We are analyzing https://link.springer.com/article/10.1186/bcr1678.

Title:
Inflammation and breast cancer. Cyclooxygenase/prostaglandin signaling and breast cancer | Breast Cancer Research
Description:
Many human cancers exhibit elevated prostaglandin (PG) levels due to upregulation of cyclooxygenase-2 (COX-2), a key enzyme in eicosanoid biosynthesis. COX-2 over-expression has been observed in about 40% of cases of invasive breast carcinoma and at a higher frequency in preinvasive ductal carcinoma in situ tumors, Extensive pharmacologic and genetic evidence implicates COX enzymes in neoplasia. Epidemiologic analyses demonstrate a protective effect of COX-inhibiting nonsteroidal anti-inflammatory drugs with respect to human cancer. Complementary experimental studies have established that both conventional nonsteroidal anti-inflammatory drugs and selective COX-2 inhibitors suppress mammary tumor formation in rodent breast cancer models. Furthermore, knocking out Cox-2 reduces mammary tumorigenesis and angiogenesis, and, conversely, transgenic COX-2 over-expression induces tumor formation. The utility of COX/PG signaling as a target for chemoprevention has been established by randomized controlled clinical trials. However, these studies also identified increased cardiovascular risk associated with use of selective COX-2 inhibitors. Thus, current efforts are directed toward identifying safer approaches to antagonizing COX/PG signaling for cancer prevention and treatment, with a particular focus on PGE2 regulation and signaling, because PGE2 is a key protumorigenic prostanoid.
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Keywords {🔍}

cox, cancer, breast, pubmed, google, scholar, cas, article, mammary, cyclooxygenase, expression, tumor, human, signaling, pge, tumors, mice, res, role, data, tumorigenesis, figure, aromatase, overexpression, cancers, prostaglandin, formation, colorectal, coxibs, reduced, carcinoma, studies, transgenic, coxpg, target, mouse, central, howe, levels, neoplasia, prevention, receptor, herneu, including, selective, models, cardiovascular, growth, null, genetic,

Topics {✒️}

population-based case-control study mammary-targeted her2/neu transgene her2/neu-induced mammary tumorigenesis nested case-control study formalin-fixed tissue sections nonsteroidal anti-inflammatory drugs steroidal anti-inflammatory drug steroidal anti-inflammatory drugs promotes cancer progression chemically-induced tumors tend tgf-beta-induced suppressor mmtv/ndl mammary glands anti-breast cancer strategies er-negative tumor formation /neu-induced breast cancer epidermal growth factor nad+-linked 15-hydroxyprostaglandin dehydrogenase antagonizing cox/pg signaling cox/pg signaling axis hormone receptor-negative disease cox-2 wild-type animals 2/neu-positive breast cancer chemotherapy-induced cox-2 upregulation cox-2 wild-type controls distant disease-free survival her2/neu transgenic mice cyclooxygenase/prostaglandin signaling axis cox-2 wild-type samples mammary tumor formation identifies cox/pg signaling mouse mammary glands pg-dependent cyp19 induction increased microvessel density small-cell lung cancers targeting pge2-driven neoplasia cox/pg signaling pathway //breast-cancer-research breast cancer research mmtv/ndl mice express visible tumor formation drive tumor formation privacy choices/manage cookies authors’ original file decreased disease-free survival rat mammary carcinomas numerous cox-independent effects high-grade ductal carcinoma mammary adipose tissue cox-derived prostanoids contribute transgenic animals relative

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Schema {🗺️}

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         headline:Inflammation and breast cancer. Cyclooxygenase/prostaglandin signaling and breast cancer
         description:Many human cancers exhibit elevated prostaglandin (PG) levels due to upregulation of cyclooxygenase-2 (COX-2), a key enzyme in eicosanoid biosynthesis. COX-2 over-expression has been observed in about 40% of cases of invasive breast carcinoma and at a higher frequency in preinvasive ductal carcinoma in situ tumors, Extensive pharmacologic and genetic evidence implicates COX enzymes in neoplasia. Epidemiologic analyses demonstrate a protective effect of COX-inhibiting nonsteroidal anti-inflammatory drugs with respect to human cancer. Complementary experimental studies have established that both conventional nonsteroidal anti-inflammatory drugs and selective COX-2 inhibitors suppress mammary tumor formation in rodent breast cancer models. Furthermore, knocking out Cox-2 reduces mammary tumorigenesis and angiogenesis, and, conversely, transgenic COX-2 over-expression induces tumor formation. The utility of COX/PG signaling as a target for chemoprevention has been established by randomized controlled clinical trials. However, these studies also identified increased cardiovascular risk associated with use of selective COX-2 inhibitors. Thus, current efforts are directed toward identifying safer approaches to antagonizing COX/PG signaling for cancer prevention and treatment, with a particular focus on PGE2 regulation and signaling, because PGE2 is a key protumorigenic prostanoid.
         datePublished:2007-07-16T00:00:00Z
         dateModified:2007-07-16T00:00:00Z
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            PGE2
            Nimesulide
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            Aromatase Expression
            Cancer Research
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            Surgical Oncology
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      headline:Inflammation and breast cancer. Cyclooxygenase/prostaglandin signaling and breast cancer
      description:Many human cancers exhibit elevated prostaglandin (PG) levels due to upregulation of cyclooxygenase-2 (COX-2), a key enzyme in eicosanoid biosynthesis. COX-2 over-expression has been observed in about 40% of cases of invasive breast carcinoma and at a higher frequency in preinvasive ductal carcinoma in situ tumors, Extensive pharmacologic and genetic evidence implicates COX enzymes in neoplasia. Epidemiologic analyses demonstrate a protective effect of COX-inhibiting nonsteroidal anti-inflammatory drugs with respect to human cancer. Complementary experimental studies have established that both conventional nonsteroidal anti-inflammatory drugs and selective COX-2 inhibitors suppress mammary tumor formation in rodent breast cancer models. Furthermore, knocking out Cox-2 reduces mammary tumorigenesis and angiogenesis, and, conversely, transgenic COX-2 over-expression induces tumor formation. The utility of COX/PG signaling as a target for chemoprevention has been established by randomized controlled clinical trials. However, these studies also identified increased cardiovascular risk associated with use of selective COX-2 inhibitors. Thus, current efforts are directed toward identifying safer approaches to antagonizing COX/PG signaling for cancer prevention and treatment, with a particular focus on PGE2 regulation and signaling, because PGE2 is a key protumorigenic prostanoid.
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      dateModified:2007-07-16T00:00:00Z
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         PGE2
         Nimesulide
         Mammary Tumorigenesis
         Aromatase Expression
         Cancer Research
         Oncology
         Surgical Oncology
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