Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The high incidence of gallium 67 accumulation in lung cencer has made radioistope scanning with this agent useful in identifying the extent of cancer locally. However, we investigated the usefulness of whole-body gallium 67 scanning, compared with physical examination, bone, liver and brain scans, and bone marrow aspirate and biopsy, in detecting metastases outside the chest in 47 patients with small cell lung cancer. In each case whole-body scanning with gallium 67 was inferior to the other methods used to detect extrathoracic tumor deposits.
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PMID:Gallium scans for staging small cell lung cancer. 20 25

Despite frequent metastatic involvement of the pancreas at postmortem examination in patients with small cell lung cancer, clinically observed pancreatitis due to metastatic pancreatic tumor rarely has been reported. This communication describes three cases of clinical acute pancreatitis occurring in a consecutive series of 40 patients with oat cell lung cancer. This complication may appear either as the initial manifestation of the neoplasm or during a recrudescent phase of the malignant growth. The diagnosis should be suspected in the presence of the clinical, laboratory, and radiologic features of acute pancreatitis in patients with known small cell carcinoma of the lung, especially if there is evidence of progression of the neoplastic disease elsewhere and no response to conservative medical management. Aggressive treatment with polychemotherapy can produce rapid clinical improvement and useful prolongation of survival.
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PMID:Metastasis-induced acute pancreatitis in small cell bronchogenic carcinoma. 22 Sep 25

A new 111Indium labeled bleomycin complex (111In-BLMC) was prepared and found to be effective for tumor imaging and therapy both in mouse glioma and human small cell lung cancer (SCLC) cells. Chromosome aberrations were studied in human SCLC cells to explore its mechanisms of killing cancer cells. SCLC cells (N417) were exposed to 111In-BLMC, BLM, or 111InCl3 (for control) for 1 hour, treated with colcemid, and chromosomal changes were analyzed. A dramatic increase in chromatic gaps, breaks, chromosome breaks, double minutes, rings, triradii, quadriradii, and chromosome stickiness were observed in the cells treated by 111In-BLMC compared to BLM or 111InCl3. These results indicated that 111In-BLMC has therapeutic potential for combination chemo-radiotherapy of cancer (e.g., by Auger electrons and local energy deposition).
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PMID:Chromosome aberrations of human small cell lung cancer induced by a new 111In-bleomycin complex. 127 17

The potential role of paraneoplastic Cushing's syndrome (CS) was assessed on the clinical course of patients with small cell lung cancer. A retrospective comparison was done of complications and survival rates according to the presence or absence of CS in patients with small cell lung cancer who died within 90 days of initial administration of chemotherapy. The setting was a comprehensive cancer center. Eleven patients with clinical and/or biochemical features of CS were identified from among 90 patients who presented between 1979 and 1989 with previously untreated small cell lung cancer. The group with CS and the control patients were compared in terms of clinicopathologic prognostic factors, treatment, and outcome. Patients with CS were comparable to the control patients in all prognostic factors, including tumor stage and cancer treatment. Eighty-two percent of patients with CS (nine of 11) died within 14 days of initiation of chemotherapy compared with 25% of the control patients (19 of 77). The median survival from initiation of chemotherapy was 12 days for the 11 patients with CS and 27 days for the 77 control patients. In 45% of the patients with CS (five of 11), death was attributed to opportunistic fungal or protozoal infection compared with 8% of control patients (six of 77). Paraneoplastic CS is a previously unrecognized adverse prognostic factor for patients with small cell lung cancer. Those with both small cell lung cancer and CS have severe opportunistic infections soon after the initiation of chemotherapy, leading to clinical deterioration and death before antineoplastic benefit from chemotherapy can be achieved. Biochemical control of CS for at least 1 to 2 weeks before initiation of chemotherapy may ameliorate the poor prognosis.
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PMID:Paraneoplastic Cushing's syndrome as an adverse prognostic factor in patients who die early with small cell lung cancer. 130 10

The survival and recurrence of 37 patients with small cell lung cancer who underwent surgical resection were compared with those of 32 patients who were excluded from surgical resection but received radiotherapy. All but 2 patients received chemotherapy. The number of patients in the resected and nonresected groups in each pretreatment clinical stage were, respectively, as follows: 13 and 2 in stage I, 12 and 7 in stage II, and 12 and 23 in stage IIIa. The main reasons for exclusion from surgical resection were locally advanced disease in 15 patients, avoidance of pneumonectomy in 7, and poor pulmonary function in 5. In stage II, the mean tumor size was larger and there were fewer patients with peripheral tumors in the nonresected group than in the resected group. In stage IIIa, there were significantly more patients with overt N2 disease and central tumors in the nonresected group than in the resected group. The 5-year survival rate of the resected group in stage I was 67.7%. Although the nonresected group in stages II and IIIa had many adverse prognostic factors, there was no statistically significant difference between the survival of the resected and the nonresected groups. With respect to the site of first recurrence, a similar pattern was observed in the two groups in each stage, whereas local disease in stage I was completely controlled by surgical resection. These observations suggest that surgical resection can be considered a modality of treatment in clinical stage I. However, the treatment role of surgical resection in clinical stages II and IIIa, even in selected patients, remains unclear.
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PMID:Comparison between resected and irradiated small cell lung cancer in patients in stages I through IIIa. 130 16

