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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relation between tumor characteristics, irradiation technique, local tumor control and survival was retrospectively studied in 323 patients with non-small cell lung cancer who started radical radiotherapy in 1974-1981. At that time three non-randomized different fractionation schedules were used: 16 x 3.25 Gy, total dose 52 Gy, 3 fractions/week (schedule 1), 11 x 4 Gy, total dose 44 Gy, 2 fractions/week (schedule 2) and 25 x 2 Gy, total dose 50 Gy, 5 fractions/week (schedule 3). The highest survival rates were observed in the patient group treated according to schedule 2. The 2-year survival rate was 30% compared with 18% and 6% in the patients treated according to schedule 1 and 3 respectively. However, this can at least partly be explained by patient selection. A correlation between size of the tumor, target volume and survival was observed: the larger the tumor, the poorer the survival. Pleural effusion showed to be an unfavorable prognostic factor. The prognosis of inoperable lung cancer on the whole remained poor: the 1-year survival rate was 43% and 2-year survival rate 16%. Only 3% of the patients lived at least five years.
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PMID:Radical radiotherapy of inoperable non-small cell lung cancer. Irradiation techniques and tumor characteristics in relation to local control and survival. 132 72

In unresectable non-small cell lung cancer (NSCLC) with a patent mainstem bronchus, some studies of obstructive tumors, showed (1) a poor role for irradiation in obtaining efficient debulking and (2) an interest in preliminary laser treatment in these patients. Cryotherapy is another method to obtain debulking. Moreover, several studies showed that cryotherapy would increase the radiosensitivity of a tumor. We performed a preliminary protocol combining successively initial cryotherapy followed by irradiation in inoperable NSCLC (either for local or functional contraindications). Thirty-eight patients were included and treated first by cryotherapy performed under general anesthesia and then with external irradiation in a curative intent. The efficiency of cryotherapy assessed on bronchoscopy was found to be volume-efficient (VE) in 26 of the 38 patients and non-volume-efficient (NVE) in the other 12 patients. After irradiation in the VE group, 17 of the 26 patients had no bronchial residual tumor (NRT). In contrast, all of the patients in the NVE group had a bronchial residual tumor (RT). Survival in the VE group (median, 397 days) was significantly higher than the survival of the NVE group (median, 144 days). Survival was found to be independent of the surgical contraindication (local or functional). The best survival was associated both with the efficiency of the initial debulking (VE) by cryotherapy and with the local control (NRT) induced by the irradiation (median, 560 days). Local control was obtained in 65 percent (17/26) of the cases in the VE group and was never observed in the NVE group. In our study the VE group's local control is better than the 35 percent usually reported after irradiation alone. These results argue for the efficient potentiation of irradiation by cryotherapy.
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PMID:Initial combined cryotherapy and irradiation for unresectable non-small cell lung cancer. Preliminary results. 133 Apr 47

Carcinoembryonic antigen (CEA), a tumor marker for lung cancers of small cell (SCLC) and non-small cell (NSCLC) types, belongs in a multigene family which includes non-specific cross-reacting antigen (NCA) and biliary glycoprotein 1 (BGP). We used specific cDNA probes and a CEA immunoassay to determine the pattern of expression in normal and malignant lung and gastrointestinal (GI) tissues. Normal lung contained high amounts of NCA and a low concentration of CEA. All 3 genes were expressed discordantly in lung tumors and cell lines. In contrast, all three genes were expressed in most G1 tumor cell lines. In both lung and colorectal cell lines expression of NCA RNA was relatively high, while BGP RNA was relatively low, and the median concentrations of CEA were greater than in corresponding non-malignant tissues. While CEA protein concentrations in lung cell lines were similar to those present in G1 cell lines, the ratio of NCA:CEA RNA was significantly higher in lung cancer lines than in colorectal lines. Thus, NCA constitutes most of the "CEA-like" immunoreactivity previously described in lung cancers. There was excellent concordance between expression of CEA RNA and CEA protein, as well as between concentrations of CEA protein in cell line pellets and supernatant fluids. Of interest, significantly higher rates of CEA expression were present in lung cancers expressing neuroendocrine (NE) markers. The association between CEA expression and NE cell properties is intriguing and may prove to be of clinical interest.
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PMID:Expression of carcinoembryonic antigen and related genes in lung and gastrointestinal cancers. 133 Sep 29

