A 15-year-old female domestic shorthair cat was presented for investigation of an 8 month history of progressive behavioural changes (episodic pacing and vocalisation), polyuria, polydipsia and periuria. At presentation the cat had a body weight of 1.98 kg and a body condition score (BCS) of 3/9. Physical examination revealed diffuse seborrhoea sicca and a palpable (approximately 10 mm diameter) mid-dorsal abdominal mass. Neurological and fundic examinations were within normal limits. Mean systolic blood pressure measured by Doppler sphygmomanometry was 176 mmHg. Clinicopathological abnormalities included mild lymphopenia (0.6 × 109/l; reference interval [RI] 1.5–7.0 × 109/l) and marginal microcytosis (38.3 fl; RI 39.0–55.0 fl). Serum biochemical analysis was unremarkable. Serum feline immunodeficiency virus and feline leukaemia virus immunochromatographic tests were both negative. Urinalysis of a cystocentesis sample yielded a specific gravity of 1.028 and urine dipstick test results were unremarkable. Urine protein:creatinine ratio was within the RI (0.25; RI 0–0.50), urine sediment examination was unremarkable and urine bacterial culture was negative. Prothrombin time was mildly increased (12.7 s; RI 7.0–11.0 s); activated partial thromboplastin and buccal mucosal bleeding times were within the RIs. Abdominal ultrasound examination revealed hetero-genous enlargement of the right ovary (11 mm diameter), the uterine wall thickness was normal and the uterine lumen contained a small volume of anechoic material. Cytological review of fine-needle aspirates from the right ovary found epithelial cells commonly arranged in acinar-like structures with bright eosinophilic granular material in the middle, consistent with Call–Exner bodies (). These findings were suggestive of a granulosa cell tumour (GCT). An aspirate of the anechoic uterine material revealed a total nucleated cell count of 0.2 × 109/l, fluid total protein of 1.8 g/l and cytological review of the fluid identified 69% poorly preserved neutrophils, 3% lymphocytes, 27% macrophages and 1% eosinophils consistent with slight neutrophilic and macrophagic inflammation. Bacterial culture of the uterine fluid was negative. Contrast-enhanced CT (Mx8000 IDT; Philips) of the brain, abdomen and thorax did not reveal evidence of gross metastatic disease. A 4 mm hypoattenuating irregularly marginated lesion was present within the parenchyma of the right liver lobe; ultrasound-guided fine-needle aspiration of the lesion yielded only occasional clusters of hepatocytes with no evidence of metastatic disease. The cat subsequently underwent therapeutic ovariohysterectomy (OHE), surgical biopsy of the liver lesion and biopsy of a regional lymph node to the uterus. Histopathological examination of the right ovary revealed a partially encapsulated, multi-lobular, densely cellular proliferation of neoplastic cells that almost completely effaced the normal architecture (). There was moderate anisocytosis and anisokaryosis, and two mitotic figures observed in 10 high power (× 400) fields. Occasional malformed Call–Exner bodies were seen and there were focal areas composed of theca cells. In one area towards the periphery of the ovary there was a large cluster of neoplastic cells within a thick-walled vessel, which raised concern for vascular invasion. The sections of examined uterus exhibited glandular cysts of varying sizes within the endometrium but no evidence of inflammation. Histopathological examination of the liver biopsy revealed diffuse, mild, periportal infiltrate of lymphocytes and plasma cells accompanied by a mild proliferation of cells with oval nuclei and a small amount of fibrous connective tissue. The periacinar hepatocytes were often mildly atrophic with thinning of cords and relative widening of sinusoids. There was mild hyperplasia of Ito cells and occasional lipogranulomas were also present. Multifocally, hepatocytes contained stippled brown intracytoplasmic material (lipofuscin), and rare plugging of bile canaliculi was also present. These changes were consistent with mild periacinar hepatocellular atrophy and mild chronic lymphoplasmacytic portal hepatitis. Examination of the lymph node biopsy revealed mild sinus histiocytosis and the tissue was otherwise unremarkable. Immunohistochemistry staining for anti-Müllerian hormone (AMH) was performed as previously described. A citrate buffer with microwave heating antigen retrieval was performed; the primary antibody was polyclonal rabbit anti-human AMH (Abcam ab84415) and immunoreactivity was visualised using biotinylated goat anti-rabbit antibody (Vectastain Elite ABC HRP Rabbit IgG; Vector Laboratories) and DAB (DAB Peroxidase [HRP] Substrate Kit; Vector Laboratories). AMH immunoreactivity was identified in developing follicles as described in humans, and within the neoplastic population of cells in a similar pattern as described for equine GCTs. Findings of ovarian histopathology, including the degree of cellular pleomorphism, high nuclear to cytoplasmic ratio and size of the neoplasm, in addition to the immunohistopathological findings of vascular invasion, resulted in a diagnosis of malignant GCT. Prior to surgery, hormone testing was undertaken to evaluate whether the tumour was endocrinologically active. A dexamethasone suppression test (0.1 mg/kg IV dexamethasone) revealed suppression of serum cortisol after 3 and 8 h (basal serum cortisol concentration 201.0 nmol/l; 3 and 8 h serum cortisol concentrations were both <27.6 nmol/l). Plasma endogenous adrenocorticotropic hormone assay (>600 pg/ml; RI 38–176 pg/ml). These results provided no evidence for excessive glucocorticoid production by the tumour. Serum oestradiol, progesterone and testosterone concentrations were within normal limits (). Serum AMH concentration was measured by a commercial laboratory (NationWide Specialist Laboratories) using sandwich ELISA for the measurement of AMH in horses. Serum AMH was 5.7 ng/ml prior to OHE, whereas the highest concentration measured in a group of healthy neutered (n = 8) and entire female (n = 4) cats was 1.7 ng/ml (). Two months following OHE, serum AMH concentration had decreased to <0.04 ng/ml. Surgical intervention resulted in complete resolution of clinical signs and BCS increased to 4/9 at re-evaluation 1 month later. A complete blood cell count and serum biochemistry performed at this time were unremarkable. However, 6 months following surgery the cat presented to the primary veterinary surgeon following several complex partial seizures. These episodes manifested as facial twitching, vocalisation, falling and circling to the right. The cat later developed central blindness and was euthanased. Post-mortem macroscopic examination did not reveal any gross abnormalities. Microscopic examination of the brain revealed a neoplasm expanding and effacing the parenchyma within the neocortex above the mid-thalamus. The neoplasm was well-demarcated, non-encapsulated, densely cellular and was composed of numerous astrocytes exhibiting moderate anisocytosis, anisokaryosis and mitotic activity. Large areas of necrosis were present and neoplastic astrocytes widely infiltrated the adjacent neuropil. The neoplasm exhibited positive immunoreactivity for vimentin and glial fibrillary acidic protein consistent with an intermediate grade (anaplastic) astrocytoma.