Diagnosis of prostate cancer in patients with persistently elevated PSA and tumor-negative biopsy in ambulatory care: performance of MR imaging in a multi-reader environment.

PURPOSE: False-negative results are obtained in approx. 20 % of prostate cancer (PCa) patients (pts) at initial systematic transrectal biopsy (Bx), in particular when digital rectal examination (DRE) or transrectal ultrasound (TRUS) is negative. The aim of this study was to assess whether MR endorectal imaging of the prostate in a multi-reader ambulatory care setting may assist in patient selection for re-biopsy. MATERIALS AND METHODS: 115 consecutive pts with persistent PSA elevation, negative Bx, DRE and TRUS were examined using T2w axial and coronal and T1w axial sequences for tumor diagnosis. MR images were prospectively read as tumor-suspicious or tumor-negative by the MR radiologist on duty. Additionally, a retrospective readout of a prostate MR expert and an abdominal imaging fellowship-trained radiologist was performed to evaluate the effect of the reader's experience on tumor detection. Imaging findings were compared to the results of the repeat Bx (61 pts) or the clinical course of at least two years. RESULTS: For the prospective reading, the sensitivity of MRI was 83 %, the specificity was 69 %, the PPV was 33 % and the NPV was 96 %. ROC analysis revealed a significantly better performance of the prostate MR imaging expert compared to the abdominal imaging radiologist (area under ROC 0.88 vs. 0.66, p < 0.001). Based on the prospective reading, a pre-test probability for PCa of 17.4 % as in our study can be reduced to 5 % when obtaining a tumor-negative result in MRI. CONCLUSION: MR imaging in a multi-reader ambulatory care setting assists in patient selection for re-biopsy. Reducing the post-test probability for PCa to 5 % allows for further follow-up instead of re-biopsy in MR tumor-negative patients. Specific training and experience improve tumor detection in prostate MR imaging.

Aneurysmal bone cyst of the mandible: a case report.

The case of a 6-year-old boy with a rapid growing mass in the right angle of the mandible that clinically and radiographically resembled a malignant lesion is presented. The biopsy specimen showed an aneurysmal bone cyst. The patient was treated surgically via extraoral approach including immediate mandibular reconstruction with with iliac crest bone. The literature is briefly reviewed.

Imaging features of subperiosteal aneurysmal bone cyst.

PURPOSE: To analyze the imaging features of subperiosteal aneurysmal bone cyst. MATERIAL AND METHODS: The imaging material of 6 patients with biopsy-proved subperiosteal aneurysmal bone cyst was reviewed. Evaluation included patient demographics, lesion location and size, radiographic features, and intrinsic characteristics on CT and MR images. Review of histologic specimens was carried out by an experienced musculoskeletal pathologist. RESULTS: All lesions were located at the surface of long tubular bones (femur 3, tibia 2, humerus 1): 3 involved the diaphysis, 2 the dia/metaphysis, and 1 exclusively the metaphysis. Lesion size ranged from 2.5 to 6 cm in maximum diameter. Radiographs and CT images always showed a superficial bone defect, which on radiographs demonstrated irregular margins in 4 cases. All lesions caused an interrupted periosteal reaction (shell 3, trabeculated shell 1, Codman angle 2). MR images always showed a multicystic appearance with a hypointense rim, contrast-enhancing cyst walls, and fluid levels. Edema of adjacent soft tissues was present in all cases. CONCLUSION: Aneurysmal bone cyst in a subperiosteal location can demonstrate an aggressive radiographic appearance. MR imaging appears to be most valuable in the differential diagnosis, since it can demonstrate typical morphological features of the underlying process.

Genetic imbalances revealed by comparative genomic hybridization in Ewing tumors.

