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 effect of fetal calf serum (FCS) on in vitro invasion by rat ascites hepatoma cells (AH130) was studied by using the in vitro invasion assay. Although the coculture of the highly invasive clone (MM1) of AH130 cells and the mesothelial cell layer or endothelial cell layer in modified minimum essential medium supplemented with 10% FCS resulted in extensive penetration of the layer by the tumor cells, the omission of FCS resulted in an almost complete elimination of the in vitro invasion. The in vitro invasiveness by human small cell lung cancer cells (OC10) was also remarkably reduced by the omission of FCS from the assay medium, suggesting a requirement of serum for the in vitro tumor cell invasion. When 10% FCS was added to the medium 2 h after the tumor cell seeding in FCS-free invasion assay system, penetration by MM1 cells was observed within an hour. This rate of penetration was almost the same as that when 10% FCS was added at the time of tumor cell seeding. FCS was also required for the penetration of a mesothelial cell monolayer by MM1 cells in a defined growth medium (SFM-101), in which MM1 cells were well maintained. The invasion-inducing activity appears to be independent of the growth-stimulating activity in serum.
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PMID:Serum requirement for in vitro invasion by tumor cells. 190 95

A great deal of information has been accumulated on the synthesis and release of AVP, oxytocin, and their associated neurophysins under normal circumstances. In 1957, Schwartz and Bartter first described SIAD in patients with lung cancer and postulated that the clinical findings were the results of excessive vasopressin secretion. Tumors have been known since 1964 to produce vasopressin, and small cell (oat cell) carcinoma of the lung is by far the most frequent malignant cause of SIAD. The biosynthetic pathway for the synthesis of AVP and its associated neurophysin (and to a lesser extent, oxytocin and its neurophysin) is well described and is similar if not identical to the synthesis of these peptides in the hypothalamus. However, there is little reliable information on the control of peptide synthesis and release by these tumors. The clinical picture of SIAD is well described and occurs in 20% to 40% of patients with SCCL, although up to 88% of patients with extensive SCCL have elevated circulating levels of one or more neurohypophyseal peptides. This information has led to considerable interest in the use of these peptides as tumor markers for the diagnosis, evaluation, and assessment of therapy in these patients. With the recognition of the high incidence of secretion of neurohypophyseal peptides by SCCL, studies have been initiated to determine the value of radioactive vasopressin neurophysin antibodies in localizing tumors that synthesize these peptides. The studies provide potentially useful information in diagnosing and following patients with SCCL and also offer some promise that radiolabeled antineurophysins could eventually be used to treat these patients.
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PMID:Ectopic secretion of neurohypophyseal peptides in patients with malignancy. 193 17

Paraneoplastic syndromes affecting the nervous system are rare and their diagnosis is often difficult when the original cancer is unknown. Recently, high levels of antineuronal antibodies (AB) have been found in serum and CSF of some patients with paraneoplastic syndromes. The anti-Yo AB recognizes 2 proteins of 34 and 62 kd in the cytoplasm of Purkinje cells and in malignant cells of patients suffering from paraneoplastic cerebellar degeneration associated with ovarian and breast cancer. The anti-Hu AB recognizes a 37-40 kd protein in nuclei of neurons and in tumor cells of patients suffering from subacute sensory neuronopathy and encephalomyelitis associated with small cell lung cancer. Other antineuronal AB have been more rarely identified. The presence of high titer of one of these AB in a patient with suspected paraneoplastic syndrome is of great practical interest since it confirms the neurological diagnosis and strongly suggests the location of the primary tumor when the malignancy is unknown. The pathogenetic role of the antineuronal AB is unknown but it is likely that some paraneoplastic syndromes affecting the nervous system are due to an immune reaction against antigens shared by the tumor and the nervous system. To date, no efficient treatment has been found.
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PMID:[Autoimmunity and paraneoplastic neurologic syndromes]. 196 63

