Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metastatic pulmonary calcinosis is a rare complication seen in malignancies accompanied by hypercalcemia, or chronic renal failure. We reviewed the clinicopathological findings of 8 cases of metastatic pulmonary calcinosis accompanied malignancy revealed at autopsy. The underlying diseases were malignant lymphoma in 3 cases (adult T cell lymphoma in 2 cases), multiple myeloma in 2, lung cancer in 2, and acute myelocytic leukemia in 1, all cases were complicated by hypercalcemia and renal failure. Chest X-ray revealed almost normal findings in 2 cases, bilateral diffuse infiltrates in 4, bilateral infiltrates in the apex in 1, and right atelectasis in 1. Bone scintigraphy was performed in 4 cases, and revealed warm pulmonary uptake in 1 patient with multiple myeloma and 1 with lung cancer, but normal findings in the 2 other cases. Histopathological examination revealed diffuse alveolar septal edema and fibrosis due to calcium deposition, which were considered to be the cause of respiratory failure. Metastatic pulmonary calcinosis is a rare but a serious complication in malignancies accompanied by hypercalcemia and renal failure, and bone scintigraphy seems to be a useful method for its diagnosis.
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PMID:[Clinicopathological features of metastatic pulmonary calcinosis with malignant neoplasm]. 175 31

The examined groups included 58 patients with cancer, 61 subjects with pulmonary tuberculosis and 50 healthy persons as controls. The content of trace elements in blood, bronchial lavage fluid from the most affected portions of the lungs, and in pathologic and healthy lung tissues was determined by a C-115 atomic absorption spectrophotometer. The examination findings demonstrated that the content of blood serum ferric zinc and magnesium, and erythrocyte zinc, manganese, potassium and calcium was higher in patients with pulmonary tuberculosis than in those with lung cancer. At the same time the content of magnesium and calcium in bronchial lavage fluid was higher in persons with a malignant process than in those with pulmonary tuberculosis. As far as differential diagnosis of pulmonary tuberculosis and lung cancer is concerned, it is advisable to measure the levels of erythrocyte trace elements since the latter most precisely reflects their content in the lung pathologic tissue.
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PMID:[Chemical elements in the blood, bronchial lavage fluid and lung tissue of patients with pulmonary tuberculosis and lung cancer]. 175 86

We report our experience of the presentation and management of symptomatic hypercalcaemia in advanced lung cancer. Between 1981 and 1987, 55 patients required urgent admission due to rapid clinical deterioration accompanied by significant hypercalcaemia (greater than 2.75 mmol l-1). Forty patients (72%) had squamous cell cancer, five small cell, three large cell, two adenocarcinoma and five unclassified. Thirty-five had evidence of bony metastases. Symptoms were categorized for each patient on the basis of being either potentially attributable to hypercalcaemia or not. All patients were rehydrated but specific treatment schedules over the period varied [1981-1985: steroids, calcitonin, mithramycin; 1985-1987: aminohydroxypropylidene bisphosphonate (APD)]. Treatment resulted in a significant reduction in the prevalence of all systems except for pain and nausea/vomiting; the greatest effect being seen on central nervous system and renal tract symptoms (75 and 80% reduction respectively; P less than 0.005 pre- versus post-treatment). Overall, 45 patients (82%) had a biochemical response; serum calcium fell from 3.28 +/- 0.33 mmol l-1 (mean +/- SE) to a nadir of 2.54 +/- 0.36 mmol l-1 (P less than 0.001). Twenty-five (49%) patients were discharged home. We conclude that despite the poor life expectancy of this group of patients (median survival 42 days) treatment of hypercalcaemia is worthwhile as it results in a significant symptomatic improvement.
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PMID:Symptomatic hypercalcaemia in lung cancer. 183 17

Concentrations of nine metals (Fe, Ca, Mg, Zn, Cu, Co, Ni, Pb and Cr) concentrations in lung tissues from 224 lung cancer cases were compared with those in other cases to achieve an understanding of their contribution to the development of lung cancer and the varieties after the development of cancer. Comparisons of metal concentrations in each cell type of lung cancer were also performed. All cases were collected from routine autopsies in Tokyo and Saitama, Japan. The copper concentration in tissue from lung cancers was significantly higher than that in other specimens, although calcium, magnesium, zinc and cobalt concentrations in lung cancers were significantly lower than those in other cases. There were no significant differences in the 99% intervals (excluding extremely high values for occupationally exposed cases) for chromium, nickel and lead concentrations between lung cancers and other cases, although these values were lower in lung cancers. However, in comparisons of men only, the chromium concentration, the degree of lung contamination and the severity of pulmonary emphysema in lung cancer cases were significantly higher than those in other specimens. Moreover, percentages of lung cancer in men at each degree of contamination and each severity of emphysema increased with increasing grades. Thus, this finding could be evidence that the exposure to contaminants other than chromium and nickel in the air had affected the development of lung cancer, except for occupationally exposed individuals. Therefore, almost all chromium and nickel in lung tissue might not deposit in carcinogenic forms such as hexavalent chromium or nickel subsulfide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metal concentrations in lung tissue of subjects suffering from lung cancer. 191 70

