Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This prospective study was designed to determine the efficacy of iodized talc pleurodesis in patients with pleural effusions. Thirty-four patients underwent this treatment (three bilaterally) between October 1, 1989, and March 31, 1991. All patients had to have complete or nearly complete lung reexpansion after tube thoracostomy with fluid drainage less than 100 ml in 24 hours. A slurry containing 5 gm of talc and 3 gm of thymol iodide was instilled into the pleural space through the chest tube. Chest tubes were removed after complete reexpansion and clearing of the effusions, usually in 3 to 5 days. The patients' ages ranged from 26 to 88 years (average 50 years). Eighteen patients had lung carcinoma, two had mesothelioma, and one each had carcinoma of the ovary, breast, or anorectum, multiple myeloma, schwannoma, or Hodgkin's lymphoma. Two patients had an unknown adenocarcinoma primary and five other patients had acquired immunodeficiency syndrome. One patient had congestive heart failure. Nineteen patients had left, 12 had right, and three had bilateral pleural effusions. The effusion was serosanguineous in 26 and serofibrinous in eight patients. Serial chest radiography showed complete response in all patients. The period of follow-up ranged from 1 to 21 (average 4.9) months, with no recurrences. Twenty-three patients have died during the follow-up period, and there was no sign that reaccumulated pleural effusion existed in any, despite clinical evidence of systemic tumor progression. These observations indicate that intrapleural instillation of a slurry of iodized talc is a safe, adequate, and effective treatment for control of neoplastic or benign pleural effusions.
J Thorac Cardiovasc Surg 1992 May
PMID:Iodized talc pleurodesis for the treatment of pleural effusions. 156 70

The curing chance of cancer disseminated to the lungs depends on the global curing chance of that specific tumor, the extent and distribution of its systemic spread and the availability of additional treatment modalities besides surgery. Of all tumors occurring in childhood and adolescence only osteosarcoma, Wilms tumor and Ewing's sarcoma preferentially disseminate to the lungs and such are the most promising candidates for successful treatment. In osteosarcoma with pulmonary dissemination surgical removal of the metastases is indispensable. In Wilms tumor chemoradiotherapy may replace or be used as an adjunct to surgery while in Ewing's sarcoma with primary pulmonary metastases chemoradiotherapy is the treatment of choice. Although metachronous lung metastases may still cured in osteosarcoma and Wilms tumor, they tend to be fatal however in Ewing's sarcoma. A small chance of success itself should not contraindicate metastasectomy but only the actual technically impossible intervention or the definite demonstration of tumor progression no longer controllable of different location. However, even palliative metastasectomy may be indicated in an individual patient.
Thorac Cardiovasc Surg 1986 Nov
PMID:Surgical treatment of pulmonary metastases in childhood. 243 85

The progression of preneoplasia into lung cancer can be serially studied in a new canine model that is simpler and more cost effective than previously reported methods of orthotopic endobronchial carcinogenesis. Short segments of bronchus, obtained by pneumonectomy, were placed on the back of 10 dogs in the form of subcutaneous bronchial autografts. These autografts (12 to 14 per dog) became vascularized and lined with normal respiratory epithelium. Four to 12 weeks after autograft implantation, 10% methylcholanthrene in crystalline form was put into 57 autografts and 10% methylcholanthrene in a silicone polymer sustained-release implant was placed into 54 autografts. Ten autografts without carcinogen (one per dog) served as controls. Serial samplings of each autograft during 9 to 97 weeks of carcinogen exposure showed the neoplastic progression from normal bronchial cells to invasive cancer through stages such as atypical squamous metaplasia and carcinoma in situ. To date, cancers have been histologically proved in 60 autografts; 36 were induced by implants and 24 by the crystalline form. Thirty-nine cancers were epidermoid, and the remainder were either adenocarcinomas (n = 3) or poorly differentiated spindle cell cancers (n = 18). The sustained-release implant method resulted in larger autografts with a greater tendency to progress to cancer than the crystalline carcinogens (p greater than 0.025). Therefore, the sustained-release implant is now considered the preferred method. Measurement of nuclear deoxyribonucleic acid by image analysis of nine histologic cancers demonstrated hyperploidy. Deoxyribonucleic acid from the L1 repeated sequence family was demonstrably hypomethylated in spindle cell tumors. Curettement of individual autografts yielded sheets of respiratory epithelium from which 43.5 to 409.5 micrograms of deoxyribonucleic acid was isolated. For the first time, deoxyribonucleic acid from each stage of the neoplastic progression in non-small cell lung cancer is available in adequate quantities for serial biochemical and therapeutic analysis.
J Thorac Cardiovasc Surg 1988 Apr
PMID:Non-small cell lung cancer in autogenous subcutaneous bronchial grafts in dogs. 283 61