Platelet counts were evaluated in 714 patients with advanced non-small cell lung cancer (N-SCLC), small cell carcinoma of the lung (SCCL), and colon cancer entered to a clinical trial. Patients had not received prior chemotherapy. Platelet counts were not different in patients who had received radiation therapy prior to entry to the study. In comparison to the other tumor types, patients with N-SCLC demonstrated an increased prevalence of thrombocytosis (counts greater than 400,000/mm3), higher platelet counts at the time of entry to the study, higher over all mean platelet counts, relative preservation of high platelet levels during disease progression, and no relationship between platelet numbers and the amount of chemotherapy given. By contrast, platelet counts in patients with SCCL were negatively correlated with the absolute amount of cyclophosphamide and adriamycin given, and declined most dramatically with disease progression and death. Platelet numbers did not correlate with fibrinopeptide A or fibrin split product levels suggesting that disseminated intravascular coagulation or fibrinolysis may have had less influence on platelet numbers than certain other factors. By contrast, significant correlations were found for all three tumor types between platelet numbers and other indicators of bone marrow function including anemia, total leukocyte count, and absolute neutrophil count; and the fibrinogen level. Based upon these findings, we postulate that the host response to malignancy, possibly in the form of production of bone marrow-stimulating cytokines, may play a prominent role in regulation of platelet counts in these (and perhaps other) neoplasms, and that a particularly prominent and persistent degree of marrow stimulation exists in patients with N-SCLC.
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PMID:The platelet count in carcinoma of the lung and colon. 196 50

The significance of neuron specific enolase (NSE) was investigated in comparison with other tumor markers (CEA, CT, CA 15-3) used in the diagnosis and treatment monitoring of lung cancer. As previously described, the calcitonin assay proved to have very low sensitivity for small cell lung cancer (SCLC). The serum NSE assay was, however, shown to be a useful diagnostic aid for discrimination between histologically different lung cancers, and therefore this assay may be a valuable tool for treatment monitoring in SCLC patients. CA 15-3, also an unspecific marker, showed similar sensitivity to the NSE assay in SCLC patients, the sensitivity being higher than CEA in non small cell lung cancer (NSCLC).
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PMID:Serum NSE, CEA, CT, CA 15-3 levels in human lung cancer. 196 44

We have examined the possible loss of 3p alleles in lung tumor samples from 28 patients with non-small cell lung cancers (non-SCLC), using tumor adjacent lung tissue from the same patients as controls. Of the 14 patients with squamous cell carcinoma only 2 (14%) displayed constitutional heterozygosity at the 3p locus and the tumors of both of these cases did not show reduction to homozygosity. Of the 14 patients with adenocarcinomas, 50% had constitutional heterozygosity, and two of the tumors displayed a loss of heterozygosity. We have also examined restriction fragment length polymorphisms (RFLPs) of the epidermal growth factor (EGF) receptor gene in 29 non-SCLC tumor samples and in the tumor adjacent lung tissue samples obtained from the same cases. Digestion of the DNA samples with the BstEII enzyme and hybridization to a HER-A64-3 probe revealed four different types of polymorphic patterns. We did not, however, detect significant differences in the specific polymorphic bands between tumor and paired non-tumor lung tissues or between the different types of carcinomas.
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PMID:Restriction fragment length polymorphism of chromosome 3 (3p) and the epidermal growth factor receptor gene in human non-small cell lung carcinomas. 197 22

