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PubMed2005

An immunohistochemical analysis to evaluate an inverse correlation between Runx2/Cbfa1 and NF kappa B in human osteosarcoma.

BACKGROUND: Dominant negative inhibition of nuclear factor kappa B (NF kappa B) signalling activity in a human osteosarcoma cell line (Saos2) results in malignant reversion and the induction of the osteoblast differentiating transcription factor, Runx2/Cbfa1. This observation suggests that there is an inverse relation between a transcription factor associated with malignant progression and chemoresistance (NF kappa B) and an osteoblast differentiating transcription factor (Runx2/Cbfa1). AIMS: To assess and correlate Runx2/Cbfa1 and NF kappa B (p65) immunoreactivity in human osteosarcoma. METHODS: Runx2/Cbfa1 and NFkappaB (p65) immunoreactivity was assessed on 11 paraffin wax embedded archival specimens of human primary osteosarcoma by standard immunohistochemical methods and scored on a scale of 0-3. A Pearson correlation analysis between Runx2/Cbfa1 and NF kappa B (p65) scores was established. RESULTS: Runx2/Cbfa1 was expressed constitutively in all pathology specimens of human osteosarcoma. Of note, a chondroblastic osteosarcoma showed the highest Runx2/Cbfa1 immunoreactivity. A Pearson correlation did not support an inverse correlation between Runx2/Cbfa1 and NF kappa B (p65) scores (r = 0.57) in human osteosarcoma. CONCLUSION: Runx2/Cbfa1 immunoreactivity does not inversely correlate with NF kappa B immunoreactivity, and thus cannot serve as an indirect measure of NF kappa B activity or an independent predictive or prognostic indicator.

Biomarkers, Tumor↗
PubMed2003

Osteosarcoma with cytokeratin expression: a clinicopathological study of six cases with an emphasis on differential diagnosis from metastatic cancer.

AIMS: To clarify the clinicopathological profile of osteosarcomas showing an intensely positive immunoreaction for cytokeratin. METHODS: Clinicopathological and immunohistochemical features were analysed in 131 patients with non-metastatic, conventional osteosarcoma, treated in Akita University and National Cancer Centre in Tokyo between 1972 and 1999. RESULTS: Six patients (4.5%; mean age, 32 years; four men, two women) had osteosarcomas showing intense cytokeratin expression. Tumours were located on the long bones of the extremities in five patients and the ilium in one. Osteoid formations were found in biopsied specimens in all cases. Three tumours were classified as osteoblastic osteosarcoma, two as fibroblastic, and one as chondroblastic. In three tumours classified as the osteoblastic subtype, epithelioid features were prominent, and four tumours showed pronounced cellular pleomorphism. In contrast to the expression of cytokeratin, epithelial membrane antigen was negative in all cases. Surgery with a wide excisional margin was performed in six patients. Preoperative and postoperative chemotherapy was given to five of the six patients, but the effects of these agents were negligible. Three of the six patients developed lung metastases, whereas the other three patients have remained well with no evidence of local recurrence or distant metastasis. CONCLUSIONS: Osteosarcoma with intense immunoreaction for cytokeratin was rare. The clinicopathological features were similar to those of patients with conventional osteosarcoma, except for a higher age, chemotherapy resistance, histological epithelioid features, and pleomorphism. This study indicates that osteoid formation and negative expression of epithelial membrane antigen are key features in the differentiation from metastatic carcinoma.

Adolescent↗
PubMed2004

Cell surface expression of epidermal growth factor receptor and Her-2 with nuclear expression of Her-4 in primary osteosarcoma.

