We are analyzing https://link.springer.com/article/10.1186/bcr1980.

Title:
Inflammation and breast cancer. Metalloproteinases as common effectors of inflammation and extracellular matrix breakdown in breast cancer | Breast Cancer Research
Description:
Two rapidly evolving fields are converging to impact breast cancer: one has identified novel substrates of metalloproteinases that alter immune cell function, and the other has revealed a role for inflammation in human cancers. Evidence now shows that the mechanisms underlying these two fields interact in the context of breast cancer, providing new opportunities to understand this disease and uncover novel therapeutic strategies. The metalloproteinase class of enzymes is well studied in mammary gland development and physiology, but mostly in the context of extracellular matrix modification. Aberrant metalloproteinase expression has also been implicated in breast cancer progression, where these genes act as tumor modifiers. Here, we review how the metalloproteinase axis impacts mammary physiology and tumorigenesis and is associated with inflammatory cell influx in human breast cancer, and evaluate its potential as a regulator of inflammation in the mammary gland.
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Keywords {🔍}

cancer, breast, pubmed, mammary, google, scholar, article, cas, timp, cell, metalloproteinase, mmp, cells, gland, expression, inflammation, tumor, metalloproteinases, matrix, immune, role, tissue, mice, adam, ductal, inflammatory, human, development, central, axis, tumorigenesis, involution, inhibitor, growth, khokha, biol, epithelial, factor, res, mmps, model, mouse, function, progression, studies, levels, macrophages, apoptosis, metastasis, overexpression,

Topics {✒️}

reversion-inducing cysteine-rich protein her2/neu-induced mammary tumorigenesis wnt1-induced mammary tumorigenesis full size image cigarette smoke-induced emphysema tumour necrosis factor-alpha transforming growth factor-α estrogen receptor-negative status komen post-doctoral fellowship atypical ductal hyperplasia beta-catenin binding domain distant relapse-free survival stromal-epithelial cross-talk enzyme-linked immunosorbent assay matrix met-alloproteinase-9 triggers real time-pcr analysis destabilizes e-cadherin function mmtv-pymt mammary tumors timp-3-deficient mammary gland terminal end buds cell type-specific expression //breast-cancer-research colony stimulating factor mouse models provide chronic hepatic inflammation related subjects lymphocytic infiltrate-positive mouse mammary gland extracellular matrix-degrading proteinases tissue-specific gene expression mammary-specific timp1 overexpression lymphocytic infiltrate-negative early mammary tumorigenesis metalloproteinases fragment e-cadherin mouse mammary development stage-specific patterns mammary tumor progression tumor necrosis factor alveolar mammary morphogenesis lymphocytic infiltrate status privacy choices/manage cookies unscheduled apoptosis early de campos jm breast cancer models gonzalez lo suggested pro-inflammatory function human breast carcinoma sympson cj tumor cell fate mammary tumor bearers

Questions {❓}

Balkwill F, Mantovani A: Inflammation and cancer: back to Virchow?
Monks J, Geske FJ, Lehman L, Fadok VA: Do inflammatory cells participate in mammary gland involution?
Vorbach C, Capecchi MR, Penninger JM: Evolution of the mammary gland from the innate immune system?

Schema {🗺️}

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         description:Two rapidly evolving fields are converging to impact breast cancer: one has identified novel substrates of metalloproteinases that alter immune cell function, and the other has revealed a role for inflammation in human cancers. Evidence now shows that the mechanisms underlying these two fields interact in the context of breast cancer, providing new opportunities to understand this disease and uncover novel therapeutic strategies. The metalloproteinase class of enzymes is well studied in mammary gland development and physiology, but mostly in the context of extracellular matrix modification. Aberrant metalloproteinase expression has also been implicated in breast cancer progression, where these genes act as tumor modifiers. Here, we review how the metalloproteinase axis impacts mammary physiology and tumorigenesis and is associated with inflammatory cell influx in human breast cancer, and evaluate its potential as a regulator of inflammation in the mammary gland.
         datePublished:2008-03-31T00:00:00Z
         dateModified:2008-03-31T00:00:00Z
         pageStart:1
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            Mammary Gland
            Mouse Mammary Tumor Virus
            Atypical Ductal Hyperplasia
            Mammary Tumorigenesis
            Cancer Research
            Oncology
            Surgical Oncology
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      headline:Inflammation and breast cancer. Metalloproteinases as common effectors of inflammation and extracellular matrix breakdown in breast cancer
      description:Two rapidly evolving fields are converging to impact breast cancer: one has identified novel substrates of metalloproteinases that alter immune cell function, and the other has revealed a role for inflammation in human cancers. Evidence now shows that the mechanisms underlying these two fields interact in the context of breast cancer, providing new opportunities to understand this disease and uncover novel therapeutic strategies. The metalloproteinase class of enzymes is well studied in mammary gland development and physiology, but mostly in the context of extracellular matrix modification. Aberrant metalloproteinase expression has also been implicated in breast cancer progression, where these genes act as tumor modifiers. Here, we review how the metalloproteinase axis impacts mammary physiology and tumorigenesis and is associated with inflammatory cell influx in human breast cancer, and evaluate its potential as a regulator of inflammation in the mammary gland.
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      dateModified:2008-03-31T00:00:00Z
      pageStart:1
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         Breast Cancer
         Mammary Gland
         Mouse Mammary Tumor Virus
         Atypical Ductal Hyperplasia
         Mammary Tumorigenesis
         Cancer Research
         Oncology
         Surgical Oncology
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