Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Leukocytosis associated with malignant disease has been known as a paraneoplastic syndrome and occurs occasionally in patients with oral malignancies. In this study, mechanisms underlying leukocytosis associated with malignancy was investigated, using a squamous cell carcinoma of the maxilla from a patient who manifested marked leukocytosis. When the patient's tumor was inoculated into nude mice, it formed squamous cell carcinoma (MH85) and induced leukocytosis and splenomegaly. Leukocytosis and splenomegaly paralleled tumor growth. Surgical excision of MH85 tumor resulted in a dramatic reduction of leukocyte count and spleen weight, indicating an involvement of humoral mediators released by MH85. MH85 cells conditioned medium (MH85CM) were shown to contain granulocyte-colony stimulating factor (G-CSF) activity, which is a potent growth factor specific for granulocytes. These results suggest G-CSF or G-CSF like substance secreted by MH85 cells is responsible for leukocytosis in MH85 bearing nude mice (MH85 mice) and in the patient. MH85 cell growth was stimulated by G-CSF and inhibited by anti-G-CSF antibody, thus suggesting that G-CSF like substance is a autocrine growth factor for MH85 cells. Splenectomized MH85 mice developed less severe leukocytosis than did non-splenectomized mice. This finding indicated that not only G-CSF like substance secreted by MH85 cells but other humoral factors released by the hyperplastic spleen contribute to the development of leukocytosis. Splenic monocytes derived from MH85 mice and MH85CM-stimulated splenic monocytes showed increased secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1), both of which have been reported to induce neutrophilia in animals. Moreover, injection of anti-TNF-antibody into neutrophilic MH85 mice significantly, although not completely, decreased leukocyte count. Thus, it seemed likely that increased secretion of TNF and IL-1 by spleen cells that are stimulated by humoral factors released from MH85 also contributes to the progression of leukocytosis. In splenectomized mice, enlargement of MH85 tumor was retarded and metastases were impaired compared these in nonsplenectomized mice. Coculture of splenocytes from MH85 mice with normal spleen cells, inhibited blastogenesis in response to mitogen. The result suggests that splenocytes from MH85 mice played as immune suppressive cells. MH85CM conferred immune suppressive activity on normal spleen cells. This suppressor cell-inducing factor (SCIF) in MH85CM was found to have an apparent molecular weight of approximately 25kd, and its biological activity was neutralized by anti-G-CSF antibody. Therefore, SCIF secreted by MH85 cells was likely to be G-CSF like substance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the pathophysiology of paraneoplastic syndromes: both cancer cells and host immune cells are responsible for the pathophysiology of leukocytosis associated with oral cancer]. 172 87

The intravenous administration of Clodronate, a strong inhibitor of osteoclastic activity provides a safe and very effective treatment of hypercalcemia whether secondary to bone metastasis or due to paraneoplastic syndrome. Its action is fast, exclusively osseous and lasts up to 7 days. The response is incomplete when increased renal absorption is the predominant mechanism of hypercalcemia. The data published by Elomaa et al on osteolytic metastases in breast cancer patients show a significant improvement with regard to pain reduction, prevention of fractures as well as hypercalcemia. The results obtained using a 1-yr oral treatment need further confirmation.
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PMID:[Value of Clodronate in the treatment of bone metastasis]. 183 87

Cancer-associated retinopathy (CAR), a paraneoplastic syndrome, is characterized by the degeneration of retinal photoreceptors under conditions where the tumor and its metastases have not invaded the eye. The retinopathy often is apparent before the diagnosis of cancer and may be associated with autoantibodies that react with specific sites in the retina. We have examined the sera from patients with CAR to further characterize the retinal antigen. Western blot analysis of human retinal proteins reveals a prominent band at 26 kD that is labeled by the CAR antisera. Antibodies to the 26-kD protein were affinity-purified from complex CAR antisera and used for EM-immunocytochemical localization of the protein to the nuclei, inner and outer segments of both rod and cone cells. Other antibodies obtained from the CAR sera did not label photoreceptors. Using the affinity-purified antibodies for detection, the 26-kD protein, designated p26, was purified to homogeneity from the outer segments of bovine rod photoreceptor cells by Phenyl-Sepharose and ion exchange chromatography. Partial amino acid sequence of p26 was determined by gas phase Edman degradation and revealed extensive homology with a cone-specific protein, visinin. Based upon structural relatedness, both the p26 rod protein and visinin are members of the calmodulin family and contain calcium binding domains of the E-F hand structure.
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PMID:A photoreceptor calcium binding protein is recognized by autoantibodies obtained from patients with cancer-associated retinopathy. 199 65

