BACKGROUND.Correlations between various patient, tumor, and treatment characteristics and complications in patients undergoing combined modality treatment for primary lower extremity soft‐tissue sarcomas were investigated.METHODS.Using the M. D. Anderson Radiation Oncology database, the records of the subset of patients treated with combined radiation and limb‐sparing surgery for primary lower extremity soft‐tissue sarcomas were retrospectively reviewed from the years 1960 to 2003.RESULTS.In all, 412 patients were identified. With a median follow‐up of 9.3 years, there were a total of 113 (27%) acute wound complications and 41 (13% at 20 years) chronic radiation‐related limb complications. Preoperative radiation and tumor sizes >5 cm were associated with an increased risk of acute wound complications (34% preoperative vs. 16% postoperative, P < .001; and 31% >5 cm vs. 17% ≤5 cm, P = .005). At 20 years the radiation‐related complication rate was higher in patients with a groin or thigh tumor location (16% vs. 4% other; P = .008), prior acute wound complications (20% vs. 10% no surgical complication), and a radiation dose ≥60 grays (Gy) (18% vs. 9% for dose < 60 Gy; P = .04). Five fractures occurred, resulting in a crude overall fracture rate of 1.2%.CONCLUSIONS.Patients treated with preoperative radiation for larger tumors are more likely to have acute surgical wound complications. Acute wound complications followed by postoperative radiation are associated with chronic radiation‐related limb problems, as are higher radiation dose and proximal tumor location. The fracture rate is so low that prophylactic fixation is not warranted. Cancer 2006. © 2006 American Cancer Society.

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Therapeutic Study, Level IV (case series). See the Guidelines for Authors for a complete description of levels of evidence.

IMPORTANCE Consensus is lacking as to the optimal radiotherapy dose and fractionation schedule for treating bone metastases.OBJECTIVE To assess the relative efficacy of high-dose, single-fraction stereotactic body radiotherapy (SBRT) vs standard multifraction radiotherapy (MFRT) for alleviation of pain in patients with mostly nonspine bone metastases. DESIGN, SETTING, AND PARTICIPANTSThis prospective, randomized, single-institution phase 2 noninferiority trial conducted at a tertiary cancer care center enrolled 160 patients with radiologically confirmed painful bone metastases from September 19, 2014, through June 19, 2018. Patients were randomly assigned in a 1:1 ratio to receive either single-fraction SBRT (12 Gy for Ն4-cm lesions or 16 Gy for <4-cm lesions) or MFRT to 30 Gy in 10 fractions. MAIN OUTCOMES AND MEASURESThe primary end point was pain response, defined by international consensus criteria as a combination of pain score and analgesic use (daily morphine-equivalent dose). Pain failure (ie, lack of response) was defined as worsening pain score (Ն2 points on a 0-to-10 scale), an increase in morphine-equivalent opioid dose of 50% or more, reirradiation, or pathologic fracture. We hypothesized that SBRT was noninferior to MFRT. RESULTSIn this phase 2 noninferiority trial of 96 men and 64 women (mean [SD] age, 62.4 [10.4] years), 81 patients received SBRT and 79 received MFRT. Among evaluable patients who received treatment per protocol, the single-fraction group had more pain responders than the MFRT group (complete response + partial response) at 2 weeks (34 of 55 [62%] vs 19 of 52 [36%]) (P = .01), 3 months (31 of 43 [72%] vs 17 of 35 [49%]) (P = .03), and 9 months (17 of 22 [77%] vs 12 of 26 [46%]) (P = .03). No differences were found in treatment-related toxic effects or quality-of-life scores after SBRT vs MFRT; local control rates at 1 and 2 years were higher in patients receiving single-fraction SBRT.CONCLUSIONS AND RELEVANCE Delivering high-dose, single-fraction SBRT seems to be an effective treatment option for patients with painful bone metastases. Among evaluable patients, SBRT had higher rates of pain response (complete response + partial response) than did MFRT and thus should be considered for patients expected to have relatively long survival.

Survival beyond twelve months is possible for a substantial proportion of patients with metastatic renal cell carcinoma. Patients with a clear-cell histological subtype, bone-only metastases, and a solitary metastasis have superior survival rates. The presence of pulmonary metastases does not predict early death in a reliable manner, and some patients may survive for years with pulmonary and systemic disease. The data are important for surgeons to consider when choosing treatment for these patients. For example, local control of disease and implant stability are important issues for patients with a potential for a long duration of survival.

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Mice bearing germ line mutations of p53 develop sarcomas at a significant rate. Since they are susceptible to a variety of other malignancies, they are not ideally suited to the study of sarcomas. To test the possibility that targeted mutation of tumor suppressor genes in early mesenchymal cells would induce formation of sarcomas, the Prx1-cre transgenic mouse was crossed to mice-bearing floxed alleles of p53 and Rb. Mice with homozygous deletion of p53 (Prx1-cre p53(lox/lox)) developed sarcomas in the extremities at a mean time of 50 weeks. Osteosarcomas (OS) were the most common type of sarcoma (61%) followed by poorly differentiated soft tissue sarcomas (PDSTS) (32%). Homozygous deletion of p53 produced sarcomas significantly more rapidly than heterozygous deletion, which resulted in sarcoma formation after a mean of 96 weeks. Mice with homozygous Rb mutation (Prx1-cre Rb(lox/lox)) developed normally and had no ostensible defects in the limbs. In contrast to p53, targeted deletion of Rb did not produce sarcomas in the limbs. However, simultaneous deletion of Rb and p53 accelerated the time to sarcoma formation, and a greater percentage of PDSTS were found. Deletion of p53 in committed osteoblasts by the Col1a1-cre transgenic mouse bearing an osteoblast-specific enhancer resulted in a high percentage of OS. These findings suggest that deletion of p53 in mesenchymal cells that give rise to osteoblasts is a powerful initiator of OS. Deletion of Rb does not initiate sarcoma formation in mice, but it accelerates formation of both soft tissue sarcomas and OS.