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

A comparative radioimmunologic study of changes in the ratio of calcitonin and parathyroid hormone secretion was carried out in healthy controls (young and older than 40 years), patients with benign tumors, inflammatory processes and malignancies of the stomach, kidney, breast, prostate and lung. A significant increase in the "calcitonin index" (ratio of molar concentrations of calcitonin and parathyroid hormone) was established in patients with cancer of the breast, prostate and skeletal metastases of lung cancer, irrespective of the presence of primary tumor. This index is irrelevant in cases of gastric and renal carcinoma and cannot be used a indication of skeletal dissemination because of the predominant level of parathyroid hormone secretion.
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PMID:[Calcitonin and parathyrin in the blood serum of cancer patients]. 710 29

Current procedures to determine the clinical staging of disease in patients with lung cancer are lacking in accuracy, particularly regarding the presence of metastatic disease. We have evaluated the use of computed tomography (CT) of the chest, brain, and upper abdomen for clinical staging of the extent of disease in 113 consecutive patients with histologically confirmed carcinoma of the lung. Comparisons with mediastinoscopy and surgical findings were made regarding the extent of primary tumor in 47 patients and nodal involvement in 41 patients. The CT scan showed a sensitivity of 86.9%, a specificity of 91.6%, and an accuracy of 89.3% for extrapulmonary extension of the primary tumor and a sensitivity of 50%, a specificity of 96.5% and an accuracy of 82.9% for mediastinal node involvement. Thirty-two of the 85 patients studied by total body CT scan had distant metastasis, of which 24 (75%) were clinically silent. Thus 28.2% of the 85 patients studied had asymptomatic metastatic disease. We conclude that CT of the chest, brain, and upper abdomen is a reliable procedure for staging lung cancer.
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PMID:TNM staging in lung cancer: role of computed tomography. 712 Oct 45

The accuracy of stage I lung cancer assessment achieved by traditional clinico-diagnostic staging was retrospectively evaluated in 164 consecutive patients who underwent thoracotomy. The diagnostic conversion rate was 6.7% (1 carcinoid and 10 innocent pulmonary lesions) and occurred only in the subset of patients lacking preoperative pathologic confirmation (15%). The conversion rate to unresectable tumor extent was 8% (11/153), and local spread was the main cause of unresectability (5.5%). The staging conversion rate was 29% (43/153): the conversion rate for nodal evaluation was double that of primary tumor evaluation (24% versus 12%), but conversion to anatomically unresectable nodal diffusion occurred in only one patient (0.6%). The ability of the surgeon to convert the wrong diagnosis was scanty without extemporary biopsy, and 7 patients with innocent lesions underwent standard resection for primary cancer. Surgical staging was a precise as pathological staging in primary tumor evaluation, but was faulty in nodal evaluation (15% error in sN- and sN1-2 assessment). It is concluded that following stage I lung cancer assessment by traditional means, supplementary examinations are requested for a better sensitivity of pathological confirmation and a better refinement of local spread. Better nodal evaluation has less value until a biologic limit to surgery for anatomically resectable nodal diffusion is universally accepted.
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PMID:Post-thoracotomy diagnostic and staging conversion rates of clinically staged I lung cancer. 728 Dec 43