Ewing tumors are characterized by reciprocal translocations involving the EWS gene on 22q12 fused to ETS transcription-factor family members. Little is known about further aberrations contributing to tumor development and progression. Sixty-two frozen tumors with known EWS rearrangements (52 primary tumors, 10 relapses) of ET patients registered in the EICESS protocol were analyzed by comparative genomic hybridization (CGH). The median number of changes in 52 primary and 10 relapsed cases was 2.5 and 5.0 per tumor (P = 0.153). Frequent abnormalities included gains of chromosomes 8, 12, 20, and 1q and losses of 16q and 19q. Neither number nor type of aberration was associated with histology, tumor size, disease stage, tumor localization, or histologic tumor response to chemotherapy. Among the 52 primary tumors, 26 with Type I fusion (EWS exon 7 to FLI1 exon 6) and 26 with other fusion types had a median of 2.0 and 3.0 aberrations per tumor, respectively (P = 0.031). Combinations of gains of chromosomes 8 and 12, gains of chromosome 20, and either gains of 8q or 18q and losses of 16q and 17p frequently occurred. The cumulative overall survival (OAS) was different between 35 patients with <5 aberrations and 13 patients with > or =5 aberrations (P = 0.009). Univariate analysis showed that patients with gains of 1q, 2q, 12, and 20 or losses of 16q and 17p had significantly lower OAS than those without aberrations. By multivariate analysis, loss of 16q (relative risk [RR] = 5.3; P = 0.0006) was an independent prognostic factor.

Alternative lengthening of telomeres is associated with chromosomal instability in osteosarcomas.

Telomere maintenance is regarded as a key mechanism in overcoming cellular senescence in tumor cells and in most cases is achieved by the activation of telomerase. However there is at least one alternative mechanism of telomere lengthening (ALT) which is characterized by heterogeneous and elongated telomeres in the absence of telomerase activity (TA). We evaluated the prevalence of TA, gene expression of telomerase subunits and ALT in relation to telomere morphology and function in matrix producing bone tumors and in osteosarcoma cell lines and present evidence of a direct association of ALT with telomere dysfunction and chromosomal instability. Telomere fluorescence in situ hybridization (T-FISH) in ALT cells revealed elongated and shortened telomeres, partly in unusual configurations and loci, dicentric marker chromosomes and signal-free chromosome ends. Free ends give rise to end-to-end associations and may induce breakage-fusion-bridge cycles resulting in an increased number of complex chromosomal rearrangements, as detected by multiplex-FISH (M-FISH). We propose that ALT cannot be seen as an equivalent to telomerase activity in telomere maintenance. Its association with telomere dysfunction and chromosomal instability may have major implications for tumor progression.

Distal chromosome 17 gains in neuroblastomas detected by comparative genomic hybridization (CGH) are associated with a poor clinical outcome.

PROCEDURE: To establish the significance of chromosome 17 aberrations in the biology of neuroblastomas, the fresh-frozen material of 53 primary neuroblastomas (average patient age: 20.8 months; stage 1 or 2: n = 10; stage 3: n = 10; stage 4: n = 10; stage 4s: n = 23) was studied by means of comparative genomic hybridization (CGH). Follow-up data were available for 52 of 53 cases studied (average follow-up period: 26.4 months). Except for one, all cases had previously been analyzed for MYCN status (semiquantitative Southern blot analysis). Studies of LOH 1p36 (VNTR-PCR) had been performed on 28 of 53 cases. RESULTS: Chromosome 17 gains were detected in 46 of 53 (86.8%) cases. Whole chromosome gains were mostly restricted to localized tumors (stage 1 or 2: 9 of 10 cases; stage 4s:19 of 23; stage 3: 2 of 10; stage 4:0 of 10 cases), whereas distal 17 gains were significantly associated with clinically advanced tumor stages and patients aged over 1 year at diagnosis. Univariate analyses revealed a statistically significant correlation of distal 17q gains with overall survival (P< 0.01, MYCN amplification: P< 0.01; 1p deletion: P< 0.01) and an elevated recurrency rate (17q: P= 0.02, MYCN amplification: P = 0.05; 1p deletion P= 0.3). There was a strong coincidence of distal 17q gains and 1p deletion or MYCN amplification (P < 0.01). CONCLUSION: Our data indicate that distal chromosome 17q gains are of major prognostic relevance for neuroblastoma patients. However, studies on a larger series of tumors have to be performed to assess whether or not these alterations are independent prognostic markers of a poor clinical outcome.

Periosteal chondroma: MR characteristics.

