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Spindle Cell Lipoma in the Dog: Histological Diagnostic Features
J. Comp. Path. 2017, Vol. 156, 54e141
ESVP and ECVP Proceedings 2016
IN-VITRO STUDY OF THE INTERACTION BETWEEN DOXORUBICIN, MELOXICAM AND SODIUM RISEDRONATE ON THE CANINE OSTEOSARCOMA CELL LINE (D-17) D. Poradowski * and B. Obmi nska-Mrukowiczy *Department of Animal Physiology and Biostructure, Division of Animal Anatomy and yDepartment of Biochemistry, Pharmacology and Toxicology, Division of Pharmacology and Toxicology, University of Environmental and Life Sciences, Wroclaw, Poland Introduction: Doxorubicin is one of the most commonly used cytostatic drugs in the treatment of canine osteosarcoma. Meloxicam reduces inflammation and pain, which sometimes accompanies neoplastic disease. Risedronate is often used in the treatment of bone diseases include Paget’s disease or post-menopausal osteoporosis. The aim of this study was to assess the viability of canine osteosarcoma cell lines treated with combinations of doxorubicin, meloxicam and risedronate. Materials and Methods: The concentration of doxorubicin used was 0.01 mg/ml, for meloxicam, concentrations of 100 and 10 mg/ ml, and for risedronate a concentration of 100 mg/ ml. The viability of the cells treated with the drugs was evaluated using the MTT assay. Four independent repetitions were performed and the results are given as the average of these values. Results: Cell viability in the presence of doxorubicin at a concentration of 0.01 mg/ml, meloxicam at 100 and 10 mg/ml and risedronate at 100 mg/ml was, respectively, 64.32 4.1%, 83.4 3.36%, 125.55 1.29% and 53.6 1.46%. Cell viability when treated by a combination of 0.01 mg/ml doxorubicin + 100 mg/ml meloxicam, 0.01 mg/ml doxorubicin +10 mg/ml meloxicam, 0.01 mg/ml doxorubicin + 100 mg/ml risedronate, 100 mg/ml risedronate + 100 mg/ml meloxicam and 100 mg/ml risedronate + 10 mg/ml meloxicam was, respectively, 46.08 2.66%, 63.99 3.58%, 15.51 3.43%, 10.01 3.13% and 41.81 5.58%. Treatment with a combination of 0.01doxorubicin + 100meloxicam + 100 risedronate and 0.01doxorubicin + 10meloxicam +100 risedronate gave viability of 23.5 3.18% and 23.76 4.57%, respectively. Conclusions: The presence of risedronate in combination with doxorubicin or meloxicam increased the cytotoxic activity of these drugs against canine osteosarcoma cells. The presence of risedronate in combination with doxorubicin and meloxicam increased the antiproliferative activity, but the effect was weaker than with combinations of doxorubicin or with meloxicam alone. The synergy between these drugs suggests that risedronate should be used more often in the treatment of canine osteosarcoma.
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SPINDLE CELL LIPOMA IN THE DOG: HISTOLOGICAL DIAGNOSTIC FEATURES G. Avallone *, V. Pellegrino *, G. Sarli * and P. Roccabiancay *Department of Veterinary Medical Sciences (DIMEVET), University of Bologna and yDIMEVET, University of Milano, Italy Introduction: Canine spindle cell lipoma (SCL) is an uncommon benign spindle cell tumour that might be misdiagnosed as soft tissue sarcoma (STS) because of the high cellularity and paucity of mature adipose tissue. The aim of this report was to define the typical histopathological features of canine SCL. Materials and Methods: Dog signalment, tumour size and site were retrieved from medical records. Haematoxylin and eosin, Masson’s trichrome, alcian blue and PAS staining and immunohistochemistry for vimentin, smooth muscle actin (SMA), S100, factor VIII-related antigen and MDM2 were performed. Mitotic count (MC) and MIB-1 based labelling index (LI) were assessed. Results: Five canine subcutaneous tumours were retrieved. Tumours contained bland spindle cells with sparse eosinophilic cytoplasm, an oval nucleus and an inconspicuous nucleolus, intermixed with ropey collagen and myxoid matrix stained by alcian blue. Three cases contained scattered mature adipocytes (!10%). MC was !1 in four cases and 1 in one case. LI range was 0.9e3.4. All cases expressed vimentin and were S100, SMA, factor VIII-related antigen and MDM2 negative, ruling out peripheral nerve, muscular/myofibroblastic and endothelial cell origin. The low proliferation rate, the absence of lipoblasts and the lack of MDM2 expression ruled out fibrosarcoma, myxoid liposarcoma and dedifferentiated liposarcoma, respectively. A fibroma was ruled out based on the high cellularity. Conclusions: Histopathological features identified in this caseload (i.e. bland spindle cells, rare adipocytes, ropey collagen and myxoid matrix) paralleled descriptions of SCL in man. The identification of these morphological hallmarks is necessary to diagnose SCL and to avoid a diagnosis of STS characterized by a poorer prognosis.
