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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical decision making is based on results from qualitative and quantitative information. To provide quantitative data, various laboratory variables are widely used in the clinical evaluation of patients with small-cell lung cancer (SCLC). The tumour marker serum neuron-specific enolase (S-NSE) and the routine laboratory parameter serum lactate dehydrogenase (S-LDH) have been investigated, mostly separately. Few studies have compared their importance in SCLC, especially in progressive disease (PD). The present investigation was undertaken to evaluate S-NSE for diagnostic efficacy in PD and compare it with S-LDH. In 27 patients in a treatment trial of SCLC, regular follow-up laboratory values were prospectively obtained. Chemotherapy was given according to trial protocols, and all clinical evaluation followed the WHO recommendations. At re-evaluation all but three values had normalised (two S-NSE, one S-LDH). S-NSE at progression was increased in 93% of the patients and S-LDH in 59%. The efficacy of S-NSE to discriminate between response and PD was superior to S-LDH (0.92 vs 0.70). There was no additive effect of the two parameters in prediction of PD, and the discriminating power was higher for S-NSE than for S-LDH (P < 0.0008). The disease status-related marker increments in relation to upper reference limits, i.e. the signal-noise relation, were higher for S-NSE than for S-LD. Both of the markers carry information on PD. S-NSE is, however, clearly superior to S-LDH in reflecting disease status during therapy. This prompts us to conclude that S-NSE should replace S-LDH as prognostic factor and disease activity monitor in SCLC.
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PMID:Serum neuron-specific enolase (S-NSE) in progressive small-cell lung cancer (SCLC). 791 35

The study set out to determine the rate of long-term survivors (LTS) in patients treated with platinum-containing chemotherapy for advanced non-small cell lung cancer (NSCLC), to identify prognostic factors predicting long-term survival (> or = 2 years) and to report the LTS natural history. Eligible patients with advanced NSCLC treated by chemotherapy in one of seven trials conducted by the European Lung Cancer Working Party from December 1980 to August 1991 were included. All patients received cisplatin and/or carboplatin. Of these, 1052 patients were eligible and 24 variables were analysed as potential prognostic factors. Actuarial 2-year and 5-year survival rates were, respectively, 7.4 and 1.8%. All patients surviving for > or = 5 years had limited disease and were treated by complementary chest irradiation and/or surgery. Univariate prognostic factor analysis for LTS identified as significant no major weight loss, limited disease, no liver metastases, normal white blood cells and neutrophils and normal lactic dehydrogenase levels. By multivariate analysis, the only significant factor was limited disease. Objective response to chemotherapy was also found to be, as disease extent, a highly significant predictor for LTS. Thus, the two best prognostic factors for LTS were non-metastatic disease and response to chemotherapy.
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PMID:Long-term survival after chemotherapy containing platinum derivatives in patients with advanced unresectable non-small cell lung cancer. European Lung Cancer Working Party. 799 23

Disease extent, performance status (PS), and serum lactate dehydrogenase (LDH) are the most important prognostic factors in both inoperable non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Hyponatremia and serum alkaline phosphatase play an additional role in SCLC. Many different stratification algorithms have been proposed in SCLC but a general consensus cannot be achieved before it is decided whether stage of disease should rank above or be included in an algorithm, along with other prognostic factors.
Lung Cancer 1994 Mar
PMID:Factors confounding evaluation of treatment effect in lung cancer. 808 32