The morphology of the tumor and the anatomic extent of the disease are important factors influencing treatment selection and ultimately survival for patients with lung cancer. The American Joint Committee TNM system provides a method for consistent reproducible description of the primary tumor (T), the status of the regional lymph nodes (N), and the presence or absence of distant metastasis (M). The TNM subsets thus classified can be grouped into three "stages" of disease such that the survival expectations for patients in each stage and cell type are similar. This classification of patients with respect to estimates of their prognosis is essential for valid comparisons of treatment modalities and meaningful communication of end results information.Clinical characteristics which influence survival are reflected in the staging recommendations. The size of the lesion, the proximal margination, and the presence or absence of other pulmonary complications are features which distinguish the T classification as T1, T2, or T3. The presence or absence of lymph node involvement has an important bearing on survival expectations. Advancing from no nodal involvement, N0, to involvement of the peribronchial and hilar nodes, N1, and then to the mediastinal nodes, N2, causes progressive erosion in survival expectations. The tumor morphology and specific nodes that are involved are important components of this relationship. The presence of distant metastasis, M1, is synonymous with an extremely poor prognosis. Using these prognostic elements, the TNM subsets are combined into three stages of disease so that patients in each group will have a generally similar life expectancy, the survival for patients with stage I disease being significantly greater than that for patients with stage II disease which is significantly greater than survival for patients with stage III disease.Improvements in the outcome for lung cancer patients depend upon the depth and scope of our scientific understandings and our ability to communicate our observations to one another. Measures of response to treatment can be translated into therapeutic practice only if uniform evaluators are used. Accordingly, a reproducible valid system for staging of lung cancer is recommended.
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PMID:Staging of lung cancer. 729 38

To improve their ability to estimate the survival of terminally ill cancer patients, palliative care physicians require accurate information on prognostic factors. The objective of this study was to assess the extent to which variables such as patient characteristics and primary tumor site affect the length of survival of terminally ill cancer patients. The study population consisted of 1081 cancer patients admitted for terminal care to a 15-bed palliative care unit from 1985 to 1991. Univariate Kaplan-Meier survival analysis and multivariate Cox regression analyses were used to examine the relationship between patient characteristics at admission and survival time. The factor most strongly associated with shorter survival was poor performance status; this strong relationship was not altered by taking into account sex and primary cancer site in the multivariate analysis. For patients who were bedridden at admission, the death rate was 5.5 times higher (95% confidence interval (Cl) 3.4-9.0) than that for ambulatory patients during the first four days of stay, and it was 2.8 times higher (95% Cl 2.0-3.9) subsequently (up to 19 days). The other prognostic factors significantly but slightly associated with poorer survival in the univariate analysis were primary lung cancer, male sex, and living with a spouse. These findings indicate that performance status is the main prognostic factor for accurately estimating the survival time of terminally ill cancer patients.
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PMID:Factors associated with length of survival among 1081 terminally ill cancer patients. 747 87

Deletions of the short arm of chromosome 9 have been observed in a number of malignant cell lines and primary tumor samples using cytogenetic and molecular techniques. These tumors include acute lymphoblastic leukemias, lymphomas, gliomas, melanomas, mesotheliomas, bladder cancer, and lung cancer. The smallest region of overlap (SRO) of these deletions is thought to contain a tumor suppressor gene. A microdissection library was constructed from bands 9p21-p23 to obtain DNA probes that would be useful in further defining the limits of the deletions. Eight single-copy probes were found to be homozygously deleted in at least 1 of the 10 cell lines examined. The mapping of these 8 clones using a panel of cell lines with deletions revealed that 3 probes mapped telomeric to the SRO and 5 clones mapped centromeric to the SRO.
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PMID:Mapping a putative tumor suppressor gene on chromosome 9 bands p21-p22 with microdissection probes. 753 86

Lung cancer is the leading cause of malignancy-related mortality in the U.S. and is predicted to increase over the remainder of this decade. Despite attempts to advance early diagnosis and use combination therapies, the clinical response of this cancer yields an overall 5-year survival rate of less than 15%. Clearly, new strategies for therapy are indicated. Although carcinogenesis is complex, tumor growth beyond 1-2 mm3 is dependent on angiogenesis. One of the potential mechanisms that allows for tumorigenesis is dysregulation of the balance of angiogenic and angiostatic factors that favors net neovascularization within the primary tumor. Numerous studies have investigated the role of a variety of molecules in the regulation of angiogenesis. Recently, interleukin-8 (IL-8), a member of the C-X-C chemokine family, has been found to be an angiogenic factor. In contrast, platelet factor 4 (PF4), another C-X-C chemokine, has been shown to have angiostatic properties. It is interesting that the major structural difference between IL-8 and PF4 is the presence of the NH2-terminal ELR (Glu-Leu-Arg) motif that precedes the first cysteine amino acid residue of IL-8 and is important in ligand/receptor interactions. We hypothesize that angiogenesis associated with tumorigenesis is dependent on members of the C-X-C chemokine family acting as either angiogenic or angiostatic factors. This paradigm predicts that the biological balance in the expression of these C-X-C chemokines dictates whether the neoplasm grows and develops metastatic potential or regresses. In this review we discuss our recent laboratory findings that support this contention and suggest that further elucidation of the biology of C-X-C chemokines in the context of neovascularization of nonsmall cell lung cancer will permit novel targeted therapy aimed specifically at attenuating tumor growth and metastasis.
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PMID:Role of C-X-C chemokines as regulators of angiogenesis in lung cancer. 753 29

