Advances in the biology of bone metastasis: How the skeleton affects tumor behavior

Sterling, Julie A.; Edwards, James; Martın, Thomas; Mundy, Gregory R.

doi:10.1016/j.bone.2010.07.015

Cited by 161 publications

(125 citation statements)

References 101 publications

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“…VEGF is also functionally linked to adhesion molecules, such as fibronectin and extracellular matrix. These proteins may assist tumor cells to attract and adhere to the bone microenvironment through the VEGF receptors VEGFR1 and VEGFR2 (Chen et al 2004, Sterling et al 2011.…”

Section: Vegf Signaling Bone Metastasis and Nichesmentioning

confidence: 99%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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Prostate cancer (PCa) is the most common malignancy affecting men in the western world. Although radical prostatectomy and radiation therapy can successfully treat PCa in the majority of patients, up to w30% will experience local recurrence or metastatic disease. Prostate carcinogenesis and progression is typically an androgen-dependent process. For this reason, therapies for recurrent PCa target androgen biosynthesis and androgen receptor function. Such androgen deprivation therapies (ADT) are effective initially, but the duration of response is typically %24 months. Although ADT and taxane-based chemotherapy have delivered survival benefits, metastatic PCa remains incurable. Therefore, it is essential to establish the cellular and molecular mechanisms that enable localized PCas to invade and disseminate. It has long been accepted that metastases require angiogenesis. In the present review, we examine the essential role for angiogenesis in PCa metastases, and we focus in particular on the current understanding of the regulation of vascular endothelial growth factor (VEGF) in localized and metastatic PCa. We highlight recent advances in understanding the role of VEGF in regulating the interaction of cancer cells with tumor-associated immune cells during the metastatic process of PCa. We summarize the established mechanisms of transcriptional and post-transcriptional regulation of VEGF in PCa cells and outline the molecular insights obtained from preclinical animal models of PCa. Finally, we summarize the current state of anti-angiogenesis therapies for PCa and consider how existing therapies impact VEGF signaling.

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Section: Vegf Signaling Bone Metastasis and Nichesmentioning

confidence: 99%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…2). The latter link has also been purported as one of the mechanism whereby the release of matrixbound TGFb facilitates the osteolytic capacity of breast cancer cells through their release of IL11 and other cytokines that stimulated the formation of bone-resorbing osteoclasts (37). Accordingly, low IL11 levels correlate with reduced resistance toward chemotherapy of human breast tumors and prolonged relapse-free survival (38).…”

Section: Il11 Promotes Tumorigenesismentioning

confidence: 99%

Molecular Pathways: IL11 as a Tumor-Promoting Cytokine—Translational Implications for Cancers

Ernst

Putoczki

2014

Clinical Cancer Research

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Emerging evidence suggests that cytokines produced by inflammatory cells act as rheostats to link the degree of wounding and local inflammation to epithelial cell survival, proliferation, and metabolism that collectively underpin the repair response. Among these cytokines, the GP130 family, which encompasses, among others, IL6 and IL11, plays a major role in orchestrating these complex processes through the activation of the latent signal transducer and activator of transcription 3 (STAT3) in the epithelium. However, many of the molecular mechanisms that govern and ensure effective epithelial wound healing and regeneration renewal also promote tumorigenesis and the progression of established cancers. Accordingly, GP130 cytokines endow the inflammatory tumor microenvironment with a capacity to promote "cancer hallmark capabilities" of the malignant epithelium, while simultaneously suppressing the antitumor response of innate and adaptive immune cells. Here, we review some recent insights derived from genetic and therapeutic inhibition of the IL6/IL11-GP130-STAT3 signaling cascade in the context of preclinical mouse models of cancer, which are likely to have implications to other solid malignancies. Clin Cancer Res; 20(22); 5579-88. Ó2014 AACR.

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“…In the case of breast cancer, the interaction of cancer cells with the bone microenvironment is crucial for their ability to colonize this tissue and their subsequent survival, growth and promotion of the feed-forward cycle of bone destruction, first described by Mundy and collaborators. [2][3][4] Thus, pharmacological interference with the microenvironmental support is an attractive strategy for repressing early bone metastasis. Toward that end, there is a need to identify the conditions and factors that make the bone microenvironment a hospitable tissue for breast cancer cell colonization and growth.…”

Section: Introductionmentioning

confidence: 99%

Chronic stress, sympathetic activation and skeletal metastasis of breast cancer cells

Elefteriou¹

2015

BoneKEy Reports

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Improved detection programs and new therapies significantly improved the 5-year survival rate of women with breast cancer. However, some women still relapse and succumb to cancer because of metastatic disease. In particular, chronically depressed patients do not seem to benefit from newly developed treatments and present with shorter survival. The reason for this association is unclear, but recent cues from preclinical studies point to the possible contribution of neuroendocrine factors generated in response to chronic stress and depression. Retrospective clinical studies also suggest a beneficial effect of sympathetic blockade in terms of less advanced disease at diagnosis, lower cancer-specific mortality, longer disease-free survival and reduced metastasis development and tumor recurrence, especially in patients who have taken propranolol before diagnosis. Therefore, b-blockers or therapies normalizing sympathetic tone might be beneficial as early adjuvant therapies to limit skeletal metastases and growth and eventually to improve prognosis in patients with breast cancers.

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Advances in the biology of bone metastasis: How the skeleton affects tumor behavior

Cited by 161 publications

References 101 publications

Regulation of vascular endothelial growth factor in prostate cancer

Regulation of vascular endothelial growth factor in prostate cancer

Molecular Pathways: IL11 as a Tumor-Promoting Cytokine—Translational Implications for Cancers

Chronic stress, sympathetic activation and skeletal metastasis of breast cancer cells

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