Chapter 094. Soft Tissue and Bone Sarcomas and Bone Metastases (Part 7)

Cancer in the bone may produce osteolysis, osteogenesis, or both. Osteolytic lesions result when the tumor produces substances that can directly elicit bone resorption (vitamin D–like steroids, prostaglandins, or parathyroid hormone–related peptide) or cytokines that can induce the formation of osteoclasts (interleukin 1 and tumor necrosis factor). Osteoblastic lesions result when the tumor produces cytokines that activate osteoblasts. In general, purely osteolytic lesions are best detected by plain radiography, but they may not be apparent until they are 1 cm. These lesions are more commonly associated with hypercalcemia and with the excretion of hydroxyproline-containing peptides indicative of matrix destruction....
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Chapter 094. Soft Tissue and Bone Sarcomas and Bone Metastases (Part 7) Chapter 094. Soft Tissue and Bone Sarcomas and Bone Metastases (Part 7) Cancer in the bone may produce osteolysis, osteogenesis, or both.Osteolytic lesions result when the tumor produces substances that can directlyelicit bone resorption (vitamin D–like steroids, prostaglandins, or parathyroidhormone–related peptide) or cytokines that can induce the formation of osteoclasts(interleukin 1 and tumor necrosis factor). Osteoblastic lesions result when thetumor produces cytokines that activate osteoblasts. In general, purely osteolyticlesions are best detected by plain radiography, but they may not be apparent untilthey are >1 cm. These lesions are more commonly associated with hypercalcemiaand with the excretion of hydroxyproline-containing peptides indicative of matrixdestruction. When osteoblastic activity is prominent, the lesions may be readilydetected using radionuclide bone scanning (which is sensitive to new boneformation), and the radiographic appearance may show increased bone density orsclerosis. Osteoblastic lesions are associated with higher serum levels of alkalinephosphatase and, if extensive, may produce hypocalcemia. Although some tumorsmay produce mainly osteolytic lesions (e.g., kidney cancer) and others mainlyosteoblastic lesions (e.g., prostate cancer), most metastatic lesions produce bothtypes of lesion and may go through stages where one or the other predominates. In older patients, particularly women, it may be necessary to distinguishmetastatic disease of the spine from osteoporosis. In osteoporosis, the corticalbone may be preserved, whereas cortical bone destruction is usually noted withmetastatic cancer. Metastatic Bone Disease: Treatment Treatment of metastatic bone disease depends on the underlyingmalignancy and the symptoms. Some metastatic bone tumors are curable(lymphoma, Hodgkins disease), and others are treated with palliative intent. Painmay be relieved by local radiation therapy. Hormonally responsive tumors areresponsive to hormone inhibition (antiandrogens for prostate cancer, antiestrogensfor breast cancer). Strontium 89 and samarium 153 are bone-seeking radionuclidesthat can exert antitumor effects and relieve symptoms. Bisphosphonates such aspamidronate may relieve pain and inhibit bone resorption, thereby maintainingbone mineral density and reducing risk of fractures in patients with osteolyticmetastases from breast cancer and multiple myeloma. Careful monitoring of serumelectrolytes and creatinine is recommended. Monthly administration preventsbone-related clinical events and may reduce the incidence of bone metastases inwomen with breast cancer. When the integrity of a weight-bearing bone isthreatened by an expanding metastatic lesion that is refractory to radiation therapy,prophylactic internal fixation is indicated. Overall survival is related to theprognosis of the underlying tumor. Bone pain at the end of life is particularlycommon; an adequate pain relief regimen including sufficient amounts of narcoticanalgesics is required. The management of hypercalcemia is discussed in Chap.347. Further Readings Borden EC et al: Soft tissue sarcomas of adults: State of the translationalscience. Clin Cancer Res 9:1941, 2003 [PMID: 12796356] Helman LJ, Meltzer P: Mechanisms of sarcoma development. Nat RevCancer 3:685, 2003 [PMID: 12951587] Mocellin S et al: Adult soft tissue sarcomas: Conventional therapies andmolecularly targeted approaches. Cancer Treat Rev 32:9, 2006 [PMID: 16338075] Pisters PW et al: Evidence-based recommendations for local therapy forsoft tissue sarcomas. J Clin Oncol 25:1003, 2007 [PMID: 17350950] Scurr M, Judson I: How to treat the Ewings family of sarcomas in adultpatients. Oncologist 11:65, 2006 [PMID: 16401715] Verweij J et al: Progression-free survival in gastrointestinal stromal tumorswith high-dose imatinib: Randomized trial. Lancet 364:1127, 2004 [PMID:15451219] Bibliography Burgert EO et al: Multimodal therapy for the management of nonpelviclocalized Ewings sarcoma of bone: IESS II. J Clin Oncol 8:1514, 1990 [PMID:2099751] Cangir A et al: Ewings sarcoma metastatic at diagnosis—results andcomparisons of two intergroup studies. Cancer 66:887, 1990 [PMID: 2201433] Hayden JB, Hoang BH: Osteosarcoma: basic science and clinicalimplications. Orthop Clin North Am 37:1, 2006 [PMID: 16311106] Jablons D et al: Metastasectomy for soft tissue sarcoma—further evidencefor efficacy and prognostic indicators. J Thorac Cardiovasc Surg 97:695, 1989[PMID: 2709861] Lindberg RD et al: Conservative surgery and post-operative radiother ...