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)

The case history of a 22-months old boy with a malignant embryonal tumor of the prostate is given. Five years after initiation and three years after termination of a combined therapy with cytostatic drugs (actinomycin D, vincristine sulfate and cyclophosphamide) and surgery he is in good health without any signs of recurrence or metastatic disease. On this moment it is still impossible to be certain whether this therapy is the key for treatment of these tumors, but the successes published and the result till now in this case can be an indication that we are going in the right direction. Perhaps we may even hope that in the future we will have cytostatic drugs and combinations of therapy which will enable us to avoid mutilating operations.
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PMID:A case of embryonal sarcoma (rhabdomyosarcoma) of the prostate treated with combined surgical and cytostatic therapy. 5 4

Intercellular glycosaminoglycans (GAGs) from various tissues were analyzed by cellulose acetate electrophoresis and enzymatic treatment with specific mucopolysaccharidases. Each tissue exhibits a particular composition of sulfate and unsulfated molecular species. Invariably, malignant human neoplasias and their metastases show striking variations in the electrophoretic pattern typical of the corresponding normal tissue. An absolute or relative increase in surface ChS A/C and HA seems to be a consistent feature of neoplastic transformation. On the other hand, the GAGs composition of benign noninfiltrative tumors does not vary greatly with respect to the original normal tissue.
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PMID:Intercellular glycosaminoglycans in human cancer. 12 Jun 29

Extensive hormonal evaluation was performed in a girl with adrenal carcinoma during the primary tumor stage, following adrenalectomy, during the period when metastases were evident and while on treatment with o,p'-DDD. At the age of 14 months a diagnosis of congenital adrenal hyperplasia was made and treatment with dexamethasone (0.125 to 0.25 mg/day) resulted in a fall-off in growth rate, normal advancement in bone age, decrease in virilization and suppression of 17- ketosteroid excretion which continued until 4 3/12 years of age when virilization increased. At five years of age elevated serum and urinary androgen levels unsuppressible with dexamethasone were noted. Following removal of a large right adrenal carcinoma, serum and urinary hormone levels returned to normal. There months following surgery, liver metastases were documented associated with elevated levels of serum androgens. With o,p'-DDD treatment, serum dehydroepiandrosterone sulfate (DS) and urinary 17-ketosteroid (17-KS) excretion fell rapidly while there was a delay in the fall of free androgens. The persistence of free steroid secretion with decreased formation of DS suggests that the o,p'-DDD may have altered sulfatase activity before causing tumor necrosis and total decrease in steroidogenesis.
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PMID:Virilizing adrenal tumor in a child suppressed with dexamethasone for three years. Effect of o,p'-DDD on serum and urinary androgens. 13 87

Urinary excretions of free cortisol and corticosteroid sulfates were determined in 31 female controls, 77 breast cancer patients, 14 cases of colonic cancer, and 7 patients with bronchial carcinoma. Elevated corticosteroid sulfate excretion was present in 38% of patients with locally recurrent breast cancer and 30% of those with distant metastases, but in only 13% of the "early" breast cancer cases. A similar abnormality was seen in colonic cancer. Urinary free cortisol was usually normal. ACTH stimulation in a normal subject produced marked increases of both urinary free cortisol and corticosteroid sulfates. It is concluded that elevated corticosteroid sulfate excretion in cancer patients arises from an increased cortisol production rate combined with increased sulfurylation of the steroid. In bronchial carcinoma patients, changes similar to those occurring in the ACTH-treated normal subject may have resulted from ectopic ACTH production in the tumor.
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PMID:The urinary excretion of corticosteroid sulfates by cancer patients. 17 59