Most lung carcinomas with hypercalcemia are usually unresectable. However, this case was resectable and the serum calcium level was normalized after the operation. Messenger RNA of the precursor of PTH-related protein (PTHrP), a substance that may be one of the causes of hypercalcemia in malignant neoplasms, was identified in the tumor tissue of the patient. The patient was a 60-year-old man with squamous cell carcinoma originating from the posterior basal segment of the left lung and invading the main bronchus and left atrium. The serum calcium level was 14.3 mg/dl, preoperatively. Pneumonectomy with partial left atrium resection was carried out and the serum calcium level became normal postoperatively. Three months following the operation, this measurement was 9.4 mg/dl, but increased to 16.2 mg/dl at four months, at which time he experienced lumbago and chest pain. The patient died eight months following the operation from uncontrollable renal failure. In the tumor tissue, mRNA of PTHrP precursor was identified. To our knowledge, this is the first case of lung cancer that could be resected, and in which PTHrP was found present.
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PMID:Hypercalcemia induced by parathyroid hormone-related protein from lung cancer tissue. 193 11

In a consecutive series of 771 patients with pathologically verified squamous cell carcinoma of the head and neck, 28 patients (3.6%) had hypercalcemia (greater than 11.0 mg/dl) during the course of their disease. The buccal mucosa (16/205, 7.8%) and tongue (8/148, 5.4%) were the most frequent primary sites. Most of the patients were stage IV patients with recurrence and advanced disease. The prognosis was poor with a median survival of only 6 weeks. The possible etiology of their hypercalcemia included humoral factors, bone metastases and independent primary lung cancer. The treatment of hypercalcemia was evaluated in 22 patients. Success was noted in all patients initially receiving chemotherapy (10 cases) or radiotherapy (3 cases) with or without saline hydration plus furosemide diuretics. However, the response rate in patients (9 cases) initially receiving hydration plus furosemide diuretics alone was 22% (2/9), with 4 of 7 failure cases later responding to chemotherapy. It is suggested that hypercalcemia be treated with chemotherapy or radiotherapy quickly, along with hydration plus diuretics. Also, the serum calcium level must be checked in patients with advanced buccal or tongue cancer.
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PMID:Hypercalcemia in squamous cell carcinoma of the head and neck. 197 96

With a newly developed monoclonal anti-PTHrP antibody, 4B3, the immunohistochemical localization of the parathyroid hormone-related protein (PTHrP) was studied on the formalin-fixed and paraffin-embedded sections of normal human tissues and various subtypes of lung cancer. Among normal epithelial tissues, keratinocytes in squamous epithelia, transitional and bronchial epithelia with squamous metaplasia, meningoepithelial cells, and mammary ductal cells with lactating changes showed positive immunoreactivity. Also, among endocrine tissues, cells in the parathyroid gland, pancreatic islets, adrenal cortex, pituitary gland, and testis were sporadically positive for PTHrP. These distribution patterns suggested that in a physiologic condition, PTHrP was closely related to keratinization and local secretion and/or the metabolism of calcium in specifically differentiated tissues. In lung cancer, however, PTHrP was detected in all cases of well-differentiated and moderately differentiated squamous cell carcinoma and in most cases of small cell carcinoma, irrespective of the patients' serum calcium level. However, PTHrP was not detected in two of five cases of poorly differentiated squamous cell carcinoma and in all cases of adenocarcinoma. Consequently, it was found that PTHrP was commonly produced by squamous cell carcinomas of the differentiated type, and that humoral hypercalcemia of malignancy could be induced when the PTHrP transgressed the homeostatic mechanisms.
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PMID:Immunohistologic evaluation of parathyroid hormone-related protein in human lung cancer and normal tissue with newly developed monoclonal antibody. 199 Dec 68