An imbalance between proliferation and apoptosis is important in tumor progression. Endothelin-1 (ET-1) has vasoconstricting and mitogenic activities and may be involved in apoptosis regulation. We found that ET-1 and FasL systems were colocalized in human colon tumors and that ET-1 was secreted by human (HT-29, SW480) and rat (PROb, REGb) colon carcinoma cell lines. Bosentan, a mixed endothelin-A- and -B- (ET(A)/ET(B)) receptor antagonist, potentiated FasL- (APO-1, CD95) induced apoptosis in these cells. The specific inhibition of enzymes involved in ceramide production did not restore survival of cells exposed to FasL and bosentan. Inhibition of PKC with bisindolylmaleimide IX enhanced FasL-induced apoptosis in HT-29, PROb and REGb cells in the absence of bosentan. These results suggest that ET-1 is an autocrine survival factor able to protect colon carcinoma cells against FasL-induced apoptosis, involving the protein kinase C (PKC) but not the sphingomyelin-ceramide signaling transduction pathways.
J Cardiovasc Pharmacol 2000 Nov
PMID:Endothelin receptor blockade potentiates FasL-induced apoptosis in colon carcinoma cells via the protein kinase C-pathway. 1107 19

Current models of oncogenesis describe cancer as a progression of genetic mutations in a tumor cell mass. However, tumors are more than a clonal expansion of malignant cells. Tumors are heterogeneous, with a complex 3D structure, analogous to organs comprised of different tissues. In a tumor mass, the component cell types interact with each other and with their microenvironment by exchanging information through cell-cell interactions and/or through interactions with the extracellular matrix (ECM). These synergetic interactions facilitate tumor progression. Furthermore, tumor invasion and metastatic development are accomplished through the breakdown of ECM. Disruption of ECM promotes abnormal inter- and/or intra- cellular signaling, leading to dysregulation of cell proliferation, growth and cytoskeleton reorganization. The disruption of the ECM in turn promotes the overproduction of growth factors, which induce elevated epithelial cell proliferation and other abnormalities including carcinogenesis. In this review we will demonstrate that hyaluronan (HA), a core component of ECM, contributes to certain types of cancer development. Additional to extracellular HA, intracellular and nuclear forms of HA have been detected. Intracellular HA is involved in cell signaling, whereas nuclear HA could promote chromatin condensation and thus facilitate mitosis. HA molecules are synthesized by hyaluronan synthases (HASs)-HAS1, HAS2 and HAS3 enzymes. Dysregulation of HAS genes results in abnormal production of HA and promotion of abnormal biological processes such as transformation and metastasis. The function of HASs appears to be cell and tissue specific. HAS1 maintains a low, basal level of HA. HAS2 is involved in embryonic and cardiac cushion morphogenesis and subsequent development through cell migration and invasion. HAS2 stimulates cell proliferation and angiogenesis. HAS3 appears to favor the malignant phenotype in many types of malignancies. However, the exact function of HAS isoenzymes and their role in cell signaling remains to be elucidated. A better understanding of HA and HASs may facilitate the design of novel therapeutic strategies to counter presumptive cancer-promoting effects of microenvironmental components.
Curr Drug Targets Cardiovasc Haematol Disord 2005 Feb
PMID:Hyaluronan and hyaluronan synthases: potential therapeutic targets in cancer. 1572 Feb 20