PURPOSE: The purpose of this study was to describe the MR characteristics of periosteal chondroma. METHOD: MR images of 12 proven cases of periosteal chondroma were analyzed with reference to tumor morphology and size. MR features were correlated with radiographic and pathologic findings. RESULTS: Tumor size ranged from 1 to 7 cm in maximum diameter with a mean value of 2.6 cm. On MR images, a soft tissue mass at the bone surface with pressure erosion of adjacent cortical bone could be identified in all cases. All lesions were bordered by a hypointense rim (100%) and frequently showed a lobulated configuration (75%). Edema of medullary bone or soft tissues was not observed in any of the cases. Signal intensity of cartilaginous tumor tissue was typically hypo-or isointense relative to muscle on T1-weighted (100%) and hyperintense relative to fat on T2-weighted (92%) and T2*-weighted (100%) MR images. Radiographically significant calcifications of the tumor matrix, present in half of the cases, caused focal signal loss on MR images of all pulse sequences. Contrast enhancement was observed predominantly at the periphery of the lesions (100%), which on pathologic examinations typically contained fibrovascular bundles, surrounding the cartilage lobules. CONCLUSION: Periosteal chondroma appears to have a relatively typical MR appearance, which reflects the histologic composition of the lesion. In addition to radiography, MRI therefore can substantially aid in the preoperative diagnosis of this rare bone lesion.

Comparative genomic hybridization (CGH) analysis of stage 4 neuroblastoma reveals high frequency of 11q deletion in tumors lacking MYCN amplification.

We have studied the occurrence and association of 11q deletions with other chromosomal imbalances in Stage 4 neuroblastomas. To this purpose we have performed comparative genomic hybridization (CGH) analysis on 50 Stage 4 neuroblastomas and these data were analyzed together with those from 33 previously published cases. We observed a high incidence of 11q deletion in Stage 4 neuroblastoma without MYCN amplification (59%) whereas 11q loss was only observed in 15% of neuroblastomas with MYCN-amplification (p = 0.0002) or 11% of cases with 1p deletion detected by CGH (p = 0.0001). In addition, 11q loss showed significant positive correlation with 3p loss (p = 0.0002). Event-free survival was poor and not significantly different for patients with or without 11q deletion. Our study provides further evidence that Stage 4 neuroblastomas with 11q deletions represent a distinct genetic subgroup that typically shows no MYCN-amplification nor 1p deletion. Moreover, it shows that neuroblastomas with 11q deletion also often present 3p deletion. This genetic subgroup shows a similar poor prognosis as MYCN amplified 4 neuroblastomas.

Desmoplastic fibroma in the thoracic spine: an unusual localization of a rare primary bone tumor.

A case of an intraspinal growing desmoplastic fibroma of the thoracic spine (T9-T11) is reported. Desmoplastic fibroma is a rare tumor of connective tissue that shows a locally infiltrative and destructive growth. An affection of the thoracic spine is an extremely rare manifestation. Preoperative CT documents the extent of osseous destruction and tumor associated cortical erosion. In central tumor areas an inhomogeneous, intermediate to low signal is demonstrated by MRI using T1- and T2-weighted spin-echo and turbo-spin-echo sequences. Contrast-enhanced MRI shows marked enhancement in peripheral areas depicting the extraosseous and intramedullary extension.

Evaluation of chemotherapy response in primary bone tumors with F-18 FDG positron emission tomography compared with histologically assessed tumor necrosis.

PURPOSE: The purpose of this study was to evaluate the potential of positron emission tomography using F-18-fluoro-2-deoxy-D-glucose (FDG PET) to assess the chemotherapy response of primary osseous tumors compared with the degree of necrosis determined histologically. PATIENTS AND METHODS: Seventeen patients with primary bone tumors (11 osteosarcomas, 6 Ewing's sarcomas) were examined using FDG PET and planar bone scintigraphy before neoadjuvant chemotherapy and before surgery. Tumor response was classified histologically according to Salzer-Kuntschik (grades I-II: good response; grades IV-VI: poor response). In both imaging methods, quantification was performed using tumor to nontumor ratios (T:NT). RESULTS: Histologically, 15 patients were classified as having good responses (grade I, n = 1; grade II, n = 6; grade III, n = 8) and two as having poor responses (grades IV and V). FDG PET showed more than a 30% decrease in T:NT ratios in all patients who had good responses. However, three of these patients had increasing bone scintigraphy T:NT ratios, and another five had decreasing ratios of less than 30%. The patients with poor responses had increasing T:NT ratios and decreasing ratios of less than 30%, respectively, using both imaging methods. CONCLUSIONS: FDG PET seems to be a promising tool for evaluating the response of primary osseous tumors to chemotherapy. In this preliminary study, FDG PET was superior to planar bone scintigraphy.

