The Experts below are selected from a list of 238662 Experts worldwide ranked by ideXlab platform
John S Condeelis - One of the best experts on this subject based on the ideXlab platform.
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mena deficiency delays Tumor Progression and decreases metastasis in polyoma middle t transgenic mouse mammary Tumors
Breast Cancer Research, 2010Co-Authors: Evanthia T Roussos, Jeffrey W Pollard, Yarong Wang, Jeffrey B Wyckoff, Rani S Sellers, Weigang Wang, Frank B Gertler, John S CondeelisAbstract:Introduction The actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic Progression of solid Tumors in humans. Mena expression level in primary Tumors is correlated with metastasis in breast, cervical, colorectal and pancreatic cancers. Cells expressing high Mena levels are part of the Tumor microenvironment for metastasis (TMEM), an anatomical structure that is predictive for risk of breast cancer metastasis. Previously we have shown that forced expression of Mena adenocarcinoma cells enhances invasion and metastasis in xenograft mice. Whether Mena is required for Tumor Progression is still unknown. Here we report the effects of Mena deficiency on Tumor Progression, metastasis and on normal mammary gland development.
Jeffrey W Pollard - One of the best experts on this subject based on the ideXlab platform.
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mena deficiency delays Tumor Progression and decreases metastasis in polyoma middle t transgenic mouse mammary Tumors
Breast Cancer Research, 2010Co-Authors: Evanthia T Roussos, Jeffrey W Pollard, Yarong Wang, Jeffrey B Wyckoff, Rani S Sellers, Weigang Wang, Frank B Gertler, John S CondeelisAbstract:Introduction The actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic Progression of solid Tumors in humans. Mena expression level in primary Tumors is correlated with metastasis in breast, cervical, colorectal and pancreatic cancers. Cells expressing high Mena levels are part of the Tumor microenvironment for metastasis (TMEM), an anatomical structure that is predictive for risk of breast cancer metastasis. Previously we have shown that forced expression of Mena adenocarcinoma cells enhances invasion and metastasis in xenograft mice. Whether Mena is required for Tumor Progression is still unknown. Here we report the effects of Mena deficiency on Tumor Progression, metastasis and on normal mammary gland development.
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the macrophage growth factor csf 1 in mammary gland development and Tumor Progression
Journal of Mammary Gland Biology and Neoplasia, 2002Co-Authors: Valerie Gouonevans, Andrew V Nguyen, Jeffrey W PollardAbstract:Colony stimulating factor 1 (CSF-1), a major regulator of the mononuclear phagocytic lineage, is expressed in more than 70% of human breast cancers and its expression is correlated with poor prognosis. Studies of CSF-1 null mutant mice demonstrated that CSF-1 plays an important role in normal mammary ductal development as well as in mammary Tumor Progression to metastasis. CSF-1 regulates these processes through the recruitment and regulation of macrophages, cells that become associated with mammary Tumors and the terminal end buds at the end of the growing ducts. This phenomenon suggests that the Tumors subvert normal developmental processes to allow invasion into the surrounding stroma, a process that gives the Tumor access to the vasculature and consequently the promotion of metastasis. In addition, soluble CSF-1 secreted from the Tumor acts to divert antiTumor macrophage responses and suppresses the differentiation of mature Tumor-antigen-presenting dendritic cells. This review discusses these observations in detail and attempts to fit them into a larger picture of CSF-1 and macrophage action in the regulation of normal mammary gland development and Tumor Progression.
Bo Zhu - One of the best experts on this subject based on the ideXlab platform.