Radiologic visualization of calcification within lung cancer is uncommon and may cause confusion and misdiagnosis. For this reason, we reviewed CT records of 353 patients undergoing initial evaluation of lung cancer for the presence of calcification within the tumor, both to document this finding and to estimate its prevalence. Twenty patients (6%) whose records indicated that CT showed calcification were identified, and their chest radiographs and CT scans were analyzed. Patients were included in the study if calcium was seen within the tumor on noncontrast pretreatment CT scans and if pathologic data were available. There were 15 lung and five mediastinal tumors. Fourteen were 5 cm or greater in diameter; three were between 3 and 5 cm, and three were 2 cm or smaller. Cell types of the tumors included small-cell carcinoma (eight patients), squamous cell carcinoma (seven patients), adenocarcinoma (four patients), and undifferentiated carcinoma (one patient). Patterns of calcification were amorphous (eight patients), punctate (10 patients), and reticular (two patients). Extent of tumor calcification and distribution (central, peripheral, or diffuse) did not correlate with cell type or size of the lesion. The visualization of calcium on chest radiographs and CT scans does not alone exclude the diagnosis of bronchogenic carcinoma.
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PMID:CT demonstration of calcification in carcinoma of the lung. 215 29

Calcium ion flux following the administration of a series of neuropeptides, N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate, and serum was monitored by flow cytometry in selected lung and breast cancer cell lines and Chinese hamster ovary cell line CHO-K1. Calcium ion flux was monitored in individual cells by flow cytometry using the indicator indo-1 AM. Five groups of neuropeptides produced calcium flux changes in lung cancer cell lines and CHO-K1 cells but not in breast cancer cells. The peak increase in free calcium was reached within 10 sec of peptide administration and declined to resting levels in 70-120 sec. When two or more members of the same group were administered simultaneously, calcium flux changes were identical to that produced by each single peptide. When two or more members of different groups were administered simultaneously, an increased calcium release occurred. When identical peptides or peptides from the same group were administered sequentially after the return of calcium concentrations to resting values, no calcium flux resulted from the second peptide. When peptides from different active groups were administered sequentially, a new calcium flux occurred after each peptide. These data are interpreted to mean that members of each active group of peptides trigger a different calcium flux pathway. Thus, many such pathways and different metabolic states exist within the cell. Elucidation of calcium flux pathways in normal and cancer cells may lead to greater understanding of the nature of the malignant defect.
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PMID:Neuropeptide stimulation of calcium flux in human lung cancer cells: delineation of alternative pathways. 215 63

Many factors, such as interleukin 1, TGF alpha, TNF alpha, and beta and prostaglandins, have been implicated in aetiological roles in HHM (Martin and Mundy, 1987). Much interest in the past has also centered upon the likelihood of ectopic secretion of PTH in this condition. We have purified a protein (PTHrP) implicated in HHM from a human lung cancer cell line (BEN). Full-length cDNA clones have been isolated and found to encode a prepropeptide of 36 amino acids and a mature protein of 141 amino acids. Eight of the first 13 amino acids were identical with human PTH, although antisera directed to the NH2-terminus of PTHrP do not recognize PTH; this homology is not maintained in the remainder of the molecule. PTHrP therefore represents a previously unrecognized hormone, possibly related to the PTH gene by a gene duplication mechanism. In support for this notion, the PTHrP gene has been localized to the short arm of chromosome 12; it is believed that chromosome 11, containing the PTH gene, and chromosome 12 are evolutionarily related. In addition, the human PTHrP gene has been isolated, characterized, and shown to have a similar intron/exon organization as the PTH gene. It is possible that the original ancestral gene is indeed the PTHrP gene; resolution of this question awaits studies in lower species. Peptides synthesized to the predicted protein sequence have enabled detailed structure-function studies that have identified NH2-terminal sequences to be responsible for the biological effects of the molecule. Antibodies raised against the various synthetic peptides have led to the immunohistochemical localization of PTHrP in many human squamous cell carcinomas as well as in subpopulation of keratinocytes of normal skin. The availability of these antibodies has opened the way for the development of a radioimmunoassay to detect PTHrP in the sera of cancer patients at risk of developing hypercalcemia. The recent characterization of PTHrP-like activity in the ovine fetus suggests some physiological function for PTHrP. It is possible that PTHrP, as the fetal counterpart of PTH, has the role of maintaining the maternal-fetal calcium gradient. The isolation and characterization of PTHrP has added to our understanding of the mechanisms of hypercalcemia, and may contribute to the understanding of other metabolic bone diseases such as osteoporosis and Paget's disease. Finally, and perhaps most importantly, PTHrP may play a hitherto unrecognized role in fetal calcium metabolism and in normal cell physiology.
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PMID:A novel parathyroid hormone-related protein: role in pathology and physiology. 218 38


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