A phase I trial of paclitaxel therapy, administered as a weekly 3-h infusion for 6 weeks with concurrent daily thoracic radiation to patients with advanced or medically inoperable non-small cell lung cancer, was performed. Paclitaxel was escalated in increments of 10 mg/m2/week in successive cohorts of three new patients as tolerated, starting at 10 mg/m2/week. Radiation was administered to the primary tumor and regional lymph nodes (40 Gy over 4 weeks), followed by a boost to the primary tumor (20 Gy in 2 weeks). Twenty-seven patients entered this study through seven dose levels of paclitaxel ranging from 10-70 mg/m2/week for the primary purpose of evaluating the toxicity of concurrent chemoradiation treatment. Esophagitis was the principal and dose-limiting toxicity. Radiation pneumonitis occurred in two patients. Other toxicities were mild. Although not designed as an efficacy study, 23 patients were available for response, and an overall response rate of 74% (confidence interval, 65-83%) was observed.
Lung Cancer 1995 Jun
PMID:Concurrent paclitaxel and thoracic radiation for advanced non-small cell lung cancer. 755 42

To study the relation between p53 mutation and metastasis in primary lung cancer, 29 pairs of primary and metastatic tumors obtained by autopsy were analyzed for abnormalities of the p53 gene, by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). The tumors consisted of 6 small cell carcinomas, 13 adenocarcinomas, 8 squamous cell carcinomas, 1 large cell carcinoma, and 1 adeno-squamous cell carcinoma. PCR-SSCP analysis showed that 3 small cell carcinomas (50%), 3 adenocarcinomas (23%), 2 squamous cell carcinomas (25%), and 1 large cell carcinoma (100%) had p53 gene mutations. The abnormalities were found between exons five and eight. The metastatic tumor and the primary tumor had similar mutations. These results suggest that p53 gene mutation may occur before distant metastasis and may be stable during the process of metastasis.
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PMID:[p53 gene abnormalities in advanced primary lung cancer and metastatic tumors]. 761 96

We have analysed our experience in 43 patients with lung cancer invading the heart or great vessels who underwent surgical resection of the invaded portion of the mediastinal organs as well as the primary tumor, and have reviewed the literature on the subject of the extended operation for lung cancer invading the heart or great vessels. Among our experience of those 43 patients, a single mediastinal organ was resected in 32 patients (the left atrium in 20, the main pulmonary artery in 7, superior vena cava in 3 and the adventitia of the aorta in 2), and more than two mediastinal organ were resected in 11 patients (the main pulmonary artery and the other in 8, and the left atrium and esophagus or trachea in 3). There were 34 squamous cell carcinomas, 4 adenocarcinomas, 3 large cell carcinomas and 3 other cell types. Pathology disclosed 6 patients had pT 3 tumor (Group 1, 24 patients had pT 4 tumor that had invaded to a single mediastinal organ (Group 2) and 11 patients had pT 4 tumor that had invaded to more than two mediastinal organs (Group 3). The 5 year survival rate in patients of Group 1, 2 and 3 were 80%, 32.2% and 0%, respectively. There were statistical differences among the survivals of those three groups. We conclude that extended resection for lung cancer invading the heart or great vessels is justified if the invasion is limited to a single mediastinal organ. Several problems on such extended resection were discussed.
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PMID:[Extended operation for lung cancer: concomitant resection of the heart or the great vessels with the lung]. 764 13


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