Osteochondromas can be complicated by mechanical irritation, compression or injury of adjacent structures, fracture, malignant transformation, and postoperative recurrence. Magnetic resonance imaging represents the most valuable imaging modality in symptomatic cases, because it can demonstrate typical features of associated soft tissue pathology, which can be differentiated from malignant transformation. Reactive bursae formation presents as an overlying fluid collection with peripheral contrast enhancement. Dislocation, deformation, and signal alterations of adjacent soft tissue structures can be observed in different impingement syndromes caused by osteochondromas. Magnetic resonance imaging provides excellent demonstration of arterial and venous compromise and represents the method of choice in cases with compression of spinal cord, nerve roots, or peripheral nerves, depicting changes in size, position, and signal intensity of the affected neural structures. Malignant transformation as the most worrisome complication occurs in approximately 1% of solitary and 5-25% of multiple osteochondromas. Magnetic resonance imaging is the most accurate method in measuring cartilage cap thickness, which represents an important criterion for differentiation of osteochondromas and exostotic (low-grade) chondrosarcomas. Cartilage cap thickness exceeding 2 cm in adults and 3 cm in children should raise the suspicion for malignant transformation. Finally, MR imaging can detect postoperative recurrence by depiction of a recurrent mass presenting typical morphological features of a cartilage-forming lesion.
Reviewing the few reported cases, osseous HD must be distinguished from systemic HD with diffuse bone marrow involvement and from osseous metastases in advanced stage of disease because it seems to have a better prognosis.
Insulin-like growth factor 1 (IGF1) reputedly opposes chemotoxicity in Ewing sarcoma family of tumor (ESFT) cells. However, the effect of IGF1 on apoptosis induced by apoptosis ligand 2 (Apo2L)/tumor necrosis factor (TNF-) related apoptosis-inducing ligand (TRAIL) remains to be established. We find that opposite to the partial survival effect of short-term IGF1 treatment, long-term IGF1 treatment amplified Apo2L/TRAIL-induced apoptosis in Apo2L/TRAIL-sensitive but not resistant ESFT cell lines. Remarkably, the specific IGF1 receptor (IGF1R) antibody α-IR3 was functionally equivalent to IGF1. Short-term IGF1 incubation of cells stimulated survival kinase AKT and increased X-linked inhibitor of apoptosis (XIAP) protein which was associated with Apo2L/TRAIL resistance. In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization. Addition of ceramide synthase (CerS) inhibitor fumonisin B1 during long-term IGF1 treatment reduced XIAP repression and Apo2L/TRAIL-induced apoptosis. Noteworthy, the resistance to conventional chemotherapeutic agents was maintained in cells following chronic IGF1 treatment. Overall, the results suggest that chronic IGF1 treatment renders ESFT cells susceptible to Apo2L/TRAIL-induced apoptosis and may have important implications for the biology as well as the clinical management of refractory ESFT.
Surgery is not the treatment of choice for soft-tissue metastases, but it may be recommended when the lesion is unique and inducing a pain resistant to anti-inflammatory drugs.
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