The p53 gene has been implicated as a tumor suppressor gene involved in the pathogenesis of lung cancer. Our previous study revealed that the p53 gene is frequently mutated with a distinct nucleotide substitution pattern in small cell lung cancer specimens in Japanese patients. In this study, we examined 30 primary, resected non-small cell lung cancer samples in Japanese patients using complementary DNA-polymerase chain reaction and sequencing. Mutations changing the p53 coding sequence were found in 14 of 30 tumor samples (47%), while G:C to T:A transversions which are uncommon in other cancers such as colon cancer were the most frequently observed mutations, in agreement with an earlier report on non-small cell lung cancer in American patients. Furthermore, the present study shows for the first time that in univariate and multivariate analyses, the presence of p53 mutations is closely associated with lifetime cigarette consumption.
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PMID:p53 mutations in non-small cell lung cancer in Japan: association between mutations and smoking. 131 70

A combination of cytogenetic and molecular studies has implicated the p21 region of human chromosome 3 as the probable site of a gene the loss of which contributes to the development of small cell lung cancer. We report here the isolation of a gene from this region which is expressed in normal lung tissue and in cell lines derived from a number of different types of tumor, but the expression of which in small cell lung cancer cell lines is undetectable by RNA blot analysis. Although the more sensitive polymerase chain reaction did detect transcripts, a novel quantitative polymerase chain reaction assay showed that their concentration in small cell lung cancer cell lines is less than 3% of that in normal lung.
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PMID:A gene from human chromosome region 3p21 with reduced expression in small cell lung cancer. 131 32

The results of nonprotocol treatment of 232 patients with small cell lung cancer seen by a group of community-based medical oncologists over a 13-year period were evaluated. Factors associated with improved survival also were assessed. The following patient characteristics significantly improved survival: limited stage of disease at diagnosis, treatment of extensive (but not limited) disease with regimens including etoposide and cisplatin, tumor resection, age younger than 70 years, radiation therapy to the chest, and female sex (extensive disease only). Comparison of the data from this study with published results of protocol studies showed similar outcomes.
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PMID:Small cell carcinoma of the lung. Treatment in the community. 131 81

Patterns of drug sensitivities in relation to topoisomerase II gene expression and activity were studied in eight human lung cancer cell lines not selected in vitro for drug resistance. The cytotoxicities of doxorubicin, etoposide, teniposide, cisplatin, camptothecin, and 5-fluorouracil were measured and, remarkably, these unselected cell lines were shown to have a common pattern of multidrug sensitivity, i.e., a multidrug sensitivity phenotype. In fact, drug sensitivities were significantly correlated with each other in the studied cell lines, the correlation being best for the topoisomerase II-targeted agents and cisplatin, less strong with camptothecin, and weak with 5-fluorouracil. Almost 1-log range difference of topoisomerase II gene expression was found in these cell lines, and this was not explained by the cell-doubling time or cell cycle distribution. The level of topoisomerase II gene expression was positively and highly correlated with the cell sensitivity to epipodophyllotoxins, doxorubicin, and cisplatin in seven cell lines. Although weaker, an association was also observed between topoisomerase II gene expression and camptothecin cytotoxicity, while no association was observed with 5-fluorouracil. However, a non-small cell lung cancer cell line with neuroendocrine properties had very low levels of expression of the topoisomerase II gene, despite being highly sensitive to all drugs tested. The levels of topoisomerase I gene expression were not found to be correlated with the cytotoxicity of any drug tested. A specific enzymatic activity assay and a teniposide-stimulated DNA cleavage assay showed that the extent of active topoisomerase II present in nuclear extracts paralleled the level of topoisomerase II gene expression. Furthermore, in addition to the normal transcript, an abnormally sized topoisomerase II message and a rearrangement of the topoisomerase II gene were detected in a poorly sensitive small cell lung cancer cell line. Therefore, low levels of topoisomerase II gene expression, and possibly mutations, may predict a reduced sensitivity of unselected human lung cancer cell lines to several drugs, including agents with a cellular target other than topoisomerase II. It is hypothesized that topoisomerase II might be involved in a common pathway of cell death induced by drugs in tumor cell lines which present a multidrug sensitivity phenotype.
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PMID:Multidrug sensitivity phenotype of human lung cancer cells associated with topoisomerase II expression. 131 95

Mutation of one p53 allele and loss of the normal p53 allele [loss of heterozygosity (LOH)] occur in many tumors including lung cancers. These alterations apparently contribute to development of cancer by interfering with the tumor suppressor activity of p53. We directly sequenced amplified DNA in the mutational hot spots (exons 4-8) of p53 in DNA samples from 40 lung cancers. Most (31 of 40) samples were preselected for LOH in the region of p53. We detected 23 p53 mutations within these exons in 22 lung cancers; no p53 mutations were found in normal tissue of the patients. One-half of the mutations were G to T transversions on the nontranscribed strand, consistent with mutagenesis by tobacco smoke. Mutations of C to A on the nontranscribed strand, which would result from G to T mutations on the transcribed strand, were detected only in one sample. Three of 23 mutations were nonsense mutations; to date, nonsense mutations of p53 have not been reported in lung cancer. Mutation of this p53-coding region was detected in 20 of 27 small cell lung cancer samples, representing a 70% occurrence. Mutation of the p53 gene is apparently very frequent in small cell lung cancers. When LOH in the p53 region could be determined, complete concordance occurred between a sample having both a p53 mutation and LOH in the region of p53 (18 of 18 samples). Twelve samples of lung cancer had LOH in the region of p53, but the samples had no detectable p53 mutations, suggesting either alterations outside the known mutational hot spots of p53 or alterations of another unidentified tumor suppressor gene in the region of p53.
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PMID:p53 mutations in human lung tumors. 131 96


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