The paraneoplastic syndrome (PNS) is an association of symptoms and signs not directly related to the site or local manifestations of a malignant tumor or its metastases. Hematologic abnormalities as PNS include erythrocytosis, anemia, neutrophilia, neutropenia, eosinophilia, thrombocytosis, thrombocytopenia, venous thromboembolism and disseminated intravascular coagulation (DIC). These abnormalities are, by and large, due to the production of biologically active growth factors, hormones or as yet unidentified "humors" by the tumor. As our understanding of growth factors controlling hematopoiesis has increased in recent years, the biologic basis of hematologic PNS are better understood. For instance, tumor-associated neutrophilia is now known to be caused by the production of G-CSF by the tumor. The mechanism by which tumor causes thromboembolism have also been extensively investigated. Cancer cells induce platelet aggregation both in vitro and in vivo. Platelet aggregating material has been isolated and partially characterized from tumor cells. The involvement of platelet glycoprotein II b/IIIa in the tumor-platelet interaction has also been shown. Malignant cells contain a unique procoagulant, cancer procoagulant A, that directly activates factor X. Together with tissue factor, this procoagulant appears to have been contribute to a high incidence of thromboembolism in cancer patients. Better understanding of hematologic PNS is important for clinical care of the patients with cancer.
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PMID:[Paraneoplastic syndrome hematologic abnormalities]. 200 36

Paraneoplastic syndromes are caused by factors produced by cancer cells that often act at a distance from both the primary site and its metastases. The most extensively characterized syndromes caused by cancer are those produced by polypeptide hormones, such as adrenocorticotropic hormone, and those produced by antibodies directed against tumor antigens that cross-react with neural tissue, such as in the Eaton-Lambert myasthenic syndrome. These syndromes develop in a minority of cancer patients, and are diagnoses of exclusion. Lung cancer, particularly small cell lung cancer, is the most common malignancy causing paraneoplastic syndromes. A large number of paraneoplastic syndromes have been described. This review focuses on the increased understanding of some of the well-documented syndromes that has occurred through recent advances principally in molecular biology and immunology.
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PMID:Paraneoplastic syndromes in thoracic malignancies. 206 93

Small cell carcinomas of the urinary tract are rare, but lethal. We report 3 cases of primary small cell carcinoma of the kidney, urinary bladder and prostate with light microscopic, immunohistochemical and electron microscopic findings. One patient with small cell carcinoma of the prostate died of disseminated disease 2 years after diagnosis and another patient with small cell carcinoma of the urinary bladder was free of tumour after 6 months. A partial remission was induced in the third patient with distant metastases of small cell carcinoma of the kidney by using chemotherapy protocols similar to the drug regimens for small cell carcinomas of the lung; the patient survived for 5 months. Immunohistochemical studies revealed the absence of argyrophilic immunostaining of tumour cells in all 3 cases, positive staining for keratin in 2 and staining for neuron-specific enolase in all 3. In the third patient, reactivity for prostate-specific antigen was negative. Dense-core, membrane-bound granules were identified in the cytoplasm of 2 patients. The paraneoplastic syndrome was not found, indicating that in considering the occurrence of ectopic hormones, specific cytoplasmic granules of origin need not be implicated. Recognition of this distinct entity requires full consideration of morphological, immunohistological, ultrastructural and biological features. In order to define the origin of this tumour more clearly and to evaluate the effectiveness of chemotherapy, larger series of patients are needed.
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PMID:Small cell carcinoma of the urinary tract. 217 13

A given cancer is a disease which combines a paraneoplastic syndrome with an invasive tumour capable of giving rise to metastases. Surgeons, radiotherapists, medical oncologists and experimental scientists are primarily interested in the tumour. Tumours of tissues and organs which do not normally produce hormones might, during the neoplastic transformation, begin to secrete hormones or substances able to mimic hormones in their effects on other tissues in the organism. The number of known hormones has increased considerably in the last 20 years. It has been found that even in the absence of clinical signs there are often secretory abnormalities and changes in the hormone balance in cancer. The tumour-paraneoplastic syndrome interaction is bidirectional. That paraneoplastic syndromes are dependent upon the tumour, is universally accepted; the reverse, that the tumour might depend on the paraneoplastic syndrome is not part of the current way of thinking. To treat cancer patients, instead of debating the cause and effect in the tumour-paraneoplastic syndrome pair with the classical idea of acting as close to the cause as possible, it seems better, in all circumstances, to treat both the tumour and the paraneoplastic syndrome, even if only subclinical.
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PMID:Paraneoplastic syndromes. 219 65

An unusual, persistent, corregated-to-honeycombed thickening of the palms accompanied by tenderness around the fingernails was found to be a cutaneous marker for internal malignancy. This combination of signs and symptoms has been reported under two clinical entities: Bazex's syndrome and tripe palm. This paraneoplastic syndrome is of interest to head and neck surgeons due to the location of the primary tumor, the site of metastatic disease, and the ability to cure the cutaneous disease by surgical removal of the primary tumor. In our patient, a squamous cell carcinoma of the lung not detectable on chest x-ray presented as a cervical mass accompanied by cutaneous changes on the palms and fingernails. Recognition of the relationship of the dermatologic changes to malignancy of a specific body region eventually led to the detection of the primary tumor. The characteristics of these paraneoplastic syndromes were reviewed in this report.
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PMID:A palmar dermatosis linked to occult carcinoma of the upper thorax, head and neck: Bazex's syndrome and tripe palm. 224 27


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