Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor invasion and metastasis are complex phenomena believed to be facilitated by the disruption of collagen and elastin fibers in the extracellular matrix. Interstitial collagenase gene expression was studied in colonic adenocarcinoma and adenoma using in situ hybridization. The data indicated that three cell types within the tumor stroma expressed collagenase transcripts; they were eosinophils, fibroblasts, and vascular endothelium. In all 12 adenocarcinomas, a high to moderate level of expression was seen in 1 to 5% of eosinophils and in occasional fibroblasts, whereas these cell types in non-neoplastic mucosa adjacent to tumor showed no detectable expression. Two adenocarcinomas showed expression in hyperplastic endothelium in vascularized granulation tissue. Two out of three adenomas showed expression in eosinophils and fibroblasts at a reduced level. Tissue inhibitor of metalloproteinase-1 gene expression was, however, negligible in all tissue examined. These results suggest that interstitial collagenase gene activation in the tumor stroma, especially eosinophils, may have an important role in tumor invasion and metastasis.
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PMID:Interstitial collagenase gene expression in colonic neoplasia. 836 69

Blood vessels within pituitary adenomas were visualized using the immunocytochemical reaction for Factor VIII (von Willebrand Factor), a specific marker of the vascular endothelium. The number of immunopositive vascular profiles were counted and expressed as a mean number per one microscopic field. The results were related to the type of adenoma, established on the basis of immunocytochemical investigation using the antibodies against pituitary hormones or a-subunit (a-SU). It was found that the richest vascularization occurred in adenomas expressing follicle-stimulating hormone (FSH). The possible role of FSH in pituitary angiogenesis is discussed.
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PMID:Immunocytochemical Investigations on the Vascularization of Pituitary Adenomas. 1211 22

Substantial evidence indicates that significant exposure to cigarette smoke is associated with an elevated risk for colorectal cancer. However, the mechanisms underlying the causal relationship between cigarette smoking and colorectal cancer remain to be investigated. Our previous study showed that cigarette smoke promotes the formation of inflammation-associated colonic adenoma in mice through an angiogenic pathway. Therefore, in the present study, we used the human colon adenocarcinoma cell line, SW1116, and human umbilical vascular endothelial cells (HUVECs) to elucidate the possible mechanisms in vitro. Results showed that cigarette smoke extract enhanced cell proliferation and the expression of 5-lipoxygenase (5-LOX), vascular endothelium growth factor (VEGF), matrix metalloproteinases (MMPs) 2 and 9 in SW1116 cells. Inhibition of 5-LOX decreased cell proliferation and expressions of VEGF, MMP-2 and MMP-9 induced by cigarette smoke extract. In addition, cigarette smoke extract indirectly stimulated HUVEC proliferation, a biological activity closely related to angiogenesis during tumor growth. This was again blocked by the 5-LOX inhibitor. Taken together, the results of the present study demonstrate the central role of 5-LOX and its relationship with angiogenic mediators in the actions of cigarette smoke in the promotion of angiogenesis during colon cancer growth.
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PMID:A mechanistic study of colon cancer growth promoted by cigarette smoke extract. 1612 68

Serum levels of vascular endothelium growth factor were measured in 43 patients with adrenal tumors and 25 healthy subjects. The mean blood levels of the factor in patients with adrenal tumors significantly surpassed the control. No correlations between the level of vascular endothelium growth factor, patients age and sex were detected. The levels of this factor were maximum in patients with adrenocortical cancer, but its mean level differed negligibly from that in other morphological variants of tumors. The level of vascular endothelium growth factor tended to increase with increasing the stage of adrenocortical cancer. A direct correlation was revealed between the level of vascular endothelium growth factor and tumor size in adrenocortical cancer and aldosterone-producing adenoma. Presumably, vascular endothelium growth factor is involved into mechanisms of growth, invasion, and metastatic growth of adrenocortical cancer.
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PMID:Vascular endothelium growth factor in the sera of patients with adrenal tumors. 1628 8

Primary aldosteronism is one of the most common causes of secondary hypertension. In recent years the prevalence has risen dramatically, from 1% to 14% of all hypertensive patients. This has been largely attributed to an increase in diagnosis. Primary aldosteronism is characterized by hypertension with or without hypokalemia and a high plasma aldosterone concentration (PAC) with a concurrent low plasma renin activity (PRA). The most common subtypes of primary aldosteronism are aldosterone-producing adenoma (42%) and bilateral idiopathic hyperaldosteronism (58%). Other less common subtypes (<1%) are glucocorticoid-remediable aldosteronism, and unilateral primary hyperplasia. Current treatment for primary aldosteronism relies on accurate subtype distinction and assessment of unilateral versus bilateral disease. Bilateral idiopathic hyperaldosteronism is best managed pharmacologically and improves with the use of aldosterone receptor antagonists. Combined treatment with sodium-channel blockers and calcium-channel blockers has also shown satisfactory results. Glucocorticoid-remediable aldosteronism responds well to treatment with low-dose glucocorticoids. Aldosterone producing adenoma and unilateral adrenal hyperplasia are appropriately treated with laparoscopic adrenalectomy. Following adrenalectomy blood pressure improves in 98% of these patients, but only about 33% require no further antihypertensive medication. Identifying the subgroups that will most benefit from adrenalectomy is paramount to formulating individual treatment strategies. In the past, treatment focused mainly on the correction of hypertension and electrolyte disturbances. Now, with accumulating evidence of the detrimental effects of aldosterone to the myocardium, vascular endothelium and kidneys, treatment also focuses on normalizing aldosterone levels or blocking aldosterone action at the receptor level. Therefore, it is essential to accurately identify the specific subtype of primary aldosteronism in order to select optimal treatment and to achieve successful patient outcomes.
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PMID:Prediction of successful outcome in patients with primary aldosteronism. 1805 76