ESVP and ECVP Proceedings 2016
IN-VITRO STUDY OF THE INTERACTION BETWEEN DOXORUBICIN, MELOXICAM AND SODIUM RISEDRONATE ON THE CANINE OSTEOSARCOMA CELL LINE (D-17) D. Poradowski * and B. Obmi nska-Mrukowiczy *Department of Animal Physiology and Biostructure, Division of Animal Anatomy and yDepartment of Biochemistry, Pharmacology and Toxicology, Division of Pharmacology and Toxicology, University of Environmental and Life Sciences, Wroclaw, Poland Introduction: Doxorubicin is one of the most commonly used cytostatic drugs in the treatment of canine osteosarcoma. Meloxicam reduces inflammation and pain, which sometimes accompanies neoplastic disease. Risedronate is often used in the treatment of bone diseases include Paget’s disease or post-menopausal osteoporosis. The aim of this study was to assess the viability of canine osteosarcoma cell lines treated with combinations of doxorubicin, meloxicam and risedronate. Materials and Methods: The concentration of doxorubicin used was 0.01 mg/ml, for meloxicam, concentrations of 100 and 10 mg/ ml, and for risedronate a concentration of 100 mg/ ml. The viability of the cells treated with the drugs was evaluated using the MTT assay. Four independent repetitions were performed and the results are given as the average of these values. Results: Cell viability in the presence of doxorubicin at a concentration of 0.01 mg/ml, meloxicam at 100 and 10 mg/ml and risedronate at 100 mg/ml was, respectively, 64.32 4.1%, 83.4 3.36%, 125.55 1.29% and 53.6 1.46%. Cell viability when treated by a combination of 0.01 mg/ml doxorubicin + 100 mg/ml meloxicam, 0.01 mg/ml doxorubicin +10 mg/ml meloxicam, 0.01 mg/ml doxorubicin + 100 mg/ml risedronate, 100 mg/ml risedronate + 100 mg/ml meloxicam and 100 mg/ml risedronate + 10 mg/ml meloxicam was, respectively, 46.08 2.66%, 63.99 3.58%, 15.51 3.43%, 10.01 3.13% and 41.81 5.58%. Treatment with a combination of 0.01doxorubicin + 100meloxicam + 100 risedronate and 0.01doxorubicin + 10meloxicam +100 risedronate gave viability of 23.5 3.18% and 23.76 4.57%, respectively. Conclusions: The presence of risedronate in combination with doxorubicin or meloxicam increased the cytotoxic activity of these drugs against canine osteosarcoma cells. The presence of risedronate in combination with doxorubicin and meloxicam increased the antiproliferative activity, but the effect was weaker than with combinations of doxorubicin or with meloxicam alone. The synergy between these drugs suggests that risedronate should be used more often in the treatment of canine osteosarcoma.
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SPINDLE CELL LIPOMA IN THE DOG: HISTOLOGICAL DIAGNOSTIC FEATURES G. Avallone *, V. Pellegrino *, G. Sarli * and P. Roccabiancay *Department of Veterinary Medical Sciences (DIMEVET), University of Bologna and yDIMEVET, University of Milano, Italy Introduction: Canine spindle cell lipoma (SCL) is an uncommon benign spindle cell tumour that might be misdiagnosed as soft tissue sarcoma (STS) because of the high cellularity and paucity of mature adipose tissue. The aim of this report was to define the typical histopathological features of canine SCL. Materials and Methods: Dog signalment, tumour size and site were retrieved from medical records. Haematoxylin and eosin, Masson’s trichrome, alcian blue and PAS staining and immunohistochemistry for vimentin, smooth muscle actin (SMA), S100, factor VIII-related antigen and MDM2 were performed. Mitotic count (MC) and MIB-1 based labelling index (LI) were assessed. Results: Five canine subcutaneous tumours were retrieved. Tumours contained bland spindle cells with sparse eosinophilic cytoplasm, an oval nucleus and an inconspicuous nucleolus, intermixed with ropey collagen and myxoid matrix stained by alcian blue. Three cases contained scattered mature adipocytes (!10%). MC was !1 in four cases and 1 in one case. LI range was 0.9e3.4. All cases expressed vimentin and were S100, SMA, factor VIII-related antigen and MDM2 negative, ruling out peripheral nerve, muscular/myofibroblastic and endothelial cell origin. The low proliferation rate, the absence of lipoblasts and the lack of MDM2 expression ruled out fibrosarcoma, myxoid liposarcoma and dedifferentiated liposarcoma, respectively. A fibroma was ruled out based on the high cellularity. Conclusions: Histopathological features identified in this caseload (i.e. bland spindle cells, rare adipocytes, ropey collagen and myxoid matrix) paralleled descriptions of SCL in man. The identification of these morphological hallmarks is necessary to diagnose SCL and to avoid a diagnosis of STS characterized by a poorer prognosis.