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Query: UMLS:C0278488 (metastatic breast cancer)
 7,812 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of cancer hypercalcaemia is an enigma that continues to challenge clinical investigators. Several possible mediators and pathways seem to be operating. To date, humoral and cellular mediators have been found to arise in tumour or normal tissues. The pathophysiological pathways that lead to osteolysis and hypercalcaemia are in large part determined by the biology of the specific tumour. Thus, the mechanisms that give rise to osteolysis in a metastatic breast cancer may be distinct from those that are operating in a non-metastatic lung carcinoma. The morbid consequences of excessive osteolysis and hypercalcaemia are usually similar and require prompt attention. Current research holds out the promise of identifying the agents and pathways responsible for cancer hypercalcaemia. Therapies may one day exist which arrest the specific pathophysiological processes which are operating.
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PMID:Hypercalcaemia in malignancy. 699 44

The aim of this paper is to explore current trends in the diagnosis, investigation and treatment of patients presenting with axillary lymph node metastases without a primary in the breast being found and, more rarely, those cases with metastatic breast cancer where the primary remains unknown--the so-called, 'occult' breast cancer. A retrospective study of 25 reported cases were selected from our database at the Royal Marsden and 6 patients were found to have true 'occult' breast cancer. These 6 patients are all still alive with no primary ever having been found in the breast. A literature review was then undertaken exploring the changing trends in this diagnostic enigma. MRI scanning, it is reported, may reveal the primary. Occult cancers in which imaging totally fails to show the primary will become increasingly rare. The prognosis of these, however, may be surprisingly better than one would expect from the nature of their presentation.
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PMID:'Occult' breast cancer. 1177 39