There is controversy over the role of Her-2 in osteosarcoma, with some investigators reporting association between expression and adverse outcome, whereas others point to the lack of gene amplification and membranous expression by immunohistochemistry (IHC) as inconsistent with biological significance. Her-2 normally requires pairing with epidermal growth factor receptor (EGFR), Her-3, or Her-4, but these have been less well studied in osteosarcoma. We evaluated the expression of each of these receptors in osteosarcoma and their potential to contribute to pathogenesis by examining a panel of low-passage primary osteosarcoma cell lines, comparing these with archival tumor specimens. Her-2 immunoreactivity was seen frequently in the diffuse staining pattern described previously. We observed EGFR in all samples by IHC. Her-3 expression was not observed. Her-4 expression was nuclear in distribution in all tumor samples and many cell line samples, consistent with activation and cleavage of the receptor. Quantified expression of Her-2 and EGFR mRNA by quantitative, real-time PCR in cell lines correlated with IHC for Her-2 but not for EGFR. Western blot identified full-length receptors for EGFR and Her-2 in all expected cell lines and showed Her-4 to be predominantly in the p80 form. Flow cytometry identified cell surface Her-2 and EGFR in all lines with receptor expression by IHC. We conclude that the cell surface expression of Her-2 and EGFR and the nuclear localization of the activated p80 fragment of Her-4 suggest that all three may be contributing to osteosarcoma pathogenesis. Therapy directed against this family of receptors may be beneficial for patients with osteosarcoma.

Bone Neoplasms↗
PubMed2004

Identification of human autologous cytotoxic T-lymphocyte-defined osteosarcoma gene that encodes a transcriptional regulator, papillomavirus binding factor.

The prognosis for patients with osteosarcoma who do not respond to current chemotherapy protocols still remains poor. Toward the goal of establishing efficacious peptide-based immunotherapy for those patients, we previously developed an autologous pair of CTLs and an osteosarcoma cell line. In the current study, we screened the cDNA library of this osteosarcoma cell line using an autologous CTL clone and identified cDNA encoding an antigen. The isolated cDNA was identical to papillomavirus binding factor (PBF), which was recently reported as a DNA binding transcription factor cooperating with RUNX1. Reverse transcription-PCR analysis revealed that PBF was expressed in 16 of 19 cases of bone and soft-tissue sarcoma cell lines (5 of 6 of osteosarcoma lines) and 57 of 76 sarcoma tissue samples (11 of 14 of osteosarcoma tissues). Also, PBF was expressed in 10 of 13 epithelial cancer cell lines and 20 of 34 of cancer tissues. In contrast, PBF was detected in some normal organs including ovary, pancreas, spleen, and liver by reverse transcription-PCR but was restricted in the cytoplasm by immunostaining and undetectable by Western blotting. Furthermore, a 12-mer peptide, CTACRWKKACQR, located at the COOH terminus of PBF, was found to be a minimum requirement for recognition by the CTL clone in the context of the HLA-B*5502 molecule. These findings suggest that PBF is a shared tumor-associated antigen, which may serve as a source of peptides applicable to peptide-based immunotherapy for osteosarcoma and other malignant tumors.

Antigens, Neoplasm↗
PubMed2004

Increased Fas expression reduces the metastatic potential of human osteosarcoma cells.

PURPOSE: The process of metastasis requires the single tumor cell that seeds the metastatic clone to complete a complex series of steps. Identifying factors responsible for these steps is essential in developing and improving targeted therapy for metastasis. Resistance to receptor-mediated cell death, such as the Fas/Fas ligand pathway, is one mechanism commonly exploited by metastatic cell populations. EXPERIMENTAL DESIGN AND RESULTS: LM7, a subline of the SAOS human osteosarcoma cell line with low Fas expression, was selected for its high metastatic potential in an experimental nude mouse model. When transfected with the full-length Fas gene (LM7-Fas), these cells expressed higher levels of Fas than the parental LM7 cells or LM7-neo control-transfected cells. These cells were also more sensitive to Fas-induced cell death than controls. When injected intravenously into nude mice, the LM7-Fas cell line produced a significantly lower incidence of tumor nodules than control cell lines. Lung weight and tumor nodule size were also decreased in those mice injected with LM7-Fas. Levels of Fas were quantified in osteosarcoma lung nodules from 17 patients. Eight samples were Fas negative, whereas the remaining 9 were only weakly positive compared with normal human liver (positive control). CONCLUSIONS: Our results demonstrate that altering Fas expression can impact the metastatic potential of osteosarcoma cells. We conclude that the increase of Fas on the surface of the LM7 osteosarcoma cells increased their sensitivity to Fas-induced cell death in the microenvironment of the lung, where Fas ligand is constitutively expressed. Thus, loss of Fas expression is one mechanism by which osteosarcoma cells may evade host resistance mechanisms in the lung, increasing metastatic potential. Fas may therefore be a new therapeutic target for osteosarcoma.

