Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149925 (small cell lung cancer)
 6,491 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung cancer is the most lethal cancer in the United States, with 143,000 deaths predicted for 1991. The cure rate is extremely low (approximately 13%), in part because the propensity for early spread precludes surgical cure in most patients. Thus, chemotherapy or other systemic therapies are the only way to improve the dismal results. Cisplatin is an active agent in small cell lung cancer (SCLC) and perhaps the most active agent in nonsmall cell lung cancer (NSCLC). The toxicities and inconvenience of cisplatin make it less than ideal for lung cancer therapy. Carboplatin was developed to provide a less toxic, more convenient alternative to cisplatin. The data presented in this review suggest that carboplatin may be substituted for cisplatin in the treatment of extensive-stage SCLC. In limited-stage SCLC, there are insufficient data to determine whether it should replace cisplatin when used simultaneously with chest irradiation and etoposide. It may be substituted for cisplatin in cycles not using irradiation. In NSCLC, carboplatin may be used alone or with etoposide for the palliative management of metastatic disease. Its role in earlier stages of NSCLC needs investigation.
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PMID:Clinical experiences with carboplatin (paraplatin) in lung cancer. 132 16

A 52-year-old man who presented symptoms compatible with paraneoplastic limbic encephalopathy (PLE) was found to have small cell lung cancer. Antineoplastic therapy resulted in complete remission. Because the neuropsychiatric symptoms are potentially reversible, it is important to recognize these symptoms as a manifestation of malignancy so that treatment can be instituted.
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PMID:Paraneoplastic limbic encephalopathy as a nonmetastatic complication of small cell lung cancer. 132 33

To analyze the region upstream of c-myc, a number of novel probes were established. These were generated by chromosomal walking starting from the breakpoint of the chromosomal translocation of the B-cell line 380 and by cloning the breakpoint of the translocation of the Burkitt lymphoma cell line IARC/BL72. Using the newly isolated probes a detailed physical map of 500 kilobases of the region upstream of c-myc was established applying pulsed-field gel electrophoresis. The chromosomal breakpoint of IARC/BL72 cells was mapped to a site 55 kilobases 5' of c-myc. A region 20 kilobases in length and containing the breakpoints of 380, EW36, P3HR-1, and Daudi cells was identified 170-190 kilobases upstream of c-myc. In addition the HPV18 integration site in HeLa cells was located between 340 and 500 kilobases 5' of c-myc. The probes were used to define the c-myc amplification units in Colo320-HSR and HL60 cells as well as in four cases of small cell lung cancer. Evidence is provided that the amplicon of HL60 cells is discontinuously organized.
Cancer Res 1992 Dec 01
PMID:Mapping chromosomal breakpoints of Burkitt's t(8;14) translocations far upstream of c-myc. 133 Feb 96

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.
Int J Cancer 1992 Nov 11
PMID:Expression of carcinoembryonic antigen and related genes in lung and gastrointestinal cancers. 133 Sep 29

The incidence and risk of septic complications in 382 patients treated for small cell lung cancer with combination chemotherapy at a single centre have been analysed. Full protocol doses were employed throughout with no dose reduction after episodes of severe or life-threatening sepsis (SLTS). 50 (13%) patients experienced 66 episodes of SLTS associated with 1978 cycles of chemotherapy (3.2% cycles affected). 20 (5.2%) patients died due to sepsis (SD) of whom only 4 had experienced SLTS with a previous cycle of treatment. The others died as a result of their first septic episode. A model comprising four variables, age (< or = 50 or > 50 years), Karnofsky performance status (KP < or = 50 or > 50), treatment (two- or three-drug regimen) and previous sepsis (SLTS or no SLTS with previous cycles) was found to satisfactorily describe the incidence of SLTS and SD in the study population and once validated in another patient groups this model should allow identification of high-risk individuals before treatment starts. If so, we propose that high-risk patients (age > 50 years, KP < or = 50, treatment with three-drug regimen) receive 50% of protocol doses in the first cycle of treatment with escalation to 75% and eventually 100% doses in subsequent cycles if sepsis does not supervene. Those with one or two risk factors present run a relatively low risk of SLTS or SD and we consider that full-dose chemotherapy should be used throughout in these individuals.
Eur J Cancer 1992
PMID:Predicting septic complications of chemotherapy: an analysis of 382 patients treated for small cell lung cancer without dose reduction after major sepsis. 133 39

Neuron specific enolase (NSE) is widely used as a neuro-endocrine marker. However the presence of NSE in many non-neuroendocrine tissues has raised questions on the specificity of NSE. We have investigated NSE immunoreactivity (NSA-ag), gamma-enolase activity and total enolase activity in small cell lung cancer (SCLC) cell lines. During well-controlled exponential growth comparison of NSE-ag content and gamma-enolase activity with the doubling-time (Td) and NSE-ag content with gamma-enolase and total enolase activity led to a clear distinction of two types of cell line: variant cell lines plus part of the classic cell lines (type I) and the remaining classic cell lines (type II). The distinction was based upon both an abrupt 6-fold increase of gamma-enolase activity and an 18-fold increase of NSE-ag, which for the larger part was enzymatically inactive. Within each group the increase of NSE-ag content was significantly correlated with the increase of gamma-enolase activity and both NSE-ag content and gamma-enolase activity increased linearly with Td. It is concluded that gamma-enolase seems to be associated with the regulation of growth rate and that a compound with the gamma-enolase antigen but without enzyme activity can distinguish two different classes of SCLC cell lines. Furthermore the demonstration that NSE-ag can represent the active enzyme as well as an enzymatically inactive compound may explain why a controversy about neuron- or non-specificity of NSE exists.
Br J Cancer 1992 Dec
PMID:Distinction of two different classes of small-cell lung cancer cell lines by enzymatically inactive neuron-specific enolase. 133 86

