to distinguish the different lung carcinomas and for investigating the different cells of origin of these tumors.
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PMID:Glycoproteins distinguishing non-small cell from small cell human lung carcinoma recognized by monoclonal antibody 43-9F. 243 33

Small cell carcinoma of the lung has reportedly been associated with structural abnormalities of the short arm of chromosome 3, but most of the previous studies were done on long-term cultures that involved cell lines. In the current study, we investigated the chromosome abnormalities in specimens from primary lung tumors grown in short-term cultures. Cytogenetic studies were done in 11 patients with small cell carcinoma of the lung, and a chromosomally abnormal clone was observed in each tumor. An abnormality of chromosome 3 was observed in six of these tumors.
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PMID:Cytogenetic studies in 11 patients with small cell carcinoma of the lung. 253 18

This study examined the lymphokine-activated killer (LAK) cell cytotoxicity on monoclonal antibody (MoAb)-bound tumor cells from the human small cell lung carcinoma cell lines H69 and H128. LAK cells were generated from normal peripheral blood mononuclear cells by incubation with interleukin 2 for 3 or more days. Cells from the LAK culture were cytotoxic to natural killer-sensitive (K562, 84% cytotoxicity) and natural killer-resistant (Daudi, 85%; H69 and H128, 69% and 97%, respectively) cell lines, and to freshly excised human lung (49%) and breast (57%) tumors. LAK cytotoxicity to H69 or H128 cells was significantly augmented by target cell preincubation with the small cell lung carcinoma-reactive MoAbs 1096 (increases of up to 271%) or 5023 (up to 223%). SCLC 5023 or 1096 did not enhance LAK cytotoxicity to Daudi cells of lymphoblastoid origin. Pretreatment of LAK cells with an anti-Fc receptor antibody blocked MoAb augmentation by 1096 or 5023 (but not LAK cytotoxicity), suggesting that LAK-MoAb interaction may be mediated by Fc binding. LAK activity coincided with emergence of a large cell [interleukin 2-stimulated large mononuclear leukocyte (LML)] subset expressing the CD16 and NKH-1 surface determinants. Serial immunophenotyping of the LAK cell culture harvested at Days 3, 5, and 7 indicated that the level of LAK cytotoxicity, with or without MoAb augmentation, correlated with frequency of NKH-1-reactive LMLs. These observations support the hypothesis that LAK cytotoxicity is mediated by a NKH-1-reactive LML subpopulation. Antitumor cytotoxicity may be augmented by tumor-reactive MoAbs through Fc binding to this LML subset.
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PMID:Augmentation of lymphokine-activated killer cell cytotoxicity by monoclonal antibodies against human small cell lung carcinoma. 254 33

The detection of bone marrow involvement might be of prognostic value and may influence therapeutic decisions in small cell lung cancer. By unilateral bone marrow aspiration and biopsy, evidence of bone marrow metastases is seen in 15-30% of patients with this disease. Since magnetic resonance imaging of the lower body and immunostaining with monoclonal antibodies have recently been shown to be very sensitive detection methods, we investigated the value of these two techniques in detecting bone marrow involvement in 35 consecutive patients with small cell lung cancer. The results were compared to those obtained with conventional cytohistological analysis. In all cases when cytology and/or bone marrow biopsy were positive, monoclonal antibodies immunostaining and magnetic resonance imaging also detected malignant cells. Furthermore, evidence of bone marrow involvement was shown with magnetic resonance imaging and/or immunostaining in 10 of 26 cases (38%) where routine procedures were unable to detect malignant cells. In one of these 26 patients, magnetic resonance imaging and immunostaining provided the only evidence of metastatic disease. These data suggest that the rate of bone marrow metastases is underestimated by routine procedures. Further investigation is needed to determine whether or not these new non-invasive methods have prognostic value or affect therapeutic choices in small cell lung carcinoma.
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PMID:Bone marrow metastases in small cell lung cancer: detection with magnetic resonance imaging and monoclonal antibodies. 255 88