Animals↗
PubMedDate not supplied

Resistance of epiphyseal cartilage to invasion by osteosarcoma is likely to be due to expression of antiangiogenic factors.

OBJECTIVES: Epiphyseal cartilage is a barrier to osteosarcoma invasion, however the mechanisms behind this resistance remain unclear. The aim of this study was to examine the chronological and spatial patterns of osteosarcoma growth and invasion of local tissue structures including epiphyseal cartilage. METHODS: We used an in vivomouse model of osteosarcoma to histologically examine tumors at different stages of disease progression. We compared the pattern of osteosarcoma penetration of epiphyseal cartilage with the expression pattern of two potent mediators of angiogenesis; proangiogenic vascular endothelial growth factor (VEGF) and antiangiogenic pigment epithelium-derived factor (PEDF). RESULTS: Epiphyseal cartilage remained intact across its entire length in all sections examined, despite increasing tumor size as well as intra- and extraosseous destruction. In the most advanced cases, only the proangiogenic lowermost layers of the hypertrophic zone of the growth plate were eroded. This corresponded with the growth plate layers which highly expressed the angiogenic factor VEGF. In contrast, the resting, proliferative and upper hypertrophic layers were resistant to osteosarcoma invasion in all cases. This corresponded to the layers with the highest expression of the potent antiangiogenic factor PEDF. CONCLUSION: Epiphyseal cartilage is resistant to local invasion by osteosarcoma. The balance of angiogenesis, influenced by pro- and antiangiogenic factors, is likely to play an important role in this resistance.

Animals↗
PubMed1980

[Results of cytostatic therapy with cyclophosphamide, vincristine, adriamycin and DTIC (CYVADIC) in localized and metastasized osteosarcoma. A retrospective analysis].

From December 1973 to november 1978, 31 patients with osteosarcoma were treated with combination chemotherapy consisting of cyclophosphamide, vincristine, adriamycin and DTIC. 11 out of 19 patients with localized osteosarcoma are alive with no evidence of disease, 14+ to 40+ months after initiation of adjuvant postoperative chemotherapy. The probability of relapse-free survival for this group was calculated as 62% at 2 years and 48% at 3 years. Considering the 15 patients with osteosarcoma of the limbs relapse-free survival will be 79% at 2 years and 62% at 3 years. In 10 of 11 patients with no relapse the primary tumor has been located in the metaphysis of the proximal tibia or the distal femur. All patients with osteosarcoma of the trunk have died from metastases. Most of the 12 patients with metastasizing osteosarcoma died within one year after onset of chemotherapy. In none of these patients a complete remission could be achieved. For patients receiving adjuvant chemotherapy results are comparable with those reported by other investigators. In patients with disseminated osteosarcoma alternative chemotherapy regimens including adriamycin, cis-dichloro-diammine-platinum and ifosfamide may prove superior. In a pilot-study using vincristine-adriamycin-DDP or ifosfamide-DDP response to chemotherapy was noted in 4 out of 7 patients with two continuing complete remissions for 13+ and 5 1/2+ months, respectively.

Adolescent↗
PubMed1998

Osteosarcoma of the larynx.

About 11,600 cases of laryngeal cancer were reported in the United States in 1995, accounting for 1% of all reported cancers. Fewer than 1% of laryngeal cancers are sarcomas, osteosarcoma being the rarest type. Twelve cases of laryngeal osteosarcoma have been cited in the literature. A 47-year-old man presented with hoarseness following a benign vocal polypectomy. The entire larynx appeared swollen, although both vocal folds moved well. Biopsies did not reveal pathologic tissue. Computed tomographic imaging revealed a destructive, expansile lesion of the thyroid cartilage. A computed tomography-guided biopsy of this cartilage revealed a high-grade sarcoma. Laryngeal osteosarcoma was diagnosed following total laryngectomy. Laryngeal osteosarcoma is a highly malignant neoplasm with early hematogenous spread. Survival statistics for peripheral osteosarcoma are poor. Limited experience reveals that a combination of surgery and radiotherapy with adjuvant chemotherapy can offer some palliation. The literature and published cases of laryngeal osteosarcoma are reviewed.