[MR morphology of primary aneurysmal bone cysts: a retrospective analysis of 38 cases]. / MR-Morphologie der primären aneurysmatischen Knochenzyste: Retrospektive Analyse von 38 Fällen.

PURPOSE: To define MR imaging characteristics of primary aneurysmal bone cyst. MATERIALS AND METHODS: MR imaging studies of 38 patients with histologically proven primary aneurysmal bone cyst were reviewed with reference to morphological features, signal characteristics, and patterns of contrast-enhancement. RESULT: Most lesions were well marginated towards bone and soft tissues (95%), either surrounded by a complete (84%) or incomplete (16%) rim of low signal intensity on images of all pulse sequences. Frequent features were polycyclic margins (84%), cortical expansion (87%), cystic spaces (100%), contrast-enhancing cyst walls (100%), internal septations (89%), fluid levels (71%) and diverticula-like projections of cyst walls (68%). Solid tissue components could be identified by MR imaging in all lesions which, on pathological examination, contained larger portions of solid material (18%). Edema of surrounding soft-tissues was observed in 29% of the cases. CONCLUSIONS: Primary aneurysmal bone cysts demonstrate a relatively uniform MR imaging appearance, which reflects the patho-anatomic composition of the lesion.

[Surgical reconstruction of fibrous dysplasia of bone in long-term follow-up]. / Operative Rekonstruktionen der fibrösen Dysplasie des Knochens im Langzeitergebnis.

PURPOSE: To examine how different operative measures influence the surgical outcome in patients with fibrous dysplasia of bone. METHODS: 118 dysplastic fibrous lesions of bone were surgically treated and reviewed in 70 patients between 1983 to 1993 (eleven years) with a median follow-up of six and a half years. Surgery consisted of intralesional curettage in 93 and marginal en bloc resection in 25 lesions. Bony defects were reconstructed with autogenous iliac crest graft in 55 lesions, with autogenous fibula graft in 9, with homologous bone chips in 28, and 5 times with a homologous fibula graft from the bone bank. In 33 lesions the entire defect was filled with polymethylmethacrylate. Osteosynthesis was performed in 41 patients. RESULTS: Recurrences requiring surgical revision were observed in 26 of 74 primary lesions (= 35% overall recurrence rate) at a mean 123.6 weeks postoperatively. The most frequent primary and recurrence location was the proximal femur (85% revision rate). 69% of all recurrences occurred under the age of 20. After intralesional curettage the reoperation rate was 32% and after marginal resection 8%. After reconstruction with autogenous iliac crest graft recurrence rate was 36%, after autogenous fibula graft 55%, after homologous bone chips 18%, after polymethylmethacrylate 9% and allograft fibula reconstruction showed no recurrences. A combined stable osteosynthesis bridging the fibrous osseous defect significantly reduced the revision rate to 3% (p = 0.01). CONCLUSION: Intralesional curettage and reconstruction with autogenous iliac crest graft in fibrous dysplasia of bone leads to a high recurrence rate. Reconstruction with cortical grafts or bone chips from the bone bank, if necessary in combination with a durable osteosynthesis in mechanically demanding locations, or solely bone cement in mechanically less demanding areas, reduces the revision rate in patients with monoostotic and polyostotic fibrous dysplasia.

A novel and consistent amplicon at 13q31 associated with alveolar rhabdomyosarcoma.

