Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of two prostaglandins (prostaglandins E and F) have been determined in a series of murine mammary lesions ranging from preneoplastic, hyperplastic alveolar nodules to highly metastatic adenocarcinomas. A highly positive correlation was seen between high levels of prostaglandin E and high tumorigenicity and metastatic potential. In addition, spontaneous metastasis of two highly metastatic tumors was partially inhibited by p.o. administration of indomethacin from the time of s.c. tumor transplantation until removal of the primary tumor at a limited size. Further, mammary tumor cells of differing metastatic potential were susceptible to polyinosinic-polycytidylic acid activated spleen lymphocytes in vitro. Cells of metastatic tumor lines (410.4 and 66) were more resistant to killing than were cells of two non-metastatic tumor lines (168 and 410). The sensitivity of all target cells was increased when endogenous prostaglandin synthesis was prevented by the addition of indomethacin (1 microM) but was not affected by the lipoxygenase inhibitor nordihydroguaiaretic acid.
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PMID:Relationships of prostaglandin E and natural killer sensitivity to metastatic potential in murine mammary adenocarcinomas. 402 66

Human breast cancer cell lines growing as xenografts in athymic nude mice have been used to examine the effects of dietary fat and fatty acids on tumor progression. The estrogen independent MDA-MB-435 cell line has the advantage that it metastasizes consistently to the lungs and forms quantifiable secondary nodules when injected into the mammary fat pads. With these breast cancer cells, the stimulating effects of polyunsaturated omega-6 fatty acids on both primary tumor growth and metastasis were demonstrated; in contrast, the long-chain omega-3 fatty acids were inhibitory. The model can also be adapted to examine dietary fatty acids, and inhibitors of their metabolism, as experimental adjuvant therapy after surgical excision of the primary tumors. Unfortunately, estrogen dependent human breast cancer cells do not metastasize, or do so rarely, in nude mice; in consequence, it is not possible to use the model to study estrogen-fatty acid interactions on the metastatic process. In addition to metastasis from a primary location, intravenous injection of MDA-MB-435 cells into the nude mouse host, particularly when combined with studies using Matrigel-based in vitro invasion assays, permits further dissection of the steps in the metastatic cascade which are influenced by dietary fatty acids. The results obtained by these several approaches have demonstrated distinct roles for the cyclooxygenase and lipoxygenase-mediated products of omega-6 fatty acid metabolism, and suggest new approaches to experimental breast cancer therapy.
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PMID:Dietary fat and breast cancer metastasis by human tumor xenografts. 947 77