Combined Modality Therapy↗
PubMedDate not supplied

Low expression of p63 and p73 in osteosarcoma.

BACKGROUND: The recent discovery of two p53-related genes, p63 and p73, has revealed an additional level of complexity to the study of p53 function. Both genes encode multiple proteins arising from alternative promoter usage and splicing, with transactivation, DNA-binding, and tetramerization domains. Recent data support a role for p63 in squamous and transitional cell carcinomas, as well as in certain lymphomas and thymomas. METHODS: To characterize the involvement of p63 and p73 in the development of osteosarcoma, we analyzed the expression and mutation of TAp63 and TAp73 in six osteosarcoma cell lines and twelve osteosarcoma specimens. RESULTS: Semiquantitative DNA/PCR analysis revealed that eight (67%) and six (50%) out of twelve osteosarcoma specimens showed significantly reduced levels of p63 and p73 transcription, respectively. Direct sequencing of the entire coding region detected no mutations in cell lines or osteosarcoma specimens. CONCLUSIONS: Our data suggest that low expression of p63 and p73 is relatively common in osteosarcomas and might contribute to their molecular pathogenesis.

Biomarkers, Tumor↗
PubMed2004

Osteosarcomas after the age of 50: a clinicopathologic study of 64 cases--an experience in northern Japan.

BACKGROUND: The clinicopathologic profile and prognostic factors of osteosarcomas after the age of 50 years have been obscure. METHODS: Clinicopathologic features were analyzed in 645 patients with osteosarcoma who were registered at the Tohoku Musculoskeletal Tumor Society and National Cancer Center in Tokyo between 1972 and 2002. RESULTS: Sixty-four patients (9.9%; 34 men and 30 women) were more than 50 years old. The most common location was the distal femur (n = 13), followed by the pelvis (n = 10), proximal femur (n = 9), and proximal fibula (n = 6). Seven (11%) patients had lung metastasis at initial presentation. On radiographs, an osteolytic appearance without periosteal reactions was a common and characteristic feature. Forty-eight tumors (75%) were classified as conventional osteosarcomas. Fourteen cases (22%) were secondary; postradiation osteosarcoma was most common in these patients, but there was no Paget's sarcoma. At the initial presentation, misdiagnoses without biopsy were made in 15 (23%) of the 64 cases. Preoperative chemotherapy was given to 22 patients, but the effect was poor in 18 cases (82%). Fifty-four patients underwent surgery, whereas the other 10 patients were treated without surgery because of systemic or inoperable local conditions. The overall survival rate at 5 years was 55.5%. Multivariate analysis showed initial pulmonary metastasis, axial tumor location, and larger tumors as significant prognostic factors. CONCLUSIONS: In northern Japan, most patients with osteosarcoma after the age of 50 had primary osteosarcoma. Careful radiological examination and biopsy are mandatory for correct diagnosis. Current systemic chemotherapy is not effective for this age group. Alternative treatment strategies should be considered.

Age of Onset↗
PubMed1981

Diaphyseal osteosarcoma.

Fifteen cases of diaphyseal osteosarcomas were found in a review of 157 cases of long bone osteosarcoma (9.5%) and two further examples were added. The clinical and histological features of the diaphyseal osteosarcomas were indistinguishable from those of the commoner juxta metaphyseal osteosarcomas. The radiological features, however, fell into four distinct patterns: Group I had the classical appearance of a conventional osteosarcoma; Group II showed dense cortical sclerosis with bony expansion but no soft tissue swelling or break of the cortex at presentation; Group III presented with a pathological fracture through a purely osteolytic lesion; Group IV usually had the classical appearances of an osteosarcoma in the diaphysis but had, in addition, dense separate sclerotic lesions which were proximal to the tumour in the humerus and distal to it in the femur. The importance of these four groups lies in the quite distinct differential diagnosis which each presents.