Ovarian carcinoma cells release high amounts of endothelin-1 and exhibit increased expression of endothelin-A receptor. Engagement of the endothelin-A receptor triggers tumor growth, survival, neoangiogenesis and invasion. Cyclooxygenase-1 and cyclooxygenase-2 are enzymes involved in the production of prostaglandins and play a role in the regulation of tumor progression in several malignancies, including ovarian carcinomas. Endothelin-1 significantly increases the expression of cyclooxygenase-1 and cyclooxygenase-2 mRNA and protein, the activity of the cyclooxygenase- 2 promoter, and the release of prostaglandin E2 from two ovarian carcinoma cell lines, HEY and OVCA 433. The cyclooxygenase- 2 inhibitor, NS-398 drastically decreased the endothelin- 1-induced prostaglandin E2 production and vascular endothelial growth factor upregulation, indicating a role for cyclooxygenase-2 in endothelin-1-induced vascular endothelial growth factor-mediated angiogenesis. In this study we demonstrated that endothelin-1-induced cyclooxygenase-2 and related prostaglandin E2 release were dependent upon the activation of endothelin-A receptor and of multiple mitogen-activated protein kinase signal pathways, including extracellular signal-regulated kinase 1/2 kinase, p38 mitogen-activated protein kinase and the transactivation of the epidermal growth factor receptor. In human ovarian xenografts, the levels of cyclooxygenase-2 protein expression were significantly reduced following treatment with the endothelin-A receptor selective antagonist, atrasentan, compared with untreated mice. These results suggest that the pharmacological blocking of endothelin-A receptor is an attractive strategy to control the cyclooxygenase-2 protein expression in ovarian carcinoma.
J Cardiovasc Pharmacol 2004 Nov
PMID:Endothelin-1 stimulates cyclooxygenase-2 expression in ovarian cancer cells through multiple signaling pathways: evidence for involvement of transactivation of the epidermal growth factor receptor. 1583 64

Experience is presented of 53 cases of diaphragm plasty of the bronchial stump, tracheobronchial anastomosis, pericardium, and esophagus wall after extended pneumonectomy on account of lung cancer. A pedicled diaphragm flap was used to prevent bronchopleural fistula in 53 patients, as well as heart dislocation after wide resection of the pericardium in 26, and esophagopleural fistula after resection of the muscle coat of the esophagus in 2. In all cases, there was a high risk of these complications. Dehiscence of the bronchial stump or tracheobronchial anastomosis occurred in 9 patients, but due to diaphragm plasty, a bronchopleural fistula formed in only 3. Restoration of the pericardium and the esophageal muscle coat was successful in all cases. Overall morbidity was 22.6%, 30-day mortality was 7.5%, hospital mortality was 11.3%. Causes of death were fulminant pneumonia of the single lung, cerebral hemorrhage, pulmonary embolism, heart failure, early tumor progression, and sepsis, in one case each. The results were compared with those in 49 patients who underwent other methods of bronchial stump or tracheobronchial anastomosis reinforcement. The analysis revealed that the diaphragm flap was highly efficacious as a multipurpose plastic material.
Asian Cardiovasc Thorac Ann 2006 Aug
PMID:Preventive diaphragm plasty after pneumonectomy on account of lung cancer. 1686 97