The influence of pretreatment serum neuron-specific enolase (S-NSE) in addition to more conventional prognostic factors on survival duration in small-cell lung cancer (SCLC) was investigated in 770 patients from nine centres in six countries. The other variables included stage of disease, performance status (PS), age, sex, serum lactate dehydrogenase (S-LDH), serum alkaline phosphatase (S-AP), and serum carcinoembryonic antigen (S-CEA). Increased values of S-NSE (> 12.5 micrograms-1 l) were observed in 81% of the patients, whereas S-LDH, S-AP and S-CEA were elevated in only half of the patients or less. Multivariable analysis by Cox's proportional hazard model disclosed S-NSE as the most powerful prognostic factor followed by poor PS and extensive stage disease. If PS was ignored, S-LDH came up as a significant prognostic factor. S-AP, S-CEA, age and sex had no significant influence on the prognosis. The three prognostic factors, S-NSE, PS and stage of disease, enabled establishment of a prognostic index (PI) based on a simple algorithm PI = zNSE + z(stage) + 2zPS. This segregated the patients into four groups with clearly different prognosis. The median survival and 95% confidence intervals of the four groups were: 468 days (540-408), 362 days (405-328), 256 days (270-241) and 125 days (179-58). Based on the present results we recommend S-NSE and PS, in addition to stage, for prognostic stratification in treatment trials on SCLC.
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PMID:Serum neuron-specific enolase (S-NSE) and the prognosis in small-cell lung cancer (SCLC): a combined multivariable analysis on data from nine centres. 869 66

The authors studied the influence on survival of 21 clinical, anatomical, haematological and biochemical factors evaluated, at diagnosis, of 411 patients (pts) with advanced Non Small Cell Lung Cancer (NSCLC) followed in our department between 1984 and 1990. Most of the patients were male (347--84.4%) and only 64 (15.6%) were females. Median age was 62 years, but was slightly higher in females. Only 34 patients were aged under 45 years. Squamous cell carcinoma (215 pts--52%) and adenocarcinoma (152 pts--37%) were the most frequent histologic types. Performance status was poor--only 103 (25%) continued active; 120 (29%) spent at least half of the time in bed; 188 (46%) were severely limited. After staging, 179 (44%) presented locally advanced disease (stage IIIB) and 232 (56%) metastatic dissemination (stage IV). Therapy was defined by the oncologic group according to individual characteristics and based on clinical grounds. Anti-neoplastic therapy was performed in 225 (55%), chemotherapy alone in 121 (30%), radiation therapy alone in 67 (16%), and sequential combined treatment (chemotherapy and thoracic radiation) in 37 (9%). Until 1987, the main chemotherapy regimen was MACC (Metrotrexate + Adriamycine + Cyclophosphamide + Lomustin), afterwards VP(M) (Cisplatin + Vimblastin + Mitomycine). Radiation therapy was performed using Co60, 2 Gy/day, 5 days a week, for 4 weeks (approximately 45 Gy total). The response rate was poor--four complete responses (2%), 42 (19%) partial responses. The overall median survival was 4.3 months and only 5% of patients were alive after 18 months of follow up. Prognostic importance of each characteristic studied was initially done by unifactorial analysis, followed by multifactorial analysis according to two methods: Cox proportional hazards model and recursive partitioning amalgamation--RECPAM. Regardless of the method used, the main determinants of survival were found to be performance status (Zubrod), weight loss and serum albumin. Other factors such as the staging (presence or absence of metastasis), lymphocytes, lactic dehydrogenase, and hoarseness were also significant. It is noteworthy that age and histological type were irrelevant; sex and hoarseness only proved important when integrated within a multifactorial model. The overall prognostic evaluation and therapeutic decision of advanced NSCLC patients could be improved by combining the prognostic value of TNM with that of performance status, weight loss and serum albumin. These prognostic guidelines must be taken into account when designing new clinical trials.
Lung Cancer 1995 Dec
PMID:Survival predictors in advanced non-small cell lung cancer. 871 65