Adolescent↗
PubMedDate not supplied

The effect of the bisphosphonate alendronate on viability of canine osteosarcoma cells in vitro.

The objective of this study was to determine the effect of alendronate on the viability of canine osteosarcoma cells and nonneoplastic canine cells. The sample population was composed of canine osteosarcoma tumor cells. Osteosarcoma cells and canine fibroblasts were maintained in culture under standard conditions. The MTT assay for cell viability was performed after 24, 48, and 72 h of incubation with alendronate (0.001 to 1000 microM) or no drug (control). Plates were set up so that each concentration and the control had a sample number of 8. The optical density (OD) of each well was measured at 540 nm using an enzyme-linked immunosorbent assay microplate reader. The percent viability was determined for each concentration and for each incubation time. After 24 h of incubation of POS (parent osteosarcoma) and HMPOS cells with alendronate, there was no significant difference in mean OD at any drug concentration when compared with control samples. A significant concentration- and time-dependent reduction in mean OD of osteosarcoma cells was observed after 48 and 72 h of incubation, with alendronate concentrations ranging from 10 to 1000 microM. The lowest percent cell viability observed in treated cells was 35%. Conversely, alendronate did not significantly affect mean OD in fibroblasts, and the lowest percent cell viability observed was 76%. Our data indicate that alendronate may have the potential to inhibit canine osteosarcoma tumor growth. It will be important to determine the clinical relevance of these in vitro findings. If similar findings are observed in vivo, use of alendronate may also be indicated as an adjuvant to existing chemotherapeutic protocols.

Alendronate↗
PubMed2000

Proficient repair of potentially lethal damage sensitive to hypertonic treatment in osteosarcoma cells.

Fast-repairing potentially lethal damage (PLD) in seven osteosarcoma cell lines was analyzed after treatment with a hypertonic 0.5 M NaCl solution for 20 min and compared to that in seven human fibroblast strains. Fixation of PLD after exposure to ionizing radiation was observed without exception in both the osteosarcoma cells and the fibroblast strains. The percentages by which the D(o)'s of the osteosarcoma cells decreased were significantly higher than the percentage decreases in the C(o)'s of the fibroblast strains (P < 0.01). Hypertonic treatment resulted in radiosensitization due to fixation of PLD in all of the osteosarcoma cell lines, demonstrating that osteosarcoma cells can repair PLD better than normal fibroblast cells. The radiobiological response of the osteosarcoma cells, with enhanced killing after hypertonic treatment, was similar to that of normal untreated fibroblast cells.

Bone Neoplasms↗
PubMed2000

Intrinsic resistance to chemotherapeutic agents in murine osteosarcoma cells.