Rhabdomyosarcomas are the most common soft-tissue sarcoma found in children. The alveolar subtype is clinically more aggressive than the embryonal subtype. In addition to the presence of specific chromosome translocations and associated fusion gene products in a high proportion of the alveolar subtype, we previously showed that tumors with this histology frequently show evidence of genomic amplification. Here, we substantially extended the number of alveolar rhabdomyosarcoma samples examined by comparative genomic hybridization analysis. Regions of loss were noted, including the smallest overlapping regions corresponding to 16q, 17/17p, and 9q32-34, in 16%, 10%, and 10% of cases, respectively (44 primary samples/6 cell lines). Amplification or gain at 12q13-15 in the region of the MDM2/GLI1/SAS/CDK4 loci and 2p24 at the MYCN locus was found in 28% and 32% of cases, respectively. Single amplicons were found at locations that in other samples showed consistent gain, including the regions 5q15-23, 7q21-31, 11p11-14, 17q23-24, and 20q13, and amplification was found in two cases at 15q24-26. However, most striking was a novel region of amplification or gain at 13q31 in 19% of cases (51 primary samples/6 cell lines). This indicates that a gene or genes at 13q31 are significant in the development or progression of alveolar rhabdomyosarcoma.

Osteochondroma: MR imaging of tumor-related complications.

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.

Correlation of morphologic and cytogenetic parameters of genetic instability with chromosomal alterations in in situ carcinomas of the breast.

Classification of preinvasive breast disease could be better founded using biologic markers, thereby increasing reproducibility. We studied 57 breast ductal and lobular in situ carcinomas by means of comparative genomic hybridization and correlated these findings with quantitative features such as the mean nuclear area, mitotic index (MI), apoptotic index (AI), and the presence or absence of necrosis. Loss of 8p and gains of 8q and 6q were associated, respectively, with a significantly higher MI and AI, whereas loss of 16q was associated with a lower MI and AI. A significantly higher number of alterations per case were seen in tumors with gains of 6q, 8q, and 17q and tumors with loss of 13q. Loss of 16q and gain of 17q correlated with the absence or presence of necrosis, respectively. Our data clearly demonstrate that distinct cytogenetic changes correlate with phenotypic changes, proliferation, and apoptosis. These data may be used to refine existing classification schemes.

Telomerase activity distinguishes between neuroblastomas with good and poor prognosis.

BACKGROUND: Treatment of neuroblastoma has remained a major challenge in pediatric oncology because the assessment of the individual prognosis, particularly in disseminated disease is still obscure. Previous studies have correlated clinical outcome with activity levels of telomerase, a cellular reverse transcriptase which has been detected in the majority of human malignant tumors. PATIENTS AND METHODS: In this blind-trial study, a non-radioactive telomeric repeat amplification protocol (TRAP) with an internal telomerase-assay standard was used on an automated laser fluorescence sequencer for the detection and semiquantitative analysis of telomerase activity (TA) in 67 neuroblastomas of all clinical stages from the German Neuroblastoma Trial and 2 ganglioneuromas. TA levels were correlated with event-free and overall survival rates and established prognostic markers such as MYCN. RESULTS: TA was present in 14 of 69 (20%) samples, including 3 of 22 stage IVS, 8 of 14 stage IV, 1 of 10 stage III, 1 of 7 stage II and 1 of 14 stage I neuroblastomas and 0 of 2 ganglioneuromas. We found a strong statistical correlation between the presence of TA and poor clinical prognosis with regard to all tumor stages. Multivariate analysis revealed TA as an independent prognostic marker. In particular, the analysis of TA in IVS neuroblastomas distinguished two different prognostic groups. CONCLUSIONS: Our data suggest that TA is an independent prognostic marker in neuroblastoma which, in combination with other markers such as MYCN, may proof useful in assessing the individual patient's prognosis.

Sublocalization of putative tumor suppressor gene loci on chromosome arm 14q in neuroblastoma.

RFLP and microsatellite analysis with 23 polymorphic markers spanning the entire long arm of chromosome 14 in 108 neuroblastomas showed allelic loss in 19 out of 107 (18%) informative tumors, placing 14q among the most frequently affected chromosomal regions in neuroblastoma. One minimal deletion region could be sublocalized in 17 of 19 cases between markers D14S1 and D14S16, and a second one between markers D14S17 and D14S23 in band 14q32. Furthermore, breakpoints in bands 14q23 and 14q12 were detected. These results suggest the presence of at least two putative tumor suppressor gene loci on chromosome 14. Survival analyses revealed no prognostic impact of allelic loss of 14q in neuroblastoma. Genes Chromosomes Cancer 26:40-46, 1999.

