Abstract

Although this might mistakenly be seen as an issue for the radiation oncology community, all of us who share in the treatment of women with early stage breast cancer should be concerned about the upcoming NRG BR007 trial, a “Phase III Randomized Trial: Evaluating De-escalation of Breast Radiation (DEBRA) for Conservative Treatment of Stage I, HR+, HER2-, RS ≤ 18 Breast Cancer), which is due to open in July. I am very supportive of the concept of using genomic testing to determine which patients between the ages of 50 and 70 with T1 N0 ER and/or PR positive breast cancers following breast conserving surgery with negative margins can be safely treated with endocrine therapy without adjuvant radiation therapy. Conceptually it is an exciting and well needed study. I am deeply concerned about the non-inferiority threshold of 4%. This has never previously been considered to be an acceptable difference in ipsilateral breast tumor recurrence (IBTR) for women between the ages of 50 and 70 with stage I, low risk cancers...

Highlights

  • Endothelin-1 initially described as a vasoconstrictor in 1988 [1] has shown to have multifunctional [1,2,3] in the development of various types of solid tumors [2]

  • Through the endothelin A receptor (ETAR) it induces a survival pathway leading to cell proliferation, escape from apoptosis, angiogenesis, invasion and metastasis formation [3, 4], elevated ET-1 levels in prostate cancer patients can be associated with higher metastatic potential [6] correlating the ET-1 levels with tumor progression [3]

  • The results presented in this study are consistent with previous reports of ET-1 overexpression in prostate cancer patients [14, 15], as it can be seen that in our Cologne collective, ET-1 levels increased significantly in comparison with the control group

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Summary

Introduction

Endothelin-1 initially described as a vasoconstrictor in 1988 [1] has shown to have multifunctional [1,2,3] in the development of various types of solid tumors [2]. Through the endothelin A receptor (ETAR) it induces a survival pathway leading to cell proliferation, escape from apoptosis, angiogenesis, invasion and metastasis formation [3, 4], elevated ET-1 levels in prostate cancer patients can be associated with higher metastatic potential [6] correlating the ET-1 levels with tumor progression [3]. Nelson, et al reported a downregulation in aggressive variants of prostate cancers (PCa) [5]. Such down-regulation of ETBR is based on promotor methylation [3]. Our group recently reported correlation between Vim overexpression and increasing migration of PCa cell lines

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