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Tumor derived tissue factor aberrantly activates complement and facilitates lung Tumor Progression via recruitment of myeloid derived suppressor cells
International Journal of Molecular Sciences, 2017Co-Authors: Xiao Han, Haoran Zha, Fei Yang, Bo Guo, Bo ZhuAbstract:The initiator of extrinsic coagulation, tissue factor (TF), and its non-coagulant isoform alternatively spliced TF (asTF) are closely associated with Tumor development. In the Tumor microenvironment, the role of TF-induced coagulation in Tumor Progression remains to be fully elucidated. Using TF-knockdown lung Tumor cells, we showed that TF is the dominant component of procoagulant activity but is dispensable in the cellular biology of Tumor cells. In a xenograft model, using immunohistochemical analysis and flow cytometry analysis of the Tumor microenvironment, we demonstrated that TF-induced fibrin deposition, which is correlated with complement activation and myeloid-derived suppressor cell (MDSC) recruitment, is positively associated with Tumor Progression. C5aR antagonism blunted the effect of TF on Tumor Progression and decreased MDSC recruitment. In conclusion, our data suggested that in Tumor microenvironment, TF-induced coagulation activated the complement system and subsequently recruited myeloid-derived suppressor cells to promote Tumor growth, which brings new insights into the coagulation-induced complement activation within the Tumor microenvironment during Tumor Progression.
Suzanne Ostrandrosenberg - One of the best experts on this subject based on the ideXlab platform.
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reduced inflammation in the Tumor microenvironment delays the accumulation of myeloid derived suppressor cells and limits Tumor Progression
Cancer Research, 2007Co-Authors: Stephanie K Bunt, Linglin Yang, Pratima Sinha, Virginia K Clements, Jeff Leips, Suzanne OstrandrosenbergAbstract:Chronic inflammation is frequently associated with malignant growth and is thought to promote and enhance Tumor Progression, although the mechanisms which regulate this relationship remain elusive. We reported previously that interleukin (IL)-1β promoted Tumor Progression by enhancing the accumulation of myeloid-derived suppressor cells (MDSC), and hypothesized that inflammation leads to cancer through the production of MDSC which inhibit Tumor immunity. If inflammation-induced MDSC promote Tumor Progression by blocking antiTumor immunity, then a reduction in inflammation should reduce MDSC levels and delay Tumor Progression, whereas an increase in inflammation should increase MDSC levels and hasten Tumor Progression. We have tested this hypothesis using the 4T1 mammary carcinoma and IL-1 receptor (IL-1R)–deficient mice which have a reduced potential for inflammation, and IL-1R antagonist–deficient mice, which have an increased potential for inflammation. Consistent with our hypothesis, IL-1R–deficient mice have a delayed accumulation of MDSC and reduced primary and metastatic Tumor Progression. Accumulation of MDSC and Tumor Progression are partially restored by IL-6, indicating that IL-6 is a downstream mediator of the IL-1β–induced expansion of MDSC. In contrast, excessive inflammation in IL-1R antagonist–deficient mice promotes the accumulation of MDSC and produces MDSC with enhanced suppressive activity. These results show that immune suppression by MDSC and Tumor growth are regulated by the inflammatory milieu and support the hypothesis that the induction of suppressor cells which down-regulate Tumor immunity is one of the mechanisms linking inflammation and cancer. [Cancer Res 2007;67(20):10019–26]
Evanthia T Roussos - One of the best experts on this subject based on the ideXlab platform.
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mena deficiency delays Tumor Progression and decreases metastasis in polyoma middle t transgenic mouse mammary Tumors
Breast Cancer Research, 2010Co-Authors: Evanthia T Roussos, Jeffrey W Pollard, Yarong Wang, Jeffrey B Wyckoff, Rani S Sellers, Weigang Wang, Frank B Gertler, John S CondeelisAbstract:Introduction The actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic Progression of solid Tumors in humans. Mena expression level in primary Tumors is correlated with metastasis in breast, cervical, colorectal and pancreatic cancers. Cells expressing high Mena levels are part of the Tumor microenvironment for metastasis (TMEM), an anatomical structure that is predictive for risk of breast cancer metastasis. Previously we have shown that forced expression of Mena adenocarcinoma cells enhances invasion and metastasis in xenograft mice. Whether Mena is required for Tumor Progression is still unknown. Here we report the effects of Mena deficiency on Tumor Progression, metastasis and on normal mammary gland development.