The cytochrome P450 (CYP) systems catalyze the metabolic transformation of a wide variety of xenobiotics including procarcinogens present in cigarette smoke condensate as well as atmospheric pollutants. The CYP1A1 isoenzyme is of particular interest because it has been implicated as a risk factor in the etiology of lung cancer in heavy cigarette smokers. The identification and expression of the structural CYP1A1 gene in either normal human lung or lung cancer cells has not been reported. Because of its potential significance in human lung cancer, we investigated the expression of the CYP1A1 structural gene in 24 established human lung cancer cell lines including 15 non-small cell (eight adenocarcinomas, three large cell undifferentiated carcinomas, two bronchioloalveolar cell carcinomas, and two squamous cell carcinomas) and nine small cell lung carcinomas. CYP1A1 mRNA was detected in 14 of 15 (93%) of the non-small cell lung carcinoma cell lines examined following 24-hour treatment with benz[a]anthracene (BA) and in nine of 15 (60%) of the non-small cell lines cultured without an inducer in the medium. When the small cell lung cancer lines were evaluated for CYP1A1 gene expression, two of nine (22%) expressed detectable CYP1A1 mRNA in both BA-induced cell cultures and constitutive (control) cultures. A positive correlation was noted between BA-induced CYP1A1 mRNA levels and the corresponding aryl hydrocarbon hydroxylase activity expressed as absolute BA-induced enzyme activity (r = 0.74; P less than .01; n = 24), which further demonstrated that CYP1A1 mRNA expression reflects CYP1A1 enzyme activity in the individual cell lines. These observations represent the first known demonstration of constitutive (non-induced) CYP1A1 gene expression in human cells and suggest altered regulation of the CYP1A1 gene in selected lung cancer cell lines. These human pulmonary carcinoma cell lines, which have documented regulatory defects, could be useful for further identification of the mechanisms associated with CYP1A1 gene regulation.
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PMID:Altered regulation of the cytochrome P4501A1 gene: novel inducer-independent gene expression in pulmonary carcinoma cell lines. 255 30

A 67 year-old man was admitted to our hospital because of cough and sputum. He smoke one pack of cigarettes a day for more than twenty years and the chest X-ray film revealed a mass in the left hilum and left sided pleural effusion. The diagnosis of small carcinoma of the lung (limited disease, T4N1MO, stage 3B) was made by trans-bronchial lung biopsy and radiographic studies. Both chemotherapy (nimustine (ACNU), cyclophosphamide, vincristine, and methotrexate) and radiation therapy was started, however, the chemotherapy was discontinued in July 1987 because of severe anemia. The diagnosis of refractory anemia with excess of blasts in transformation (RAEB in T) was made by bone marrow aspiration and the patient was treated by transfusion (400-800 ml/week). In December 1987 transition to acute myeloblastic leukemia was confirmed by another bone marrow aspiration biopsy and the patient was given low dose cytosine arabinoside (Ara-C). The response was favorable in the beginning but in about two months pancytopenia became refractory and the patient died in June 1988. Clinically there was no sign of local or distal recurrences of lung cancer, and the complete remission of small cell lung cancer (SCLC) was confirmed by autopsy. Survival in SCLC remains poor, so that the choice of treatment is still the primary concern, however, development of other malignancies which include acute leukemia is another problem which should be taken into account when the treatment is extensive.
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PMID:[Acute myeloblastic leukemia development in a patient with small cell lung cancer in complete remission]. 256 Sep 98

In small cell lung carcinoma, one of the short arms of chromosome 3 is typically lost. To investigate chromosome 3 in extrapulmonary small cell carcinoma, we used DNA probes that detect restriction-fragment-length polymorphisms at loci on 3p. These probes were used to study DNA extracted from tumors and normal tissues and/or tumor cell lines from five patients with extrapulmonary small cell cancer. Tumor DNA from four of the five patients with extrapulmonary small cell cancer retained heterozygosity at loci on 3p. Cytogenetic studies of the tumor cell lines established from these four patients showed retention of both short arms of chromosome 3. We conclude that the loss of genetic material from 3p observed in small cell lung cancer is not typical in extrapulmonary small cell cancer.
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PMID:Retention of chromosome 3 in extrapulmonary small cell cancer shown by molecular and cytogenetic studies. 256 43


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