Journal of Tumor
http://ghrnet.org/index.php/JT
ISSN-Online: 1819-6187<br />Frequency: Annual, Instant published<br />Journal Access: Open Access<br />The first Issue: June, 2013<br /><br />en-USJournal of Tumor1819-6187<p>Submission of a manuscript implies that the work described is not simultaneously being considered by other journals or is already published elsewhere; That the material contained within the manuscript is original, with all information from other sources appropriately referenced, and that written specific permission has been granted by any existing copyright holders prior to publication and is clearly cited and available. That its publication has been approved by all co-authors; That the author(s) agree to transfer to ACT Publishing Group Inc exclusive copyright ownership for all formats of the manuscript, including print and electronic formats, English and non-English language formats, and subsequent editions; That the author(s) acknowledge that all articles published by ACT Publishing Group Inc are selected by an in-house editor and fully peer-reviewed by external reviewers. ACT Publishing Group Inc applies the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: <a href="http://creativecommons.org/licenses/by-nc/4.0/">http://creativecommons.org/licenses/by-nc/4.0/</a>. The corresponding author and all co-authors, signs a copyright transfer form at the time of submission of the manuscript; That all figures and tables have been correctly placed and clearly identified, and meet the journal’s standards of high-resolution quality. The Journal or the publisher will not be held legally responsible should there be any claims for compensation. The journal allows the authors to hold the copyright without restrictions and to retain publishing rights without restrictions.</p>Key Players and Potential Therapies in the Development of Breast Cancer Metastasis to the Spine
http://ghrnet.org/index.php/JT/article/view/3290
<p><strong>Background: </strong>Breast cancer metastasis to the spine causes severe morbidity due to pathological fractures, spinal cord compression, pain, loss of mobility and paralysis. An improved understanding of the biology behind metastatic breast cancer growth and invasion to the bony vertebral column is essential in order to control local tumour growth and progression of metastasis.</p><p><strong>Aim: </strong>To identify and characterise the presence of six key markers involved in spinal metastasis progression, RANKL, OPG, MMP-9, PTHrP, VEGF and IL-6. To determine the effectiveness of inhibitory agents, bisphosphonate Zoledronic Acid and RTK inhibitor Sorafenib on cancer cell growth and survival, as well as the expression of tumour markers in vitro.</p><p><strong>Materials and Methods and Results: </strong>The presence of RANKL, OPG, MMP-9, PTHrP, VEGF and IL-6 was confirmed in the cytoplasm of secondary breast cancer cell lines MDA-MB-231, MDA-MB-453 and MCF-7 in vitro. This was further supported by histological analysis of tumour-containing spinal sections from an established mouse model of spinal cancer. Zoledronic Acid and Sorafenib reduced proliferation rates in all cell lines and Sorafenib caused significant apoptosis of MDA-MB-231 and MDA-MB-453 cells.</p><p><strong>Conclusion: </strong>This study highlights a potential role for the markers VEGF, RANKL and IL-6 in promoting breast cancer growth, bone degradation and angiogenesis during spinal metastases. Both Zoledronic Acid and Sorafenib displayed anti-tumour effects on cancer proliferation and to a lesser extent apoptosis. These findings highlight the importance of tumour and bone-derived factors and their therapeutic application in breast cancer spinal metastasis.</p>Zumana KhairEffie MouhtourisJulia L. GregoryGerald Quan2022-07-222022-07-2210