Seventy-five patients with locally advanced non small cell lung carcinoma were entered in a phase II study combining chemotherapy (vindesine, lomustine, cisplatin and cyclophosphamide) and radical thoracic radiotherapy delivering a total dose of 60-65 Gy. Patients were regularly assessed by radiological and fiberoptic bronchoscopy examinations in order to evaluate local control. An objective response was observed in 22 patients (29%) after initial chemotherapy (2 complete remissions and 20 partial responses). The complete response rate after the combined schedule was 30%. Toxicity of this combination was acceptable. Median survival was 13.5 months. Actuarial risk of developing distant metastases at 3 years was 60%. However, the main cause of failure was local with 80% of uncontrolled or recurrent thoracic tumor in the first 2 years of follow-up. The present study shows that local control remains a major problem in the management of patients with inoperable non metastatic non small cell lung cancer.
Bull Cancer 1992
PMID:[Combination of chemotherapy (vindesine, lomustine, cisplatin, cyclophosphamide) and thoracic radiotherapy in nonresectable non-small cell bronchial carcinoma: final results of a phase II clinical trial]. 133 40

Subacute paraneoplastic cerebellous degeneration is a rare syndrome which is found in less than 1% of patients with cancer. Small cell cancer of the lung and of the ovary are the two neoplasms most frequently associated to this entity. Two patients with small cell lung cancer who initially had a cerebellous syndrome in which no sign of macroscopic cerebellous lesion could be demonstrated by either computerized tomography or nuclear magnetic resonance of the head are presented. One of the patients was evaluated at autopsy. Both patients were treated with polychemotherapy with which partial response was obtained. Neurologic symptomatology was not alleviated in the first patient with death due to bronchopneumonia at 5.5 months of initiation of the disease, while improvement of the cerebellous paraneoplastic syndrome was achieved in the second patient. The different evolution of subacute paraneoplastic cerebellous degeneration in two patients in whom antibodies were not demonstrated and in whom initial response of the tumor to chemotherapy was achieved may be explained by the second patient having undergone prolonged treatment of 6 cycles suggesting a strict relation ship between the tumor and subacute cerebellous degeneration which, to date, remains unknown.
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PMID:[Subacute paraneoplastic cerebellar degeneration in microcytic carcinoma of the lung. Presentation of 2 cases]. 133 85

Paraneoplastic neurological syndromes are mostly associated with small cell lung cancer. Lambert-Eaton myasthenic syndrome appears to be caused by anti-presynaptic calcium channel antibodies. Calcium channels are also present in the cell membrane of small cell lung cancer, which may trigger the formation of anti-calcium channel antibodies. It is the most convincing argument in support of the auto-immune paraneoplastic theory, which refers to cross-antigenicity. Serum of patients with small cell carcinoma and cancer-associated retinopathy contains immunoglobulins against several antigens in the retinal and tumor cells. Patients with chronic intestinal pseudoobstruction (gastrointestinal neuropathy) associated with small cell lung cancer displayed circulating IgG antibodies reactive with neurons of myenteric plexus (anti-enteric neuronal antibodies). On the other hand, high levels of anti-neuronal antibodies (anti-Hu) have been found in the serum and cerebrospinal fluid of patients suffering from subacute encephalomyelitis (limbic encephalitis, cerebellar degeneration, sensory neuronopathy) associated with small cell lung cancer. The pathogenic role of the anti-neuronal antibody is not well established. Nevertheless, the finding of high titer antineuronal antibody in patients with a suggestive clinical syndrome is of great interest since it confirms the paraneoplastic syndrome and suggests the location of the primary tumor when the cancer is unknown.
Bull Cancer 1992
PMID:[Autoimmunity and cancer: paraneoplastic neurological syndromes associated with small cell cancer]. 133 87

Chronic administration of etoposide over multiple days has proved to be an effective schedule against a variety of neoplasms. The usual duration of etoposide administration is 3 to 5 days. However, recent studies have demonstrated this agent can be administered for up to 21 consecutive days with acceptable toxicity. Studies are currently under way to determine whether more protracted etoposide administration will prove to be more efficacious in the management of selected malignancies. Previous work at our institution has confirmed the activity of protracted administration of single-agent etoposide against small cell lung cancer and non-small cell lung cancer. More recently, we have combined either cisplatin or carboplatin with etoposide given orally for 21 consecutive days in phase II trials in patients with small cell lung cancer and non-small cell lung cancer. The results of these trials are reviewed.
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PMID:Combination chemotherapy with oral etoposide. 133 96


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