Aggressive squamous cell carcinoma of the cranium of a dog.

BACKGROUND: The authors report a case of keratinized squamous cell carcinoma (SCC) in a 14-year-old dog with extensive cranial bone invasion. To our knowledge, this is the first description of such a case of cranial keratinized SCC with aggressive generalized osteolysis described in a dog. CASE PRESENTATION: The 14-year-old dog was referred for radiological examination with suspicion of head trauma with clinical signs of head deformation, exophthalmos and nasal discharge. The skull radiographs showed a large osteolytic defect of the frontal bone and parietal bone in the region of the external sagittal crest. Findings from the skull CT scan included generalized osteolysis in the region of parietal bone, frontal bones, maxilla on the right side and the nasal bone including the dorsal nasal concha. In the area of bone loss, new soft tissue formation with multifocal foci of mineralization was visible. The ultrasound examination revealed hypoechogenic changes with hyperechoic foci consistent with mineralization and poor vascularization. The brain and ocular structures were without visible changes. Fine needle aspiration cytology (FNAC) was performed, and squamous cell carcinoma was suspected. After 3 months, the re-presented to the clinic. The dog became progressively listless, his appetite was decreased, and he became acutely blind. Follow-up skull CT scan revealed significant osteolysis, which affected a significant aspect of the cranium. All bone defects had been replaced by new 3.5 cm-thick soft tissue formations with multifocal small 1-2 mm areas of mineralization. There was no evidence of metastasis. Histological examination confirmed the suspicion of squamous cell carcinoma. CONCLUSIONS: This paper is the first report of cranial SCC in a dog causing extensive bone osteolysis. The lesions in this dog originated from the frontal and parietal bones including frontal sinuses. There are variants of tumors that arise from squamous epithelium or resemble SCC in the skull. These examples include adenosquamous carcinoma and proliferating trichilemmal tumours. In addition, there is possible malignant transformation caused by papilloma viruses. In the veterinary literature, there is only one similar description of adenosquamous carcinoma in a cat with similar clinical manifestations. It is justified to suspect a process of neoplastic epithelial origin in all cases of aggressive and extensive skull bone lysis. This issue should be subject to further investigation.

Surface-Modified Poly(l-lactide-co-glycolide) Scaffolds for the Treatment of Osteochondral Critical Size Defects-In Vivo Studies on Rabbits.

Poly(l-lactide-co-glycolide) (PLGA) porous scaffolds were modified with collagen type I (PLGA/coll) or hydroxyapatite (PLGA/HAp) and implanted in rabbits osteochondral defects to check their biocompatibility and bone tissue regeneration potential. The scaffolds were fabricated using solvent casting/particulate leaching method. Their total porosity was 85% and the pore size was in the range of 250-320 µm. The physico-chemical properties of the scaffolds were evaluated using scanning electron microscopy (SEM), energy dispersive X-ray spectroscopy (EDX), X-ray diffractometry (XRD), X-ray photoelectron spectroscopy (XPS), Fourier transform infrared spectroscopy (FTIR), sessile drop, and compression tests. Three types of the scaffolds (unmodified PLGA, PLGA/coll, and PLGA/HAp) were implanted into the defects created in New Zealand rabbit femoral trochlears; empty defect acted as control. Samples were extracted after 1, 4, 12, and 26 weeks from the implantation, evaluated using micro-computed tomography (µCT), and stained by Masson-Goldner and hematoxylin-eosin. The results showed that the proposed method is suitable for fabrication of highly porous PLGA scaffolds. Effective deposition of both coll and HAp was confirmed on all surfaces of the pores through the entire scaffold volume. In the in vivo model, PLGA and PLGA/HAp scaffolds enhanced tissue ingrowth as shown by histological and morphometric analyses. Bone formation was the highest for PLGA/HAp scaffolds as evidenced by µCT. Neo-tissue formation in the defect site was well correlated with degradation kinetics of the scaffold material. Interestingly, around PLGA/coll extensive inflammation and inhibited tissue healing were detected, presumably due to immunological response of the host towards collagen of bovine origin. To summarize, PLGA scaffolds modified with HAp are the most promising materials for bone tissue regeneration.

Testicular disorder of sex development in four cats with a male karyotype (38,XY; SRY-positive).

The molecular background of disorders of sex development (DSD) in cats is poorly recognized. In this study we present cytogenetic, molecular and histological analyses of four cats subjected for the analysis due to ambiguous external genitalia. Three cases, with rudimentary penises and an abnormal position of the urethral orifice, represented different types of hypospadias. The fourth case had a normal penis, a blind vulva and spermatogenetically active testes. Histological studies showed structures typical of testes, but spermatogenic activity was observed in two cats only. All the cats had a normal male chromosome complement (38,XY) and the Y-chromosome linked genes (SRY and ZFY) were also detected. Fluorescent in situ hybridization (FISH), with the use of the feline BAC probe harboring the SRY gene, excluded the possibility of chromosome translocation of the Y chromosome fragment carrying the SRY gene onto another chromosome. Sequencing of four candidate genes (SRY--sex determining region Y; AR--androgen receptor; SRD5A2--steroid-5-alfa reductase 2 and MAMLD1--mastermind-like domain containing (1) revealed one SNP in the SRY gene, one common polymorphism in exon 1 of the AR gene (tandem repeat of a tri-nucleotide motif--CAG), six polymorphisms (5 SNPs and 1 indel) in the SRD5A2 gene and one SNP in the MAMLD1 gene. Molecular studies of the candidate genes showed no association with the identified polymorphisms, thus molecular background of the studied DSD phenotypes remains unknown.

Mitochondrial D-loop mutations and polymorphisms are connected with canine malignant cancers.

Abstract The aim of the conducted investigations was to identify differences in the D-loop nucleotide sequence between neoplastic tissue, normal tissue, and blood and to determine their correlation with the type of cancer in dogs. In 62.5% of the analyzed tumors of epithelial origin and 25% tumors of mesenchymal origin, substitution was detected within the D-loop sequence between the neoplastic tissue, normal tissue, and blood. Two mutations occurring in the carcinogenic process in position T15620C have been identified in epithelioma glandulae sebacei and carcinoma planoepithelialae keratodes. Blood and cancer heteroplasmy was diagnosed for carcinoma planoepithelialae keratodes and "Comedo" carcinoma. The results of the study indicate that polymorphic changes in the D-loop sequence promote carcinogenesis in dogs. Heteroplasmy diagnosed in blood and tumor cells and absence thereof in normal tissue may imply mtDNA recombination. High prevalence of mtDNA mutations in canine tumors may suggest mtDNA genetic instability, which is likely to play a role in carcinogenesis.