Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors investigated the clinical and radiological features and the treatment strategy for bone metastasis from a rare tumor, intracranial meningeal hemangiopericytoma. The clinical presentations and characteristic imagings were retrospectively reviewed in 15 bony metastatic lesions of four patients with this tumor. All four cases were initially diagnosed as atypical meningioma, and all of the bone metastases developed more than 10 years after the initial intracranial surgery. The common symptom induced by the metastatic lesions was pain. On plain roentgen films and computed tomography (CT), the involved bones showed thinning and expansion. On bone scintigraphy, a "cold-in-hot" appearance was typically observed. The clinical and radiological findings were diagnosed as bone metastasis from intracranial meningeal hemangiopericytoma. The prognosis after bone metastasis was relatively short compared to the long duration before bone metastases, because of the coexistence of other, visceral, metastasis. Combined with effective radiation therapy, surgical intervention for bone metastasis of this tumor should be carefully considered.
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PMID:Bone metastasis of intracranial meningeal hemangiopericytoma. 1599 Sep 73

Bone metastases are severely debilitating and have a significant impact on the quality of life of women with metastatic breast cancer. Treatment options are limited and in order to develop more targeted therapies, improved understanding of the complex mechanisms that lead to bone lesion development are warranted. Interestingly, whilst prostate-derived bone metastases are characterised by mixed or osteoblastic lesions, breast-derived bone metastases are characterised by osteolytic lesions, suggesting unique regulatory patterns. This study aimed to measure the changes in bone formation and bone resorption activity at two time-points (18 and 36 days) during development of the bone lesion following intratibial injection of MDA-MB-231 human breast cancer cells into the left tibiae of Severely Combined Immuno-Deficient (SCID) mice. The contralateral tibia was used as a control. Tibiae were extracted and processed for undecalcified histomorphometric analysis. We provide evidence that the early bone loss observed following exposure to MDA-MB-231 cells was due to a significant reduction in mineral apposition rate, rather than increased levels of bone resorption. This suggests that osteoblast activity was impaired in the presence of breast cancer cells, contrary to previous reports of osteoclast-dependent bone loss. Furthermore mRNA expression of Dickkopf Homolog 1 (DKK-1) and Noggin were confirmed in the MDA-MB-231 cell line, both of which antagonise osteoblast regulatory pathways. The observed bone loss following injection of cancer cells was due to an overall thinning of the trabecular bone struts rather than perforation of the bone tissue matrix (as measured by trabecular width and trabecular separation, respectively), suggesting an opportunity to reverse the cancer-induced bone changes. These novel insights into the mechanisms through which osteolytic bone lesions develop may be important in the development of new treatment strategies for metastatic breast cancer patients.
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PMID:Breast cancer cells induce osteolytic bone lesions in vivo through a reduction in osteoblast activity in mice. 2406 36