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

Survival and histologic subtype were compared in 61 patients with small cell anaplastic lung cancer. Patients with lymphocyte-like (oat cell) and fusiform histologies treated with chemotherapy had longer median survivals than the polygonal and other varieties on the same treatment. Likewise, when detectable disease was confined to the chest and supraclavicular nodes, the patients with lymphocyte-like and fusiform types lived longer. The improved survival in the lymphocyte-like and fusiform categories accounted for most of our improved overall median survival rates with the COPP regimen in small cell lung cancer. Survival in the polygonal and other types was not appreciably different from that seen in non-small cell lung cancer (squamous and adenocarcinoma). It may be possible to refine treatment plans on the basis of cell type so as to further increase survival in small cell anaplastic lung carcinoma.
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PMID:Relationship between survival and histologic type in small cell anaplastic carcinoma of the lung. 22 3

The Ludwig Lung Cancer Group was created in 1977. Participants are from Austria, Denmark, Germany, Norway, Sweden, Switzerland, and Yugoslavia. 400 patients are randomized yearly. The clinical trial I investigating the role of C. parvum intrapleurally as adjuvant therapy in operable non-small cell lung cancer patients has been closed in February 1979 with a total accrual of 475 patients. The average follow-up time for these cases is approximately 8 months. It is early to make any definitive comparisons of the treatment groups (C. parvum versus placebo). However, it is possible to identify a few high-risk patient groups. Preliminary indications are that surgical T- and N-stage, type of resection, histological type of tumor as well as degree of tumor dedifferentiation (central histology review) are prognostic factors with regard to disease-free interval and survival. In the same, the disease-free interval appears to become shorter for patients experiencing high fever after C. parvum administration. The Ludwig Lung Cancer Group offers a sharp tool for investigating the possible role of adjuvant therapies in non-small cell lung cancer and for gathering new information on the biology of the disease.
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PMID:[Postoperative prevention of recurrence with intrapleural Corynebacterium parvum in patients with stage I and II bronchial carcinomas. Ludwig lung cancer study I]. 46 60

Lung cancer arises after a series of morphological changes, which take several years to progress from normal epithelium to invasive cancer. The morphological changes progress from hyperplasia, to metaplasia, to dysplasia, to carcinoma in situ, to invasive cancer and finally to metastatic cancer. Multiple molecular changes have been documented in lung cancers, both small cell (SCLC) and non-small cell (NSCLC) types. The number of changes has been estimated to be in double digits. These changes include activation of dominant oncogenes myc family, (K-ras and neu genes), as well as loss of recessive growth regulatory genes or anti-oncogenes (p53, and RB as well as unidentified gene or genes on chromosome 3). However, cytogenetic and molecular genetic studies indicate that multiple other specific sites of actual or potential DNA loss may be present in lung cancers. Other changes may include development of drug resistance, and production of growth factors and their receptors. It is tempting to associate specific molecular changes with specific morphological changes, as has been attempted in the colon. However, because of the difficulties in serially sampling the respiratory tract, such studies have not been performed to date. Documentation of molecular changes in premalignant lesions and prospective studies of their prognostic effects will be necessary for the design of rational chemoprevention trials.
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PMID:The molecular biology of lung cancer. 130 9

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

Molecular probes for lung cancer have greatly increased the understanding of the biology of this disease and the preneoplastic changes that precede it. They have confirmed and extended the clinical, pathologic, and biologic reasons for the primary division of lung cancers into small cell and non-small cell lung cancer types. Many molecular changes are present in lung cancers and involve dominant oncogenes and recessive growth regulatory genes. Clinical application of these markers will aid diagnosis, classification, and clinical management.
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PMID:Molecular markers for the diagnosis and prognosis of lung cancer. 131 27

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

To evaluate the utility of nuclear morphometry as a prognostic indicator in lung cancer, 5-year follow-up information was obtained in 46 cases of surgically resected Stage I non-small cell lung cancer (NSCLC). Nuclear area, perimeter, major diameter, minor diameter, and nuclear shape factor were determined from representative histologic sections of the tumors with a computer-assisted digitizing system. The morphometric parameters were compared between patients with favorable outcome (Group I: alive with no evidence of disease, n = 17) and those with poor outcome (Group II: dead of disease or with recurrence of disease, n = 29). No significant differences in any of the morphometric parameters were found between tumors in Groups I and II for individual tumor cell types or the combined cases. Failure to demonstrate a correlation between morphometric parameters and prognosis in Stage I NSCLC indicates that future efforts to determine objective prognostic factors should concentrate on other variables, such as specific genetic abnormalities.
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PMID:Absence of correlation between nuclear morphometry and survival in stage I non-small cell lung carcinoma. 131 90

