Bone islands incidentally detected on computed tomography: frequency of enostosis and differentiation from untreated osteoblastic metastases based on CT attenuation value.

OBJECTIVE: The frequency of enostosis incidentally found on CT and CT attenuation value to distinguish them from untreated osteoblastic metastases (UOM). METHODS: Enostosis group: 46 polytrauma patients underwent thoracoabdominal CT. Inclusion criteria: age range 14-35 years. Exclusion criteria: cancer, previous fractures. UOM group: 20 patients with radiological diagnosis of UOM. Analyzed data: number, size, location and density of enostoses and metastases. The density was measured with the broadest possible region of interest at the center of the lesion by two radiologists independently. Receiver operatingcharacteristic analysis to determine the sensitivity and specificity, area under the curve 95% confidence intervals and cutoff values of CT density to differentiate metastases from enostoses. RESULTS: Patients were 28 ± 7 years old (72% males). 41 (89%) patients had 124 enostoses (2-15 mm) with an average density of 1007 ± 122 Hounsfiled unit (HU, observer1) and 1052 ± 107 (observer2). The most common sites of occurrence were the proximal femur (34%), the pelvis (22%), the acetabulum (20%), the proximal humerus (11%), the vertebrae (11%) and the rib (2%). 13 patients had 1 bone island, 8 patients had 2, 9 cases had 3 and 11 cases had more than 3 enostoses. Overall, 114 UOM were evaluated, their average density was 728 ± 163 HU (observer1) and 712 ± 178 HU (observer2). The area under the curve value of mean density to distinguish enostoses from UOM was 0,982. Using a cut-off of 881 HU for mean density, sensitivity was 98% and specificity 95%. CONCLUSION: The frequency of enostosis in this study is 89%. The average density identified can help to distinguish enostoses from UOM. ADVANCES IN KNOWLEDGE: We report the exact frequency of enostosis.

Malignant behavior and resistance to cisplatin of human ovarian carcinoma xenografts established from the same patient at different stages of the disease.

Three human ovarian carcinoma lines (HOC8) derived from the same patient before (P-HOC8) and after (R-HOC8 and Y-HOC8) cycles of chemotherapy were established i.p. in nude mice. The biological characterization showed that these tumor lines had various features in common. Cytological and histopathological characteristics and the expression of tumor-associated antigens OC125 and MOV18 were maintained in the three variants and were comparable to the patient's primary tumor. The HOC8 variants were aneuploid with a chromosome mode number of 80-81. All three tumor lines grew better i.p. than s.c. in nude mice. After i.p. injection the HOC8 lines produced ascites in all the mice, infiltration of pancreas, liver, diaphragm, and lung metastases. The sensitivity to cisplatin was evaluated for HOC8 lines growing in nude mice and mirrored the clinical development of resistance. Treatment with cisplatin of mice transplanted i.p. with P-HOC8 (obtained before the patient received chemotherapy) resulted in a significant increase in survival time; the R-HOC8 and Y-HOC8 lines (obtained after chemotherapy) were less sensitive. HOC8 xenografts, which represent the course of a single patient's disease, are a useful model for investigating the development of drug resistance in ovarian carcinoma.

Organ-specific growth of a murine lymphoma of spontaneous origin in nude mice.

The MOC-25 tumour arose spontaneously in a female nude mouse and was established as a continuous line intraperitoneally in nude mice, where it reproduces the topological features of its origin, growing preferentially in the uterus, ovaries and liver. Karyotype analysis showed that MOC-25 cells are hyperdiploid. Tumorigenicity and malignant behaviour were studied by transplanting tumour cells into different sites in nude mice. The comparison of tumour take after i.p. and s.c. injections of scaled concentrations of MOC-25 cell suspension showed preferential growth in the peritoneum. Regardless of the route of implantation (s.c., i.v., i.p.), this tumour rapidly and preferentially disseminated to the liver, uterus, ovaries, spleen and bone marrow. No significant differences in tumour growth and metastatic behaviour were observed when MOC-25 was injected in ovariectomized nude mice or in male nude mice. Morphology studies using light and electron microscopy, immunophenotyping and molecular analysis indicated a B-lymphoid origin of the MOC-25 tumour.

Intraperitoneal and subcutaneous xenografts of human ovarian carcinoma in nude mice and their potential in experimental therapy.

Human ovarian carcinomas (HOC) were established s.c. and i.p. in nude mice and the biological characteristics were investigated for 4 xenografts. HOC8 and HOC18, derived respectively from a primary tumor of the ovary and a pleural effusion (from 2 different patients) were established s.c. in nude mice. HOC10 and HOC22, derived from the ascites of 2 patients, were directly established as ascites after i.p. injection in nude mice. The s.c. and i.p. growth behavior of the 4 HOC lines was investigated. HOC18, HOC8 and HOC22 cells produced progressively growing tumor after s.c. injection but HOC10 ascites would not grow s.c. The cell suspension derived from HOC18 only produced carcinomatosis upon i.p. injection, while HOC8 cells produced both ascites and carcinomatosis. The 2 ascites HOC10 and HOC22 produced ascites in nude mice, but only HOC22 formed i.p. carcinomatosis. Histopathological characteristics of the patients' primary tumors persisted in nude mice, regardless of the site of tumor implantation. DNA histograms of the xenografts closely matched the patients' tumors and remained stable at different passages. Cisplatin, adriamycin and cyclophosphamide given i.v. were tested against HOC8 and HOC18 growing s.c. and HOC22 and HOC10 growing i.p. HOC8 showed a significant response to DDP and almost no sensitivity to ADR and CTX. HOC18 showed only moderate growth delay with all 3 drugs. Mice bearing HOC10 and HOC22 ascites had a prolonged survival time after DDP and ADR treatment.