CPT-11 and Topotecan are a new semisynthetic derivative of CPT, and have been shown to inhibit DNA topoisomerase I and to have a strong antitumor activity with low toxicity against murine tumor. On the other hard, the new antitumor compounds, NC-190 and IST-622 have been shown to inhibit DNA topoisomerase II, and the clinical study are currently under progress. A phase II study of CPT-11 demonstrated that CPT-11 was a very active agent which a acceptable toxicities against patient with advanced non-small cell lung cancer and small cell lung cancer.
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PMID:[DNA topoisomerase inhibitor]. 133 23

The expression of transforming growth factor-alpha (TGF alpha) was assessed by immunohistochemical staining in 52 human lung tumor samples. All of the 8 small cell lung cancers were negative whereas all of the 18 adenocarcinomas and 23 of the 26 squamous cell carcinomas showed positive immunoreaction to TGF alpha. Distribution of TGF alpha stainings in the squamous cell carcinomas was weaker and more heterogeneous as compared to the adenocarcinomas. Ultrastructural localization of TGF alpha in the squamous cell lung carcinomas by indirect immunogold staining revealed that TGF alpha is present in the cytoplasm as well as the cell membrane but not in the nucleus. This suggests that the lung cancer cells are not only the producer of TGF alpha, but also the target cells of the TGF alpha action. The expression of TGF alpha in lung tumors may be useful diagnostically in differentiating small cell lung cancer from non-small cell lung cancer and may also be important in the study of the biological properties of primary lung cancers.
Tumour Biol 1992
PMID:Immunohistochemical study of transforming growth factor-alpha in human lung cancers. 133 97

Using single-strand conformation polymorphism we have found two polymorphic sites, AAC to AAT at codon 511 (exon 12) and GCT to GCG at codon 708 (exon 15), in the MCC gene. These sites and an RsaI polymorphic site in APC allowed us to study 23 human small cell lung cancer (SCLC) and 7 non-small cell lung cancer samples for allele loss. Of the 23 SCLC samples, 21 (91%) were informative for one or more of these markers, and we found allele loss in more than 80% (17 of 21). In non-small cell lung cancer samples, 5 of 7 (71%) were informative, and reduction or loss of one allele was found in 2 of 5 (40%). Seven cases were informative for both genes, loss of heterozygosity occurred for both genes in five, one retained heterozygosity for both, and one SCLC had loss of heterozygosity for APC but not for MCC. We conclude that loss of heterozygosity occurs frequently for MCC and APC in lung cancer of all histological types and is very frequent in SCLC. This suggests the presence of tumor suppressor gene(s) in the MCC/APC region of 5q21 involved in human lung cancer.
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PMID:Polymorphic sites within the MCC and APC loci reveal very frequent loss of heterozygosity in human small cell lung cancer. 134 17

Frequent loss of heterozygosity at chromosomal loci in a specific tumor type may indicate the presence of a tumor suppressor gene. We have examined loss of heterozygosity on chromosome 8p in paired tumor and constitutional DNA from 346 patients representing seven different types of human cancer. Frequent allelic losses were observed in hepatocellular carcinoma (22 of 46 cases, 47.8%), in colorectal cancer (12 of 26, 46.2%), and in non-small cell lung cancer (14 of 35, 40.0%), in contrast to low frequencies detected in breast cancer (5 of 56, 8.9%) and renal cell carcinoma (2 of 27, 7.4%). Ovarian cancer and gastric cancer showed intermediate frequencies of 33.3% and 22.2%. Subsequent analysis of 120 hepatocellular carcinomas and 94 colorectal cancers with five polymorphic markers along the short arm of chromosome 8 defined commonly deleted regions within the same chromosomal interval, 8p23. 1-8p21.3, suggesting that one or more tumor suppressor genes for both cancers may be present in that region.
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PMID:Frequent loss of heterozygosity for loci on chromosome 8p in hepatocellular carcinoma, colorectal cancer, and lung cancer. 135 16