We examined two recently described cytokeratin markers, CYFRA 21-1 (cytokeratin fragment recognized by KS 19-1 and BM 19-21 antibodies) and TPS (specific M3 epitope of the tissue polypeptide antigen), in 405 lung cancer patients (91 small-cell and 314 non-small-cell lung cancers) and 59 patients presenting with nonmalignant pulmonary disease. Sensitivity-specificity relationship, as analyzed by receiver operating characteristic curves, demonstrated a higher accuracy of CYFRA 21-1 in comparison with TPS in both small-cell and non-small-cell lung cancers. Thresholds of 3.6 ng/ml and 140 U/L for CYFRA 21-1 and TPS respectively gave a 90% to 95% specificity. Sensitivity of CYFRA 21-1 was the highest in squamous-cell carcinomas (0.61) and the lowest in small-cell lung cancers (0.36), whereas sensitivity of TPS did not vary significantly according to histology (overall sensitivity, 0.40). In non-small-cell lung cancers, both serum CYFRA 21-1 and serum TPS distributions varied significantly according to Mountain's stage of the disease, nodal status, tumor status, and performance status, inasmuch as the worse each above-mentioned variable became, the higher the median and interquartile serum marker level was. Neither CYFRA 21-1 nor TPS was able to accurately discriminate between stage IIIa (marginally resectable) and stage IIIb (unresectable) non-small-cell lung cancers, however. In both small-cell and non-small-cell lung cancers, univariate survival analyses demonstrated that either a CYFRA 21-1 level over 3.6 ng/ml or a TPS level over 140 U/L significantly indicated a poor survival rate. In the whole population, taking into account other significant variables, Cox's model analysis demonstrated that a poor performance index, an advanced stage of the disease, the presence of metastases, elevated serum lactate dehydrogenase, and high serum CYFRA 21-1 (odds ratio, 1.74; 95% confidence interval, [1.33-2.27] were independent prognostic variables. We concluded that CYFRA 21-1 is a significant determinant of survival. Other applications of cytokeratin markers in lung cancer are still limited.
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PMID:Cytokeratins as serum markers in lung cancer: a comparison of CYFRA 21-1 and TPS. 881 Jun 12

Epidemiological evidence suggests that cadmium (Cd) exposure causes pulmonary damage such as emphysema and lung cancer. However, relatively little is known about the mechanisms involved in Cd pulmonary toxicity. In the present study, the effects of Cd exposure on human fetal lung fibroblasts (MRC-5 cells) were evaluated by determination of lipid peroxidation, intra-cellular production of reactive oxygen species (ROS), and changes of mitochondrial membrane potential. A time- and dose-dependent increase of both lactate dehydrogenase leakage and malondialdehyde formation was observed in Cd-treated cells. A close correlation between these two events suggests that lipid peroxidation may be one of the main pathways causing its cytotoxicity. It was also noted that Cd-induced cell injury and lipid peroxidation were inhibited by catalase and superoxide dismutase, two antioxidant enzymes. By using the fluorescent probe 2',7'-dichlorofluorescin diacetate, a significant increase of ROS production in Cd-treated MRC-5 cells was detected. The inhibition of dichlorofluorescein fluorescence by catalase, not superoxide dismutase, suggests that hydrogen peroxide is the main ROS involved. Moreover, the significant dose-dependent changes of mitochondrial membrane potential in Cd-treated MRC-5 cells, demonstrated by increased fluorescence of rhodamine 123 examined using a laser-scanning confocal microscope, also indicate the involvement of mitochondrial damage in Cd cytotoxicity. These findings provide in vitro evidence that Cd causes oxidative cellular damage in human fetal lung fibroblasts, which may be closely associated with the pulmonary toxicity of Cd.
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PMID:Cadmium-induced oxidative cellular damage in human fetal lung fibroblasts (MRC-5 cells). 929 17

