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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological analysis of the sclerotic changes in peripheral lung carcinoma (PLC) and nephrosclerosis in renal-cell carcinoma (RCC) established a promoting role of sclerosis in carcinoma development. The pneumosclerosis role as a background process in the PLC development is proved by the following facts: high proportion (83%) of the carcinoma in the scar among PLC; identity of the scar collagen composition in PLC and that in metatuberculosis and metapneumonic pneumosclerosis foci; detection of metatuberculosis foci in 75% of PLC; the presence of the precancerous changes in the epithelium entrapped in the pneumosclerotic foci, not only with signs of morphological atypia, but with the disturbance of nuclear DNA and cellular oncogene expression as well. The association of RCC with nephrosclerosis is shown by a high proportion (82.7%) of the RCC development against the background of nephrosclerosis; the dependence of the so-called cortical adenoma development on the degree of nephrosclerosis; epithelial proliferation in the nephrosclerotic foci with the appearance of undifferentiated cells with the altered DNA content and the expression of cytokeratins and vimentine. Carcinoma morphogenesis against the background of sclerosis may be described as follows: development of sclerosis (focal and/or diffuse), the appearance of the focal epithelial hyperplasia in the scar, dysplasia or adenoma and finally carcinoma.
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PMID:[Sclerosis and carcinogenesis]. 128 96

Squamous, large cell, and adenocarcinoma, collectively termed non-small cell lung cancer (NSCLC), are diagnosed in approximately 75% of patients with lung cancer in the United States. The treatment of these three tumor cell types is approached in virtually identical fashion because, in contrast to small cell carcinoma of the lung, NSCLC more frequently presents with localized disease at the time of diagnosis and is thus more often amenable to surgical resection but less frequently responds to chemotherapy and irradiation. Cigarette smoking is etiologically related to the development of NSCLC in the great majority of cases. Genetic mutations in dominant oncogenes such as K-ras, loss of genetic material on chromosomes 3p, 11p, and 17p, and deletions or mutations in tumor suppressor genes such as rb and p53 have been documented in NSCLC tumors and tumor cell lines. NSCLC is diagnosed because of symptoms related to the primary tumor or regional or distant metastases, as an incidental finding on chest radiograph, or rarely because of a paraneoplastic syndrome such as hypercalcemia or hypertrophic pulmonary osteoarthropathy. Screening smokers with periodic chest radiographs and sputum cytologic examination has not been shown to reduce mortality. The diagnosis of NSCLC is usually established by fiberoptic bronchoscopy or percutaneous fine-needle aspiration, by biopsy of a regional or distant metastatic site, or at the time of thoracotomy. Pathologically, NSCLC arises in a setting of bronchial mucosal metaplasia and dysplasia that progressively increase over time. Squamous carcinoma more often presents as a central endobronchial lesion, while large cell and adenocarcinoma have a tendency to arise in the lung periphery and invade the pleura. Once the diagnosis is made, the extent of tumor dissemination is determined. Since most NSCLC patients who survive 5 years or longer have undergone surgical resection of their cancers, the focus of the staging process is to determine whether the patient is a candidate for thoracotomy with curative intent. The dominant prognostic factors in NSCLC are extent of tumor dissemination, ambulatory or performance status, and degree of weight loss. Stages I and II NSCLC, which are confined within the pleural reflection, are managed by surgical resection whenever possible, with approximate 5-year survival of 45% and 25%, respectively. Patients with stage IIIa cancers, in which the primary tumor has extended through the pleura or metastasized to ipsilateral or subcarinal lymph nodes, can occasionally be surgically resected but are often managed with definitive thoracic irradiation and have 5-year survival of approximately 15%.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-small cell lung cancer. Part I: Biology, diagnosis, and staging. 164 34