The rapid pace of research in the genetics of human cancer will predictably render any review of the topic out of date by the time of its publication. Prospects for the near future will likely include the identification of a chromosome 3p gene(s) linked with the development of familial renal cancer and, perhaps, also lung cancer. In addition, the availability from the Human Genome Project of an increasing number of well-characterized markers will accelerate the search for additional human recessive oncogenes. Many questions still remain about the etiology of lung cancer and how to apply this information for patient care. For example, identification of the cell of origin for small cell and non-small cell lung cancers will facilitate our understanding of the development of these tumors and improve the possibilities for future preventive strategies. In addition, we now realize that these cancers arise from the sequential accumulation of multiple genetic mutations (Table 3; Fig. 1). Therefore, a central question is which of these targets are essential for the process of carcinogenesis, and whether there is a critical temporal order for this process with a defined premalignant phase in a discrete field of bronchial tissue. In addition, are there genetically inherited susceptibilities to the development of lung cancer (either directly or via variabilities in carcinogen metabolism) that could be accurately identified in the general population? Finally, is there a rate-limiting mutation and will the genetic correction of this defect suffice to restore growth regulation, or will the replacement of multiple gene products be required for tumor suppression? We are already witnessing the beginnings of the use of molecular diagnostic markers as a research tool for assigning prognostic information. The expression of neuroendocrine markers in non-small cell lung cancer has recently been applied as an indicator of the potential response to combination chemotherapy [15]. Similar methods are being applied to the expression of tumor suppressor genes or the presence of somatic mutations in dominant oncogenes such as the ras gene. However, the clinical benefit of this prognostic information with currently available treatment programs is still uncertain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oncogenes in human lung cancer. 136 67

A murine monoclonal antibody designated 4B5 was raised against the high molecular weight fraction of pooled sputum from patients with non-small cell lung cancer (NSCLC). Immunohistochemical staining indicated that 4B5 binds to histologically normal bronchial epithelium distant from tumor in 72% (39 of 54) of patients with NSCLC, but it binds to the primary cancer in only 13% (7 of 54) of the same patients. The antibody reacted less intensely with the bronchial epithelium in 16.6% (3 of 18) of autopsied patients without significant lung disease. The antigen recognized by 4B5 is a high molecular weight glycoprotein of more than 400 kilodaltons, judged by gel filtration and sodium dodecyl sulfate-polyacrylamide gel electrophoresis and western blot analysis. Antigenic activity persisted after heating and resisted treatment with neuraminidase, but it was destroyed using protease and periodate. Multiple epitopes were present on each molecule recognized by 4B5. The determinants recognized by this antibody deserve additional study as possible markers of premalignant change in patients with NSCLC.
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PMID:Detection of a novel marker in the bronchial secretions of patients with non-small cell lung cancer using the 4B5 monoclonal antibody. 137 28

The distribution of O6-methylguanine-DNA methyltransferase (MGMT) activity in extracts of tumors from 74 patients was measured. The results demonstrated that there was considerable variation of MGMT activity in different human tumor tissues as well as in different individuals. The mean values (X +/- SD, pmol/mg of protein) in breast cancer, stomach cancer, small cell lung cancer, non-small cell lung cancer, renal cell carcinoma, esophageal carcinoma, brain tumors, colon carcinoma and malignant melanoma were 1.071 +/- 0.374 (9), 0.515 +/- 0.107 (5), 0.509 +/- 0.251 (5), 0.461 +/- 0.227 (24), 0.329 +/- 0.246 (5), 0.273 +/- 0.376 (5), 0.244 +/- 0.175 (14), 0.242 +/- 0.308 (5) and 0.201 +/- 0.161 (2) respectively. It was notable that six samples (1/24 non-small cell lung cancer, 3/5 esophageal carcinoma, 1/14 brain tumors and 1/5 colon carcinoma) did not have any detectable level of MGMT activity. Activity of glutamine pyruvic transaminase (GPT) was also measured in the same extracts used for the assay of MGMT activity. The activity of GPT in these samples with undetectable level of MGMT activity was similar to those with significant MGMT activity. These results further strengthen the assumption that a certain fraction of human tumors are Mer-.
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PMID:O6-methylguanine-DNA methyltransferase activity in human tumors. 139 31


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