In order to elucidate factors influencing the prognosis of small-cell lung cancer (SCLC), we reviewed the records of 253 patients with SCLC and evaluated 20 pretreatment prognostic factors by univariate analysis and Cox's multiple regression analysis. Recursive partitioning and amalgamation (RPA) was employed to identify subgroups with similar survival rates. Cox's multiple regression analysis identified five significant factors: extent of disease, number of metastatic sites, serum albumin, serum lactate dehydrogenase, and presence of weight loss. Among these, extent of disease was the most influential factor. RPA analysis revealed three subgroups predicting significantly different prognoses. The median survival time and 3-year survival rate were 18.4 months and 20.6%, respectively for the good-risk group (limited disease without weight loss), 13.5 months and 9.1%, respectively for the intermediate-risk group (limited disease with weight loss or extensive disease with less than two metastatic sites), and 9.2 months and 0%, respectively for the poor-risk group (extensive disease with two or more metastatic sites). These results will be useful for development of new staging system or subsequent stratification for randomized trials.
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PMID:Prognostic factors of small-cell lung cancer in Okayama Lung Cancer Study Group Trials. 1035 26

Based on an increased frequency of early death (death within the first treatment cycle) in our two latest randomized trials of combination chemotherapy in small-cell lung cancer (SCLC), we wanted to identify patients at risk of early non-toxic death (ENTD) and early toxic death (ETD). Data were stored in a database and logistic regression analyses were performed to identify predictive factors for early death. During the first cycle, 118 out of 937 patients (12.6%) died. In 38 patients (4%), the cause of death was sepsis. Significant risk factors were age, performance status (PS), lactate dehydrogenase (LDH) and treatment with epipodophyllotoxins and platinum in the first cycle (EP). Risk factors for ENTD were age, PS and LDH. Extensive stage had a hazard ratio of 1.9 (P = 0.07). Risk factors for ETD were EP, PS and LDH, whereas age and stage were not. For EP, the hazard ratio was as high as 6.7 (P = 0.0001). We introduced a simple prognostic algorithm including performance status, LDH and age. Using a prognostic algorithm to exclude poor-risk patients from trials, we could minimize early death, improve long-term survival and increase the survival differences between different regimens. We suggest that other groups evaluate our algorithm and exclude poor prognosis patients from trials of dose intensification.
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PMID:Early death during chemotherapy in patients with small-cell lung cancer: derivation of a prognostic index for toxic death and progression. 1002 22

Patients recruited for phase I trials are considered to have a poor prognosis, because the majority of them have already been heavily treated. We examined the survival of lung cancer patients admitted to phase I trials and treated with single new investigational chemotherapeutic agents or new investigational biological modifiers in the Division of Thoracic Oncology of the National Cancer Center Hospital between 1987 and 1993. Eighty-two patients had lung cancer among 121 patients registered in phase I trials. To identify prognostic factors, univariate and multivariate analyses were conducted. Median survival time (MST) from beginning of the phase I trial was 9.4 months, and the response rate was 4.2%. There were 11 (13.4%) early deaths within 3 months, and the death of 1 (1.2%) patient was treatment-related. Univariate analysis demonstrated that performance status, body weight loss, chemotherapy regimen, liver metastasis, number of metastatic sites, prior chemotherapy, and serum levels of hemoglobin, and lactate dehydrogenase were significant prognostic factors for survival. Among these factors, performance status >1, body weight loss >/=10%, and number of the metastatic sites >1 were selected as risk factors in multivariate regression analysis. The low-risk group, which included the 36 patients with no risk factors, had an MST of 13.9 months and an early death rate of 0%. The intermediate-risk group of 31 patients was characterized by patient having only one risk factor. These patients had an MST of 7.6 months and an early death rate of 13%. The high-risk group of 9 patients had two or three risk factors. These patients had an MST of only 1.5 months and a high early death rate of 78%. We conclude that the MST of lung cancer patients who participated in the phase I trials was 9.4 months. Therefore, it appears reasonable to have admitted these patients to the phase I trials. However, as the patients in the high-risk group had a poor outcome and high early death rate, they should not have been admitted to phase I trials. This prognostic model should be validated in other patient series.
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PMID:Survival and prognostic factors in lung cancer patients treated in phase I trials: Japanese experience. 1049 56


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