Squamous, large cell, and adenocarcinoma, collectively termed non-small cell lung cancer (NSCLC), are diagnosed in approximately 75% of patients with lung cancer in the United States. The treatment of these three tumor cell types is approached in virtually identical fashion because, in contrast to small cell carcinoma of the lung, NSCLC more frequently presents with localized disease at the time of diagnosis and is thus more often amenable to surgical resection but less frequently responds to chemotherapy and irradiation. Cigarette smoking is etiologically related to the development of NSCLC in the great majority of cases. Genetic mutations in dominant oncogenes such as K-ras, loss of genetic material on chromosomes 3p, 11p, and 17p, and deletions or mutations in tumor suppressor genes such as rb and p53 have been documented in NSCLC tumors and tumor cell lines. NSCLC is diagnosed because of symptoms related to the primary tumor or regional or distant metastases, as an incidental finding on chest radiograph, or rarely because of a paraneoplastic syndrome such as hypercalcemia or hypertrophic pulmonary osteoarthropathy. Screening smokers with periodic chest radiographs and sputum cytologic examination has not been shown to reduce mortality. The diagnosis of NSCLC is usually established by fiberoptic bronchoscopy or percutaneous fine-needle aspiration, by biopsy of a regional or distant metastatic site, or at the time of thoracotomy. Pathologically, NSCLC arises in a setting of bronchial mucosal metaplasia and dysplasia that progressively increase over time. Squamous carcinoma more often presents as a central endobronchial lesion, while large cell and adenocarcinoma have a tendency to arise in the lung periphery and invade the pleura. Once the diagnosis is made, the extent of tumor dissemination is determined. Since most NSCLC patients who survive 5 years or longer have undergone surgical resection of their cancers, the focus of the staging process is to determine whether the patient is a candidate for thoracotomy with curative intent. The dominant prognostic factors in NSCLC are extent of tumor dissemination, ambulatory or performance status, and degree of weight loss. Stages I and II NSCLC, which are confined within the pleural reflection, are managed by surgical resection whenever possible, with approximate 5-year survival of 45% and 25%, respectively. Patients with stage IIIa cancers, in which the primary tumor has extended through the pleura or metastasized to ipsilateral or subcarinal lymph nodes, can occasionally be surgically resected but are often managed with definitive thoracic irradiation and have 5-year survival of approximately 15%.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-small cell lung cancer. Part II: Treatment. 171 39

Histospectrophotometric study of DNA content shows that, at the lung periphery, oval structures with atypia, adenomatosis with atypia, dysplasia and basal cell hyperplasia with bronchial epithelium atypia should be regarded as precancerous lesions. Carcinoma in situ and bronchoalveolar carcinoma are distinguished from the foci of epithelial dysplasia by an increase of DNA content and appearance of hetero- and aneuploidy. Aneuploidy is observed in 97% peripheral lung carcinoma and is combined with a heterogeneity of cells by their DNA content. Poorly differentiated squamous cell carcinoma, adenocarcinoma and large cell carcinoma are characterized by a marked heterogeneity which correlates with a degree of tumour morphological atypia. Bronchoalveolar carcinoma is a heterogeneous group of tumours with a different histogenesis and pronounced anaplasia which is expressed in a various degree of polyaneuploidy and heteroploidy. Small cell lung carcinoma, a special group of tumours, which, as distinct from other carcinoma types, is characterized by a low, sometimes diploid DNA content which does not correlate with its malignancy.
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PMID:[The DNA content in precancer, peripheral cancer and carcinoids of the lung (histospectrophotometric research)]. 195 57

Operative material obtained from patients with lung cancer and precancer, carcinoids, secondary tuberculosis, chronic nonspecific diseases and pulmonary lymphosarcoma was examined immunohistochemically. Expression of the oncogenes was higher in lung carcinoma than in the foci of lung epithelium regeneration, metaplasia and dysplasia. All the oncogenes in precancer and cancer may be divided into two groups by the degree of their expression: oncogenes the activation of which occurs in the same way at certain stages of tumour progression regardless of the lung carcinoma histogenesis and oncogenes expressed at certain stages depending upon the carcinoma histogenesis. The majority of oncogenes studied may be included into the second group (C-myc, ras, sis, src) and only one c-fos into the first group. The oncogenes expression may occur at the precancerous stage and precede the morphological changes in cells and tissues. The expression of some oncogenes (C-myc, sis) takes place not only in the tumour parenchyma but in the cancer stroma as well thus making the immunohistochemical method most reliable that permits one to study a true expression of oncogenes by cancer cells.
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PMID:[The immunohistochemistry of cellular oncogenes in precancer and cancer of the lung]. 228 84

