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  MTE 17 - Dealing with Metastatic Bone Disease in Lung Cancer - Prevention of SREs and Pain (Ticketed Session) (ID 69)

  • Event: WCLC 2015
  • Type: Meet the Expert (Ticketed Session)
  • Track: Palliative and Supportive Care
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/08/2015, 07:00 - 08:00, 102+104+106

  • 14289

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    MTE17.01 - Dealing with Metastatic Bone Disease in Lung Cancer - Prevention of SREs and Pain (ID 2002)

    07:00 - 08:00  |  Author(s): V. Hirsh
    • Abstract
    • Presentation
    • Slides

    Abstract:
    Approximately 30-40% of patients with advanced lung cancer develop bone metastases, but as the newer therapies are extending survival, the chance of developing bone metastases increases. Bone metastases cause skeletal-related events (SREs) such as pathologic fractures, spinal cord compression, radiation therapy or surgery to bone, or hypercalcemia – all of which can have debilitating consequences (including pain) affecting patients' health-related quality of life (HR-QOL) and performance status (PS)[1]. Bone metastases are the most common cause of cancer-associated pain in patients with advanced malignancies[2]. Poor PS prevents the patients from receiving further lines of treatments available today. SREs are associated with increased economic costs. In one clinical trial, the median time to first SRE was only 5 months[3]. Early detection of bone metastases can prevent SREs and avoid inappropriate implementation of major surgery or chemoradiation therapy. With the new generation bisphosphonate zoledronic acid or denosumab (anti-RANKL activity), one can reduce the number of patients who experience SREs, decrease the annual incidence of SREs, and delay the median time-to-first SRE[3]. These agents are effective even after the onset of SREs. They are well tolerated, with manageable side effects. The biochemical markers of bone metabolism especially N-telopeptide of type I collagen (NTX) and bone specific alkaline phosphatase (BALP) can be both prognostic and predictive markers for the patients with bone metastases from NSCLC[4-6]. Anticancer activity of zoledronic acid and denosumab further supports their use as soon as bone metastases are diagnosed in patients with non-small cell lung cancer (NSCLC). Further trials will inform us about the efficacy of these agents for prevention of bone metastases and even about possible effects on visceral metastases, with a significant impact on overall survival[7, 8]. These trials will be discussed, as well as the explanation for the longer survival on the bone-targeted agents. The new targeted agents which are being investigated will be mentioned too[9, 10]. References 1. Coleman RE (1997). Skeletal complications of malignancy. Cancer 80 (suppl.): 1588- 1594 2. Mercadante S (1997). Malignant bone pain: pathophysiology and treatment. Pain 69: 1-18. 3. Rosen LS, Gordon D, Tchekmedyian S, et al (2003). Zoledronic acid versus placebo in the treatment of skeletal metastases in patients with lung cancer and other solid tumors: a phase III, double-blind, randomized trial – the Zoledronic Acid Lung Cancer and other Solid Tumors Study Group. J Clin Oncol 21: 3150-3157. 4. Coleman RE, Major P, Lipton A, et al (2005). Predictive value of bone resorption and formation markers in cancer patients with bone metastases receiving the bisphosphonatezoledronic acid. J Clin Oncol 23: 4925-4935. 5. Lipton A, Cook R, Saad F, et al (2008). Normalization of bone markers is associated with improved survival in patients with bone metastases from solid tumors and elevated bone resorption receiving zoledronic acid. Cancer 113: 193-201. 6. Hirsh V, Major PP, Lipton A, et al (2008). Zoledronic acid and survival in patients with metastatic bone disease from lung cancer and elevated markers of osteoclast activity. J Thorac Oncol 3: 228-236. 7. Luo FR, Camuso A, McGlinchey K, et al (2005). Evaluation of anti-osteoclastic activity of the novel, oral multi-targeted kinase inhibitor Dasatinib (BMS- 354825). AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics, November 14-18, 2005, Philadelphia, PA, p173 [Abstract B178]. 8. Borgstein NG, Yang Y, Condon CH, et al (2008). ACE-011, a soluble activin receptor type IIA IgG-Fc fusion protein decreases follicle stimulating hormone and increases bone- specific alkaline phosphatase, a marker of bone formation in postmenopausal healthy women. Cancer Research 69 (2 Suppl): Abstract 1160. 9. Hellerstedt BA, Edelman G, Vogelzang NJ, et al (2012). Activitiy of cabozantinib (XL 184) in metastatic NSCLC: Results from a phase II randomized discontinuation trial (RDT). J Clin Oncol 30(suppl): Abstract 7514. 10. Parker C, Nilsson S, Heinrich D, et al (2013). Alpha Emitter Radium-223 and Survival in Metastatic Prostate Cancer. New Engl J of Med 369(3): 213-223.
    
    

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