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      Validity of Osteoprotegerin and Receptor Activator of NF-κB Ligand for the Detection of Bone Metastasis in Breast Cancer

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          Abstract

          Osteoprotegerin (OPG) is a robust antiresorptive molecule that acts as a decoy receptor for the receptor activator of nuclear factor κB ligand (RANKL), the mediator of osteoclastogenesis. This study was designed to explore the possible role of serum OPG and RANKL in detecting bone metastasis in breast cancer and its interaction with clinicopathologic parameters. Serum levels of RANKL and OPG were estimated in 44 metastatic and 36 nonmetastatic breast cancer patients using ELISA kits. Serum OPG levels were significantly reduced in patients with bone metastasis and correlated negatively with the number of bone lesions and CA 15-3 levels. At concentrations ≤82 pg/ml, OPG showed a high specificity in identifying the presence of bone metastasis (92%), albeit with low sensitivity (59%), which improved after the exclusion of diabetics and patients treated with aromatase inhibitors (AI). Serum RANKL levels were significantly higher in the presence of bone metastasis and hypercalcemia. At concentrations >12.5 pg/ml, RANKL had an associated sensitivity of 86%, albeit with low specificity (53%), in detecting bone metastasis. The RANKL/OPG ratio significantly increased in the presence of bone metastasis with appropriate sensitivity and specificity (73% and 72%, respectively) at a cutoff of ≥0.14 for the detection of bone metastasis. Serum OPG and RANKL/OPG ratios are promising biomarkers for detecting bone metastasis in breast cancer patients.

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          Cancer statistics, 2015.

          Rebecca Siegel, Kimberly D Miller, Ahmedin Jemal (2015)
          Each year the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data were collected by the National Cancer Institute (Surveillance, Epidemiology, and End Results [SEER] Program), the Centers for Disease Control and Prevention (National Program of Cancer Registries), and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics. A total of 1,658,370 new cancer cases and 589,430 cancer deaths are projected to occur in the United States in 2015. During the most recent 5 years for which there are data (2007-2011), delay-adjusted cancer incidence rates (13 oldest SEER registries) declined by 1.8% per year in men and were stable in women, while cancer death rates nationwide decreased by 1.8% per year in men and by 1.4% per year in women. The overall cancer death rate decreased from 215.1 (per 100,000 population) in 1991 to 168.7 in 2011, a total relative decline of 22%. However, the magnitude of the decline varied by state, and was generally lowest in the South (∼15%) and highest in the Northeast (≥20%). For example, there were declines of 25% to 30% in Maryland, New Jersey, Massachusetts, New York, and Delaware, which collectively averted 29,000 cancer deaths in 2011 as a result of this progress. Further gains can be accelerated by applying existing cancer control knowledge across all segments of the population. © 2015 American Cancer Society.
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            Bone cancer pain: causes, consequences, and therapeutic opportunities.

            Patrick Mantyh (2013)
            Common cancers, including cancers of the breast, lung, and prostate, frequently metastasize to multiple bones where they can cause significant and life-altering pain. Similar to cancer itself, the factors that drive bone cancer pain evolve and change with disease progression. Once cancer cells have metastasized to bone, both the cancer cells and their associated stromal cells generate pain by releasing algogenic substances including protons, bradykinin, endothelins, prostaglandins, proteases, and tyrosine kinase activators. The release of these factors by cancer/stromal cells can induce sensitization and activation of nerve fibers that innervate the bone. Additionally, these factors can drive a remarkable increase in the number, size, and activity of bone-destroying osteoclasts, which can ultimately result in fracture of the tumor-bearing bone. Tumor growth in bone can also generate a neuropathic pain by directly injuring nerve fibers as well as inducing an active and highly pathological sprouting of both sensory and sympathetic nerve fibers that normally innervate the bone. This structural reorganization of sensory and sympathetic nerve fibers in the bone, combined with the cellular and neurochemical reorganization that occurs in the spinal cord and brain, appears to contribute to the peripheral and central sensitization that is common in advanced bone cancer pain. These mechanistic insights have begun to lead to advances in both how we understand and treat bone cancer pain. Copyright © 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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              Endothelial Dysfunction, Inflammation, and Apoptosis in Diabetes Mellitus

              Inge van den Oever, Hennie Raterman, Mike T. Nurmohamed … (2010)
              Endothelial dysfunction is regarded as an important factor in the pathogenesis of vascular disease in obesity-related type 2 diabetes. The imbalance in repair and injury (hyperglycemia, hypertension, dyslipidemia) results in microvascular changes, including apoptosis of microvascular cells, ultimately leading to diabetes related complications. This review summarizes the mechanisms by which the interplay between endothelial dysfunction, inflammation, and apoptosis may cause (micro)vascular damage in patients with diabetes mellitus.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Res
                Journal ID (iso-abbrev): Oncol Res
                Journal ID (publisher-id): OR
                Title: Oncology Research
                Publisher: Cognizant Communication Corporation (Elmsford, NY )
                ISSN (Print): 0965-0407
                ISSN (Electronic): 1555-3906
                Publication date Collection: 2017
                Publication date (Electronic): 14 April 2017
                Volume: 25
                Issue: 4
                Pages: 641-650
                Affiliations
                [1]*Biochemistry Department, Faculty of Pharmacy, Mansoura University , Mansoura, Egypt
                [2]†Clinical Pharmacy, Oncology Center, Mansoura University , Mansoura, Egypt
                [3]‡Medical Oncology Unit, Oncology Center, Mansoura University , Mansoura, Egypt
                Author notes
                Address correspondence to Mohamed A. Ebrahim, M.D., Associate Professor of Medical Oncology, Faculty of Medicine, Oncology Center, Mansoura University, Gehan Al Sadat, Mansoura, Dakahlia Governorate 3516, Egypt. Tel: +201002057451; E-mail: drmohamedawad@ 123456gmail.com or Laila A. Eissa, Ph.D., Professor and Head of Clinical Biochemistry Department, Faculty of Pharmacy, University of Mansoura, Mansoura 33516, Egypt. E-mail: lailaeissa2002@ 123456yahoo.com
                Article
                Publisher ID: OR1000
                DOI: 10.3727/096504016X14768398678750
                PMC ID: 7841017
                PubMed ID: 27983911
                SO-VID: 2f015250-0539-451d-89c2-433faff96a1f
                Copyright © Copyright © 2017 Cognizant, LLC.
                License:

                This article is licensed under a Creative Commons Attribution-NonCommercial NoDerivatives 4.0 International License.

                History
                Page count
                Figures: 7, Tables: 3, References: 22, Pages: 10
                Categories
                Subject: Article

                Keywords: breast cancer,bone metastasis,osteoprotegerin (opg),receptor activator of nuclear factor κb ligand (rankl)
                Data availability:
                Keywords: breast cancer, bone metastasis, osteoprotegerin (opg), receptor activator of nuclear factor κb ligand (rankl)

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