Small cell lung cancer (SCLC) is the most malignant of the pulmonary neoplasms and is associated with a poor local cellular immune response. 16 patients with non small cell lung cancer (NSCLC) and 11 patients with SCLC underwent bronchoalveolar lavage (BAL) in the lung which harbored the tumor in order to investigate the lymphocyte surface antigens utilizing the immunoperoxidase technique. Analysis of blood lymphocytes was performed in parallel. 8 patients with previous sarcoidosis in complete remission who underwent BAL and 10 normal blood donors served as controls. Among blood lymphocytes the CD3+, CD4+ and CD16+ cell populations were elevated significantly and the T4/T8 ratio was elevated in NSCLC patients, but only CD16+ were augmented in SCLC. Cell populations expressing the activation markers transferrin (TF) receptor, interleukin-2 (IL-2) receptor and the very late antigen VAL-1 were also increased in NSCLC, while SCLC was associated with antigen distributions similar to controls. No differences between the cohorts were seen in the expression of human leukocyte antigen (HLA)-DR. In BAL the population of CD3+ and CD4+ cells were reduced in SCLC and the T4/T8 ratio was diminished in contrast to controls and NSCLC patients, whereas these two latter groups did not differ from each other. The distribution pattern of CD16, TF receptor and IL-2 receptor in the study groups resembled that of cells of the blood stream, but CD16+ natural killer cells were additionally down regulated to control values in SCLC. No differences were seen in the distribution of VLA-1. HLA-DR+ cells were clearly elevated in both cancer groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of local cellular immunity in lung cancer by bronchoalveolar lavage. 197 83

Clearcut progress has been achieved in the treatment of lung cancer in the last decade. While small cell lung cancer has proven a highly chemosensitive tumor, only remissions of relatively short duration are obtained. The high relapse rate is probably due to the reappearance of chemoresistant subclones. In contrast, non small cell lung cancer is often chemoresistant from the outset, a fact which limits the therapeutic possibilities in these tumors. Different forms of chemoresistance are described and potential modalities of circumventing or reversing it are discussed. In recent years, greater insight into molecular mechanisms of tumor formation has been achieved. The role of activation or overexpression of oncogenes has been demonstrated. More recently the role of tumor suppressor gene inactivation has become evident. By means of restriction fragment length polymorphism (RFLP) a combination of gene deletions in various chromosomes has been demonstrated in lung cancer. The pattern of chromosomes involved appears to vary between small cell and non small cell lung cancer. It is to be hoped that these new insights will be translated into new treatment modalities for lung cancer.
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PMID:[Therapy of bronchus carcinoma: therapeutic possibilities and current molecular biology trials]. 197 58

Etoposide (VP-16-213) is an antineoplastic agent with demonstrated efficacy against a broad spectrum of human malignancies, including testicular, germ cell, lung, and other cancers. Etoposide can be synergistic with other agents. As part of combination chemotherapy, etoposide has become a so-called standard in therapies for testicular cancer and small cell lung cancer. Its activity in tumors such as lymphoma and leukemia, as well as solid tumors, identifies etoposide as a highly important chemotherapeutic agent. Cellular and animal models have shown that the cell kill and tumor response depend on both dose and time of exposure. Recent clinical studies again show that dose and schedule of etoposide can have important effects on clinical response to the drug. Further research should now continue: (1) on the use of etoposide as part of initial therapy in several cancers, and (2) in higher doses and prolonged schedules to optimize this agent's potential.
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PMID:Etoposide. Current and future status. 198 22

Over the past 200 years, a bewildering array of chemical, physical, and viral agents has been identified that can cause cancer, but the mechanisms involved are only now becoming clear. In the leukemias and lymphomas, it appears that the activation of cellular oncogenes is important. The genes involved are present in all normal cells and are often associated with cell growth and regulation. When activated, they act in a dominant fashion to cause a cell to express the malignant phenotype. There is increasing evidence that in solid tumors, a more important mechanism may be the loss of a suppressor gene. The classic example is retinoblastoma, in which the retinoblastoma gene has been cloned and is also found to be associated with several other common cancers including sarcomas and small cell lung cancer. It is likely to be one of a family of such genes. It may well be that the activation of one or more oncogenes or the loss of one or more suppressor genes, or both, is required for a tumor to progress from initiation through promotion to a metastasizing malignancy.
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PMID:From chimney sweeps to oncogenes: the quest for the causes of cancer. 201 68


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