The urinary excretion of corticosteroid sulfates and free cortisol were determined in 150 breast cancer patients. Four of 60 cases of early breast cancer (7%) and 26 of 90 patients with advanced breast cancer (29%) showed an elevated urinary corticosteroid sulfate excretion. Urinary free cortisol was usually normal. Estrogen receptor assays were performed on tumor samples from 67 breast cancer patients; 24 were from primary lesions obtained at mastectomy, 3 from inoperable primaries in patients with systemic metastases, and 40 from metastases. Sixteen of the primary breast cancers (67%), 26 of the metastases (65%) and 1 of the 3 inoperable primaries contained estrogen receptors. With 2 exceptions, patients with an increased urinary corticosteroid sulfate excretion also had estrogen receptor-containing tumors.
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PMID:Corticosteroid sulfate excretion and estrogen receptors in breast cancer. 17 41

During the past ten years, the histiogenesis of malignant histiocytomas and a group of related benign and malignant lesions have been the source of speculation. Although of heterogeneous histological appearance, it is believed that there is a common cell of origin for these neoplasms--the histiocyte. From 1966 to 1974, 16 patients were encountered who had neoplasms that fell into the general group of malignant histiocytomas. These tumors were variously located in the extremities, head, chest wall, retroperitoneum, lung, spermatic cord, and lower abdomen. Surgical treatment included radical amputations, wide local excision, pulmonary lobectomy, and nephrectomy. Cobalt therapy and chemotherapy with vincristine sulfate, cyclophosphamide, doxorubicin hydrochloride, and chlorambucil were also used. Ten of 16 patients are alive after treatment, two are alive with metastatic disease, but four have died of malignant disease.
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PMID:Malignant histiocytomas. 20 92

2,4-Diaminoanisole sulfate was fed at dietary levels of 0.12% (low dose) or 0.5% (high dose) to groups of 50 male and 50 female inbred F344 rats for 78 weeks. By 107 weeks after the initial exposure, 58% of the male rats and 42% of the female rats administered the high dose had thyroid neoplasms, whereas only 7--8% of the controls developed them. Follicular cell carcinomas were the primary type of neoplasm induced. None of the controls had these tumors. The carcinomas, which were papillary, cystic, or solid, were highly invasive but did not metastasize. A brown pigment was present as granules primarily in thyroid follicular cells in all exposed rats. The amount of pigment as determined by an image-analyzing computer revealed that the cross-sectional area occupied by the pigment granules and the optical density of the granules were dose related.
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PMID:Neoplasms and pigmentation of thyroid glands in F344 rats exposed to 2,4-diaminoanisole sulfate, a hair dye component. 28 80

Interaction of T and B lymphocytes, platelets, granulocytes, macrophages and mast cells with the subendothelial extracellular matrix (ECM) is associated with degradation of heparan sulfate (HS) by a specific endoglycosidase (heparanase) activity. The enzyme is released from intracellular compartments (i.e., lysosomes, specific granules) in response to various activation signals (i.e., thrombin, calcium ionophore, immune complexes, antigens, mitogens), suggesting its regulated involvement in inflammation and cellular immunity. In contrast, various tumor cells appear to express and secrete heparanase in a constitutive manner, in correlation with their metastatic potential. Heparanase enzymes produced by different cell types may exhibit different molecular properties and substrate cleavage specificities. The platelet enzyme appears also in a latent form. It can be activated by tumor cells and thereby facilitate their extravasation in the process of metastasis. Degradation of ECM-HS by all cell types was facilitated by a proteolytic activity residing in the ECM and/or expressed by the invading cells. This proteolytic activity produced a more accessible substrate for the heparanase enzymes. Heparanase-inhibiting, nonanticoagulant species of heparin markedly reduced the incidence of lung metastasis in experimental animals. These species of heparin also significantly impaired the traffic of T lymphocytes and suppressed cellular immune reactivity and experimental autoimmune diseases. Heparanase activity expressed by intact cells (i.e., platelets, mast cells, neutrophils, lymphoma cells) was found to release active HS-bound basic fibroblast growth factor from ECM and basement membranes. Heparanase may thus elicit an indirect neovascular response in processes such as wound repair, inflammation and tumor development. The significant anticancerous effect of heparanase-inhibiting molecules may therefore be attributed to their potential inhibition of both tumor invasion and angiogenesis. Both normal leukocytic cells and metastatic tumor cells can enter the bloodstream, travel to distant sites and extravasate to the parenchyma at these sites. We suggest that heparanase is utilized for this purpose by both types of cells. Other functions (i.e., enzyme activities, adhesive interactions, chemotactic and proliferative responses) of metastatic tumor cells seem to mimic the equivalent functions of leukocytes as they migrate across blood vessels to gain access to sites of inflammation.
Invasion Metastasis 1992
PMID:Expression of heparanase by platelets and circulating cells of the immune system: possible involvement in diapedesis and extravasation. 139