BACKGROUND: There are two general categories of drug resistance: acquired and intrinsic. The mechanisms involved in acquired drug resistance have been extensively studied, and several mechanisms have been described. However, the mechanisms responsible for intrinsic drug resistance have not been elucidated, to our knowledge. The purpose of the present study was to investigate the cytological and biochemical differences between acquired and intrinsic drug resistance in osteosarcoma cells. METHODS: We previously isolated a clonal cell line (MOS/ADR1) to study acquired resistance in osteosarcoma by exposure of parental murine osteosarcoma cells (MOS) to doxorubicin. In the present study, we cloned a new, intrinsically resistant cell line (MOS/IR1) by single-cell culture of MOS cells and we investigated the differences in cell phenotype and the mechanisms of resistance in both of these resistant clones. RESULTS: The MOS/ADR1 and MOS/IR1 cells were sevenfold and fivefold more resistant to doxorubicin than the parental murine osteosarcoma cells. Morphologically, the MOS/ADR1 cell line was composed of polygonal cells, whereas the MOS/IR1 cell line consisted of plump spindle cells with long cytoplasmic processes. The MOS/IR1 cells showed a much lower level of alkaline phosphatase activity than did the MOS/ ADR1 and MOS cells. There were no substantial differences in the cellular DNA content or the doubling time among these three lines. Overexpression of the P-glycoprotein involved in the function of an energy-dependent drug-efflux pump was detected in the MOS/ADR1 cells but not in the MOS/ IR1 cells. After the cells were incubated with doxorubicin for one hour, the two resistant lines had less accumulation of the drug than did the parent line (p < 0.05). The addition of a P-glycoprotein antagonist, verapamil, or the depletion of cellular adenosine triphosphate resulted in a marked increase in the accumulation of doxorubicin in the MOS/ADR1 cells (p < 0.05) but not in the MOS/ IR1 cells. The MOS/ADR1 cells were found to exhibit cross-resistance only to substrates for P-glycoprotein (such as doxorubicin, vincristine, and etoposide), whereas the MOS/IR1 cells were resistant to all of the drugs studied (including cisplatin and methotrexate). The degree of drug resistance in the MOS/IR1 cells was found to be associated with the molecular weight of the drugs (p < 0.05). Permeabilization of the plasma membrane by saponin increased both the accumulation of doxorubicin (p < 0.05) and the cytotoxic activity of this drug in all lines, but the effects were most pronounced in the MOS/IR1 cells. CONCLUSIONS: Taken together, this data suggests that reduced drug accumulation in the MOS/IR1 cells may be due to the effect of decreased permeability of the plasma membrane on the transport of drugs from the extracellular environment into the cytosol of the cell and that this may be the mechanism responsible for intrinsic resistance to multiple drugs in the MOS/IR1 cell line. CLINICAL RELEVANCE: Current drug treatment for human osteosarcoma may include multiple chemotherapeutic agents, such as doxorubicin, cisplatin, and methotrexate. These drugs exhibit different cytotoxic actions and, thus, the mechanisms of resistance to individual drugs vary. Clinical resistance to multidrug chemotherapy may be observed in tumors that recur after repetitive chemotherapy and in previously untreated tumors. In the former group, a tumor cell may express multidrug resistance by combining several different mechanisms due to its exposure to various drugs. In the latter group, however, this is not likely. Decreased intracellular drug accumulation due to reduced permeability of the plasma membrane, found in the MOS/IR1 cells, is one possible mechanism and may explain the intrinsic resistance to multidrug chemotherapy for the treatment of osteosarcoma. Further study regarding the resistance mechanism in the MOS/IR1 cells may help to overcome the intrinsic drug resistance in oste

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Parosteal osteosarcoma of the posterior aspect of the distal part of the femur. Oncological and functional results following a new resection technique.

BACKGROUND: Parosteal osteosarcoma is a low-grade malignant bone tumor that arises from the surface of the metaphysis of long bones. Parosteal osteosarcoma is usually well differentiated and displays a low propensity to metastasize. Wide resection of a parosteal osteosarcoma has been shown to provide a relatively risk-free method of preventing local recurrence. We propose a new method of resection of parosteal osteosarcomas located in the popliteal paraosseous space of the distal part of the femur. This method involves resection of the mass through separate medial and lateral incisions, which allows for wide margins yet limits the amount of dissection of the soft tissues and the neurovascular bundle. METHODS: Six patients with parosteal osteosarcoma located on the posterior aspect of the distal part of the femur underwent resection of the lesion and reconstruction with a posterior hemicortical allograft through dual medial and lateral incisions. The patients were evaluated with regard to pain, postoperative function, union of the allograft (osteosynthesis), and the prevalence of local recurrence. RESULTS: The average time until the last follow-up assessment was 4.3 years. No metastases developed, and there were no local recurrences. All patients were free of disease at the last follow-up evaluation. Postoperatively, the average range of motion of the knee was 0 to 122 degrees. Five of the six patients were free of pain at the time of the latest follow-up. Five of the six patients returned to their preoperative active functional status. CONCLUSIONS: We recommend resection of a parosteal osteosarcoma located on the posterior surface of the femur through separate medial and lateral incisions. This approach provides minimal dissection of the neurovascular bundle but ample exposure for reconstruction with a hemicortical allograft.