It is known that interleukin-2 (IL-2) plays an important role in the activation of host antitumor immune response. In addition to IL-2 cell surface receptor, a soluble form of IL-2 receptor (SIL-2R) may be released in the blood and potentially be involved in the regulation of IL-2 availability. High SIL-2R levels have been found in patients with lung cancer. The current study evaluated the influence of changes in SIL-2R serum levels during the perioperative period on early relapse rate in patients with operable non-small cell lung cancer. The study included 60 patients (epidermoid carcinoma, 33; adenocarcinoma, 27). Serum levels of SIL-2R were measured with an enzyme immunoassay before surgery and 7 and 30 days after surgery. A surgery-induced increase in SIL-2R levels was seen 7 days after surgery in 38 of 60 patients. On the 30th day after surgery, SIL-2R values were lower than the preoperative values in 32 patients (Group A) or still greater in the other 28 patients (Group B). After a median follow-up of 10 months, relapse occurred in 19 of 60 patients. The relapse rate was significantly higher in Group B than in Group A patients (16 of 28 versus 3 of 32, respectively; P less than 0.001). This difference also was significant in relation to histotype and node status. This study shows that the persistence of increased SIL-2R levels in the postoperative period is associated with a higher early relapse rate in patients with operable non-small cell lung cancer. The impact of SIL-2R levels on relapse suggests that host immune defenses may influence the clinical course of patients with lung cancer. Therefore, the evaluation of SIL-2R in the perioperative period may represent a new prognostic biologic factor in operable non-small cell lung cancer.
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PMID:Postoperative increase in soluble interleukin-2 receptor serum levels as predictor for early recurrence in non-small cell lung carcinoma. 131 91

Between August 1985 and September 1989, 62 patients with medically inoperable or surgically unresectable, non-small cell lung cancer were treated with both external beam radiotherapy and high dose rate bronchial brachytherapy. Treatment consisted of external beam radiotherapy (5000-6000 cGy in 5-6 1/2 weeks) and weekly high dose rate bronchial brachytherapy (three to five fractions, 500 cGy at 1 cm from the source) delivered either concurrently or sequentially. Median survival for all patients was 13 months (m). Stage I and Stage IIIA-B patients had median survivals of 20 m and 10 m, respectively. Patients without nodal disease (No) had a significantly longer median survival compared to patients with regional node metastases (N1-3), 17 m versus 9 m. A total of 54 patients were evaluable for local tumor control analysis. Local tumor control was achieved in six of eight patients who had a normal pre-treatment radiograph. Patients with measurable tumor on the pre-treatment radiograph and negative regional nodes had local tumor control in eight of twenty-two (36%) cases. In patients with regional lymphadenopathy, loco-regional tumor control was achieved in four of eight cases. Additionally, there were sixteen patients with non-measurable tumor due to associated effusion, atelectasis and/or infiltrate. Four of these (25%) were considered to have local tumor control. Of 60 evaluable patients, there were nine occurrences of fatal hemorrhage, one of whom was disease-free (NED) at autopsy. The remaining eight patients had either clinical or pathological evidence of recurrent or persistent tumor. Patients who had follow up bronchoscopies were found to have varying degrees of concentric narrowing in the treated areas. One such patient had total lung collapse with no evidence of tumor. While this form of treatment may yield high local control rates in earlier stages, this study suggests the potential risk of fatal complication. Additional studies are warranted to further investigate the use of this modality in the treatment of lung cancer.
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PMID:Treatment of non-small cell lung cancer with external beam radiotherapy and high dose rate brachytherapy. 157 23

We studied the effects of Cepharanthin (CEP) on bone marrow suppression induced by chemotherapy in 18 primary lung cancer patients (14 NSCLC, 4 SCLC). NSCLC patients received IP (IFM+CDDP) therapy and SCLC patients received ION (IFM+VCR+ACNU) therapy. For the control, we chose the first course and we administered CEP (1 mg/kg) during the second course. The rate of leukopenia and neutropenia was significantly lower during the CEP course than during the control (p less than 0.01). The recovery rate (at 3 weeks) of leukopenia and neutropenia was significantly higher during the CEP course than during the control (p less than 0.05). But, obvious effects of CEP for lymphopenia and thrombocytopenia were not obtained. Side effects by CEP were not observed in this study. These data suggest that the large dose of CEP contributes to the prevention of leukopenia, especially neutropenia, in patients who receive a sufficient amount of anticancer drugs.
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PMID:[Effects of cepharanthin on leukopenia and thrombocytopenia induced by chemotherapy in lung cancer patients]. 131 1


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