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10.1158/1078-0432.CCR-13-1590 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-13-1590 C4058425!4058425!24677373     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Cancer+Res 2014 ; 20 (12): 3071-7 Nephropedia Template TP {{tp|p=24677373|t=2014. Molecular Mechanisms of Bone Metastasis and Associated Muscle Weakness |pdf=|usr=}}{{24677373}} gab.com Text Molecular Mechanisms of Bone Metastasis and Associated Muscle Weakness JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24677373 #FOAvip Bone is a preferred site for breast cancer metastasis and leads to pathological bone loss due to increased osteoclast-induced bone resorption. The homing of tumor cells to the bone depends on the support of the bone microenvironment in which the tumor cells prime the pre-metastatic niche. The colonization and growth of tumor cells then depends on adaptations in the invading tumor cells to take advantage of normal physiological responses by mimicking bone marrow cells. This concerted effort by tumor cells leads to uncoupled bone remodeling in which the balance of osteoclast-driven bone resorption and osteoblast-driven bone deposition is lost. Breast cancer bone metastases often lead to osteolytic lesions due to hyperactive bone resorption. Release of growth factors from bone matrix during resorption then feeds a ?vicious cycle? of bone destruction leading to many skeletal related events. In addition to activity in bone, some of the factors released during bone resorption are also known to be involved in skeletal muscle regeneration and contraction. In this review, we discuss the mechanisms that lead to osteolytic breast cancer bone metastases and the potential for cancer-induced bone-muscle cross-talk leading to skeletal muscle weakness. Twit Text FOAVip Molecular Mechanisms of Bone Metastasis and Associated Muscle Weakness ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24677373 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24677373 #FOAvip English Wikipedia <ref>{{Cite pmid|24677373}}</ref> Molecular Mechanisms of Bone Metastasis and Associated Muscle Weakness #MMPMID24677373 Waning DL; Guise TA Clin Cancer Res 2014[Jun]; 20 (12): 3071-7 PMID24677373show ga Bone is a preferred site for breast cancer metastasis and leads to pathological bone loss due to increased osteoclast-induced bone resorption. The homing of tumor cells to the bone depends on the support of the bone microenvironment in which the tumor cells prime the pre-metastatic niche. The colonization and growth of tumor cells then depends on adaptations in the invading tumor cells to take advantage of normal physiological responses by mimicking bone marrow cells. This concerted effort by tumor cells leads to uncoupled bone remodeling in which the balance of osteoclast-driven bone resorption and osteoblast-driven bone deposition is lost. Breast cancer bone metastases often lead to osteolytic lesions due to hyperactive bone resorption. Release of growth factors from bone matrix during resorption then feeds a ?vicious cycle? of bone destruction leading to many skeletal related events. In addition to activity in bone, some of the factors released during bone resorption are also known to be involved in skeletal muscle regeneration and contraction. In this review, we discuss the mechanisms that lead to osteolytic breast cancer bone metastases and the potential for cancer-induced bone-muscle cross-talk leading to skeletal muscle weakness. äMolecular Mechanisms of Bone Metastasis and Associated Muscle Weakness(epmc).pdf DeepDyve Pubget Overpricing