Adult↗
PubMed1988

Craniofacial osteosarcomas: plain film, CT, and MR findings in 46 cases.

Forty-six osteosarcomas of the cranial and facial bones were reviewed radiographically by using the conventional parameters for long bone tumors. There were 32 de novo osteosarcomas (11 maxillary, 13 mandibular, and eight cranial) and 14 postradiation osteosarcomas. All the maxillary tumors originated from the alveolar ridge, and the majority of mandibular lesions began in the body of the mandible. The postradiation osteosarcomas occurred in portions of bones at the borders of the radiation field; the latent period ranged from 4 years, 2 months to 50 years (mean, 14 years). The majority of de novo or postradiation craniofacial osteosarcomas were osteolytic with a long transition zone and no periosteal reaction; the exception was in the mandible, where nearly half the cases were osteoblastic and periosteal reaction was occasionally present. Tumor matrix mineralization occurred in more than 75% of the cases, and osteoid matrix calcification was most frequent, even though most tumors were chondroblastic. Soft-tissue extension of tumor was present in all cases and contained calcifications in more than half. Conventional radiographs are of limited value in evaluating head and neck osteosarcomas because of the superimposed bony structures. CT provides excellent detection of tumor calcification, cortical involvement, and, in most instances, soft-tissue and intramedullary extension. MR is even more effective in demonstrating the intramedullary and extraosseous tumor components on both T1- and T2-weighted images. However, CT and plain films are superior to MR in detecting the matrix calcifications and bone destruction or reaction.

Adolescent↗
PubMed2005

Investigation of the effect of pamidronate disodium on the in vitro viability of osteosarcoma cells from dogs.

OBJECTIVE: To determine the effect of pamidronate disodium on the in vitro viability of osteosarcoma cells and non-neoplastic cells from dogs. SAMPLE POPULATION: 3 osteosarcoma and 1 fibroblast cell lines derived from dogs. PROCEDURE: Cell counts and cell viability assays were performed in cultures of osteosarcoma cells (POS, HMPOS, and COS31 cell lines) and fibroblasts after 24, 48, and 72 hours of incubation with pamidronate at concentrations of 0.001 to 1000 microM or with no drug (control treatment). Percentage viability was determined in cell samples for each concentration of pamidronate and each incubation time. A DNA fragmentation analysis was performed to assess bisphosphonate-induced apoptosis. RESULTS: Osteosarcoma cell viability decreased significantly in a concentration- and time-dependent manner at pamidronate concentrations ranging from 100 to 1000 microM, most consistently after 48 and 72 hours' exposure. In treated osteosarcoma cells, the lowest percentage cell viability was 34% (detected after 72 hours' exposure to 1000 microM pamidronate). Conversely, 72 hours' exposure to 1000 microM pamidronate did not significantly reduce fibroblast viability (the lowest percentage viability was 76%). After 72 hours of exposure, pamidronate did not cause DNA fragmentation in POS or HMPOS cells. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that pamidronate may have the potential to inhibit osteosarcoma growth in dogs, possibly through a nonapoptotic mechanism. The clinical relevance of these in vitro findings remains to be determined, but administration of pamidronate may potentially be indicated as an adjuvant treatment in chemotherapeutic protocols used in dogs.

Animals↗
PubMed1999

Parosteal osteosarcoma of the scapula.

Parosteal osteosarcoma is a low-grade osteosarcoma, which occurs on the surface of the bone. We had experienced a parosteal osteosarcoma involving the flat bone, the scapula of a 21-year-old man. This is an extremely rare location for a parosteal osteosarcoma. Plain radiograph showed broad-based, well-defined radiodense lesion at the scapula. Computed tomogram demonstrated an intact cortex and absence of a medullary involvement. Tumor showed a lobulated, high-density lesion, indicating bone formation. Histologically, parosteal osteosarcoma is a well-differentiated osteosarcoma. The tumor is composed of a hypocellular proliferation of spindle cells, with minimal cytologic atypia. The bone is in the form of a well-formed bony trabeculae. Occasional cartilage is present in the form of a cap.

Adult↗