The cytograms of smears, obtained in bronchoscopic examinations of 59 patients with bronchial epithelium dysplasia and 44 patients with initial forms of squamous-cell carcinoma of the lung are analyzed. A histologic control has been made in all the cases. The authors classify the cytomorphologic criteria, they have statistically processed 140 signs, minimizing their number and selecting their combinations for the differential diagnosis between dysplasia and carcinoma of the lung. Cytologically dysplasia in squamous-cell metaplasia of the bronchial epithelium and dysplasia of the cylindrical epithelium have been distinguished. Three degrees of dysplasia have been singled out: (I) weak, (II) moderate, (III) grave.
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PMID:[Differential diagnostic cytochemical signs of dysplasia of the bronchial epithelium and squamous cell carcinoma of the lung]. 248 Nov 34

The present report considers the autopsic study of an homograft recipient who had been living for 18.5 years after a cardiac transplantation. The patient was treated by immunosuppressive therapy associating azathioprine and steroids. During the exceptionally long follow-up, two skin carcinomas and a lung carcinoma occurred successively. In addition, the autopsy allowed observation of a kidney adenocarcinoma associated to a polycystic disease, and a liver regenerative nodular hyperplasia containing several areas of severe dysplasia. These findings, when compared with those usually observed in immunodeficient patients, suggested the possibility that long-term immunosuppressive therapy may give rise to malignancies other than those arising after a short therapy.
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PMID:An exceptional 18-year follow-up after cardiac transplantation. How can malignancies occur during immunosuppressive therapy? 264 24

We have experienced 11 cases of lung carcinoma in workers at a chromate factory during the past 14 years. All patients were males. The age of onset ranged from 41 to 68 years. Ten of the 11 were heavy smokers. The time of exposure to chromate was from 17 to 29 years and the average was 23.9 years. Seven patients had perforation of their nasal septa. The primary sites of the cancers were from the lobar to the subsegmental bronchi. There were nine squamous cell carcinomas and three small cell carcinomas. Four squamous cell carcinomas were hilar type early stage cancers and two of them were found in one patient at the same time. The chromium content of the lung tissue in the seven patients tested was from 13.9 to 2,368.4 micrograms/g of dry tissue and was higher than that of lung cancer or non-lung cancer cases without chromate exposure. There was no severe dysplasia of the bronchial epithelium in these 11 patients.
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PMID:Lung cancer in chromate workers--analysis of 11 cases. 299 8

Morphological analysis of 90 observations with a clinical diagnosis of a small peripheral lung carcinoma is performed. The examination of an operation material confirmed diagnosis in 71 cases. Tuberculomas are found in 19 cases. The peripheral lung carcinoma was found to develop in 91.5% (65 cases) against the background of preexisting scars which in 73.8% (48 cases) had a post-tuberculosis and 26.2% (17) post-pneumonia origin. Scars were most frequently related to the healed forms of a focal secondary tuberculosis (30 cases) and sclerotic changes around tuberculomas (8). Post-tuberculosis scars provoking sclerosis and deformation of vessels, bronchi, bronchioles and alveoles with the development of an epithelial dysplasia, are one of the risk factors in the development of a peripheral lung carcinoma. The degradation and fibrinoid changes of a scar tissue infiltrated by a tumour and followed by destruction of scars are observed in peripheral lung carcinomas with a diameter more than 3 cm.
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PMID:[Peripheral cancer of the lung and tuberculosis]. 301 Sep 15

Epidemiological studies have demonstrated that workers in the nickel refinery industry have an increased risk for respiratory tract carcinoma. In the present study, serum from 51 workers at a Norwegian nickel refinery have been tested against lung, nasal and breast carcinoma antigens in the humoral leukocyte adherence inhibition test. The breast cancer antigen was used as a non-specific antigen. The frequency of positive response against the lung carcinoma antigen was significantly higher among the refinery workers (21/51) than in the controls (3/17) (P = 0.07). Moreover, among workers employed for 10 years or more, the response was higher than found for workers with shorter employment. Of the nickel workers with nasal dysplasia, 56% (15/27) gave a positive reaction against the lung carcinoma antigen compared to 25% (6/24) of the workers without dysplasia (P = 0.03). The same trends were also found for the nasal carcinoma antigen. The study gives further support for the usefulness of the humoral leukocyte adherence inhibition test in identification of individuals with an increased risk for developing cancer.
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PMID:A serum immune factor in detection of an occupational group with increased risk for lung and nose cancer. 689 46


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