pubmed-article:18691115 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18691115 | lifeskim:mentions | umls-concept:C0376545 | lld:lifeskim |
pubmed-article:18691115 | lifeskim:mentions | umls-concept:C0387583 | lld:lifeskim |
pubmed-article:18691115 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:18691115 | lifeskim:mentions | umls-concept:C2699007 | lld:lifeskim |
pubmed-article:18691115 | lifeskim:mentions | umls-concept:C1555307 | lld:lifeskim |
pubmed-article:18691115 | pubmed:issue | 21 | lld:pubmed |
pubmed-article:18691115 | pubmed:dateCreated | 2008-8-11 | lld:pubmed |
pubmed-article:18691115 | pubmed:abstractText | There is much interest in the potential use of Cox-2 selective inhibitors in combination with other cancer therapeutics. Malignancies of hematopoietic and non-hematopoietic origin often have increased expression of cyclooxygenase-2 (Cox-2), a key modulator of inflammation. For example, hematological malignancies such as chronic lymphocytic leukemia, chronic myeloid leukemia, Hodgkin's lymphoma, non-Hodgkin's lymphoma and multiple myeloma often highly express Cox-2, which correlates with poor patient prognosis. Expression of Cox-2 enhances survival and proliferation of malignant cells, while negatively influencing anti-tumor immunity. Hematological malignancies expressing elevated levels of Cox-2 potentially avoid immune responses by producing factors that enhance angiogenesis and metastasis. Cellular immune responses regulated by natural killer cells, cytotoxic T lymphocytes, and T regulatory cells are also influenced by Cox-2 expression. Therefore, Cox-2 selective inhibitors have promising therapeutic potential in patients suffering from certain hematological malignancies. | lld:pubmed |
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