Comparative genomic hybridization of ductal carcinoma in situ of the breast-evidence of multiple genetic pathways.

There is strong evidence that ductal carcinoma in situ (DCIS) represents a precursor lesion of invasive breast cancer. In order to analyse specific chromosomal alterations of DCIS, 38 paraffin-embedded specimens of DCIS and six associated invasive carcinomas were examined by means of comparative genomic hybridization (CGH). Losses of 16q material were seen almost exclusively in well- and intermediately-differentiated DCIS. These two subgroups differed in the average number of genetic imbalances, 2.5 and 5.5 respectively. Additionally, a higher frequency of gains of 1q and losses of 11q material was seen in intermediately-differentiated in contrast to well-differentiated DCIS. Poorly-differentiated DCIS displayed a higher frequency of amplifications (17q12, 11q13) and a higher average rate of genetic imbalances (7.1). Analysis of adjacent invasive breast carcinoma revealed a genetic pattern almost identical to the one seen in the DCIS counterpart. These data characterize DCIS as a genetically far-advanced, heterogeneous lesion and as a direct precursor of invasive breast cancer.

Gain of chromosome arm 17q and adverse outcome in patients with neuroblastoma.

BACKGROUND: Gain of genetic material from chromosome arm 17q (gain of segment 17q21-qter) is the most frequent cytogenetic abnormality of neuroblastoma cells. This gain has been associated with advanced disease, patients who are > or =1 year old, deletion of chromosome arm 1p, and amplification of the N-myc oncogene, all of which predict an adverse outcome. We investigated these associations and evaluated the prognostic importance of the status of chromosome 17. METHODS: We compiled molecular cytogenetic analyses of chromosome 17 in primary neuroblastomas in 313 patients at six European centers. Clinical and survival information were collected, along with data on 1p, N-myc, and ploidy. RESULTS: Unbalanced gain of segment 17q21-qter was found in 53.7 percent of the tumors, whereas the chromosome was normal in 46.3 percent. The gain of 17q was characteristic of advanced tumors and of tumors in children > or =1 year of age and was strongly associated with the deletion of 1p and amplification of N-myc. No tumor showed amplification of N-myc in the absence of either deletion of 1p or gain of 17q. Gain of 17q was a significant predictive factor for adverse outcome in univariate analysis. Among the patients with this abnormality, overall survival at five years was 30.6 percent (95 percent confidence interval, 21 to 40 percent), as compared with 86.0 percent (95 percent confidence interval, 78 to 91 percent) among those with normal 17q status. in multivariate analysis, gain of 17q was the most powerful prognostic factor, followed by the presence of stage 4 disease and deletion of 1p (hazard ratios, 3.4, 2.3, and 1.9, respectively). CONCLUSIONS: Gain of chromosome segment 17q21-qter is an important prognostic factor in children with neuroblastoma.

[Primary bone tumors and "tumor-like lesions" of the shoulder. Their histopathology and imaging]. / Primäre Knochentumoren und "Tumorlike Lesions" der Schulter. Histo-Pathologie und Bildgebung.

Purpose of this review is to demonstrate typical X-ray, CT and MR morphology of primary bone tumors and "tumor-like lesions" of the shoulder in correlation with histopathology. 711 primary bone tumors of the shoulder and proximal humerus were studied. 602 were localized in the humerus, 90 in the scapula and 19 in the clavicula. The most frequent benign tumors were osteochondromas (n = 143), simple bone cysts (n = 115), enchondromas (n = 75) and aneurysmal bone cysts (n = 50). Fibrous dysplasia (n = 25), chondroblastoma (n = 15), osteoid osteoma (n = 13), giant cell tumors (n = 12) and non ossifying fibroma (n = 11) were less frequent. The most frequent malignant bone tumors were osteosarcoma (n = 72), chondrosarcoma (n = 52) and Ewing's sarcoma (n = 46). Focal plasmocytoma (n = 20) and lymphoma (n = 10) were less frequent. The average age of the patients was 31.5 years. Some of these tumors were typically located in the shoulder, i.e. simple bone cysts and chondroblastoma. In summary the shoulder was a rather infrequent site of primary bone tumors, but since most of these tumors were benign, the radiologist should be aware of the differential diagnosis to guide therapy.