A case report of mucoepidermoid carcinoma of the thymus, aggressively treated by multimodality therapy including surgery, radiotherapy, chemothermotherapy, and systemic chemotherapy is presented. The patient, a 53-year-old man, underwent potentially complete resection for an anterior mediastinal tumor, histologically diagnosed as a mucoepidermoid carcinoma of the thymus with Masaoka stage II disease. However, because of local recurrences in the left chest wall and pleura, re-resection was twice performed 4 years and 5 months, and 5 years and 7 months after the initial surgery, in combination with intrathoracic chemothermotherapy and irradiation. Seven years and 1 month after the initial operation, in vitro chemosensitive test based-chemotherapy using vinorelbine for pleural disease was performed, resulting in maintenance of good quality of life (QOL) due to dramatic decrease in pleural effusion. He died of tumor progression, 7 years and 9 months after the initial treatment. Although the clinical aspects of thymic mucoepidermoid carcinoma are little known, it is assumed that such aggressive therapeutic multimodalities as repeated surgical resection, irradiation and chemothermotherapy, and chemotherapy based on in vitro chemosensitivity tests contributed to long-term survival for this unusual disease.
Ann Thorac Cardiovasc Surg 2006 Aug
PMID:Mucoepidermoid carcinoma of the thymus treated by multimodality therapy: a case report. 1697 99

In the nearly 130 years since Trousseau first described migratory thrombophlebitis in cancer patients, thromboembolism has become a well-established presenting sign and complication of cancer. The coagulation system is activated in cancer and is further amplified by treatment with chemotherapy, radiation or surgery. Hypercoagulation is documented in virtually all cancer types, albeit at different rates, and is the second leading cause of death in cancer patients. The relationship between clotting activation and carcinogenesis supports the view of cancer as a hypercoagulable state and holds implications for the development of thrombosis, enhancement of tumor growth and risk of poor clinical outcomes. Although it is well recognized that cancer can activate the coagulation cascade, it is less well known that activation of the coagulation system may also support tumor progression. Additionally, platelet activation in cancer patients and its impact on tumor progression and metastasis further expand the role of the hemostatic system in malignancy. The problem of thrombosis in patients with metastatic diseases is a serious concern for clinicians. This review explores the mechanisms and clinical implications of coagulation and platelet activation in cancer. The prevention and treatment of venous thromboembolism in cancer will also be discussed by reviewing data from key clinical investigations. Finally, the emerging role of low-molecular-weight heparin as an antineoplastic agent will be explored. Warfarin and unfractionated heparin have been in clinical use for more than 50 years. Both are effective anticoagulants, but their use is associated with a number of impediments, including the need for intensive coagulation monitoring, wide variation in dose-response relationships, multiple drug interactions (in the case of warfarin), and serious immune-mediated thrombocytopenia (in the case of heparin). The introduction of low-molecular weight heparin advanced anticoagulation therapy by enhancing efficacy and eliminating the need for intensive coagulation monitoring. Fondaparinux, the first selective factor Xa inhibitor, represents yet another improvement in anticoagulation therapy. By binding rapidly and strongly to antithrombin, its sole physiologic target in plasma, fondaparinux catalyzes specifically the inhibition of factor Xa, which results in effective and linear dose-dependent inhibition of thrombin generation. Additionally, efficient inhibition of factor Xa activity impairs the activation of tissue factor/factor VIIa complex leading to downregulation of procoagulant state, pro-angiogenesis, and proinflammatory factors induced by tissue factor/factor VIIa. Furthermore, a number of orally active direct antithrombin and anti-factor Xa are in advanced clinical development for various thromboembolic disorders.
Timely Top Med Cardiovasc Dis 2006 Aug 01
PMID:Role of current and emerging antithrombotics in thrombosis and cancer. 1680 96

We performed percutaneously radiofrequency (RF) ablation of 5 renal cell carcinomas (mean diameter 26 +/- 15 mm) with computed-tomography (CT) fluoroscopic guidance using the transhepatic route. The RF electrode was successfully advanced into all tumors. RF ablation caused one minor complication (small asymptomatic perirenal hematoma); no major complications occurred. The follow-up contrast-enhanced CT images showed no local tumor progression of any tumors in a median period of 10 months (range 3-14 months). In conclusion, it seems that this transhepatic approach is safe and can be an alternative method for electrode insertion during RF ablation of selected renal tumors.
Cardiovasc Intervent Radiol
PMID:Transhepatic approach for percutaneous computed-tomography-guided radiofrequency ablation of renal cell carcinoma. 1750 40


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