To assess the safety and efficacy of concomitant pulmonary resection and cardiac operation requiring cardiopulmonary bypass, the records of 19 patients were reviewed. Eighteen patients (94.7%) presented with cardiac symptoms and were found to have pulmonary pathology of indeterminate etiology. Pulmonary resections were performed through a median sternotomy in all but 1 patient, who underwent posterolateral thoracotomy and right middle lobectomy after repositioning because dense adhesions prevented adequate dissection through the initial incision. A total of 24 resections were performed. Sixteen (66.7%) were performed on cardiopulmonary bypass. Six wedge resections (25.0%) were performed before bypass. Two lobectomies (8.3%) were performed after infusion of protamine sulfate. Nine patients (47.4%) had benign pathology, 7 (36.8%) had primary carcinoma, and 3 (15.8%) had metastatic disease. Bleeding complications occurred in 15.8% of patients (3/19). There was 1 perioperative death (5.3%), which was due to adult respiratory distress syndrome after intraoperative hemorrhage followed lobectomy for bullous disease. Another patient required lateral extension of the sternotomy during an episode of exsanguinating intraparenchymal pulmonary hemorrhage, which resulted in lobectomy, as well as costochondral and sternal osteomyelitis. A third patient required exploration for bleeding at the staple line. Postoperative complications occurred in 7 patients (36.8%) and were predominantly respiratory (5/7, 71.4%) (p = 0.006). The median postoperative hospitalization was 15 days. Although comparison of patients who underwent pulmonary resection during bypass with those who had resection either before heparinization or after protamine infusion showed no significant difference with respect to age, incidence of malignancy, operation performed, complications, postoperative hospitalization, or survival, this was probably due to the small number of patients in the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Concomitant cardiac and pulmonary operation: the role of cardiopulmonary bypass. 163 22

We have examined the binding and functional activity of monoclonal antibody (MAb) SG-1 that was raised by immunization against embryonal carcinoma cells and screened using KHT fibrosarcoma cells. Quantitative absorption, binding and in situ immunochemical staining assays indicate that the MAb SG-1-defined epitopes are expressed preferentially by the highly metastatic KHT35-L1 cells relative to the weakly metastatic, parental KHTp cells. Furthermore, there was a significant correlation (p less than 0.05) between the expression of MAb SG-1-defined antigen on the cells, following trypsin treatment, and their metastatic ability. Binding of MAb SG-1 to antigen was inhibited by specific sulfated polysaccharides including cerebroside sulfate (brain sulfatide), fucoidan, and dextran sulfate (500 kD) but not by heparan, chondroitin, keratan or dextran (5 kD) sulfates. Initial characterization of antigen from KHT cells indicates that the epitope of MAb SG-1 is defined by sulfated glycoconjugates containing galactose and sulfate but not N-acetylglucosamine. In the total lipid extracts of KHT35-L1 cells the antigen was detected in the delipidated protein fraction as well as in the chloroform/methanol fraction. These results suggest that the sulfated glycoconjugate determinants identified by MAb SG-1 may be relevant to the metastatic process of KHT fibrosarcoma cells.
Clin Exp Metastasis
PMID:Sulfated glycoconjugate determinants recognized by monoclonal antibody, SG-1, correlate with the experimental metastatic ability of KHT fibrosarcoma cells. 169 55


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