ABSTRACTS
Background: Triple negative breast cancers (TNBC) generally show a very poor prognosis with a need for targeted therapy. Expression of MET is elevated in 15–20% of breast cancers. Overexpression is a prognostic marker of poor survival, is associated with TNBCs and high risk of metastatic progression. MET is rarely mutated in breast cancer, however limited studies have indicated that MET overexpression is due to elevated copy number. Targeted inhibition of MET may provide a much needed therapeutic opportunity for treating TNBC. Methods: 89 TNBC cases were analysed for MET copy number using fluorescence in situ hybridisation [Vysis MET SpectrumRed FISH Probe Kit and CEP 7 (D7Z1) SpectrumGreen Probe, Abbott Molecular]. MET protein expression was analysed using immunohistochemistry (SP44 clone antibody, Roche). Results: One case (1.5%) showed elevated copy number for both MET and the CEP7 enumeration probe (average MET ¼ 9.2, average CEP7 ¼ 7.8, ratio ¼ 1.2). This case was not associated with recurrence or poor survival. Forty-seven of 89 (53%) showed MET immunoreactivity. Discussion: Compared with another study1 reporting MET amplificatopm in 14% of TNBC, we have found elevated MET copy number occurs at a low frequency (1.5%) within our cohort and does not account for MET overexpression. Further investigation of MET copy number in larger cohorts is warranted. Reference 1. Gonzalez-Angulo AM, Chen H, Karuturi MS, et al. Frequency of mesenchymal-epithelial transition factor gene (MET) and the catalytic subunit of phosphoinositide-3-kinase (PIK3CA) copy number elevation and correlation with outcome in patients with early stage breast cancer. Cancer 2012; 119: 7–15.
DIABETIC DERMANGIOPATHY – A MICROMETRIC STUDY Mohit Shahi1,2, Prakash R. Malur2 and Carol Fernandes3 1School of Medicine, Taylor’s University, Malaysia, 2Pathology, and 3Skin, KLES’ JN Medical College, Belgaum, India Aim: Diabetes mellitus (DM) is the most common endocrine disorder and cutaneous disorders associated with DM are thought to occur in about one-third of patients. The present study was undertaken to assess the alterations in the small blood vessels. Methods: Skin biopsies from 100 type 2 diabetic patients and 15 non-diabetic controls were studied to observe the dermangiopathic changes. The lumen diameter and basement membrane width were measured. Depending on deposition of PAS-positive material in the vessel wall, the dermangiopathic changes were graded as 1 þ , 2 þ and 3 þ . Results: 80% of the cases showed 2 þ (69%) or 3 þ (11%) changes. The other 20% cases showed 1 þ change and were not taken as positive evidence of microangiopathy. Mean BMT was measured as 6.06 microns and mean LD was 53.9 microns. The mean BMT:LD ratio was 0.11. No correlation was observed between age, duration of diabetes, severity of disease, diabetic complications and microangiopathy. A positive correlation was observed between the grades of microangiopathy and the basement membrane thickness. Discussion: Characteristic angiopathy is demonstrable in vessels of diabetic patients and the vessel basement membrane thickness is an important criterion to grade diabetic dermangiopathy.
S81
IMMATURE OVARIAN TERATOMA. A CASE REPORT AND REVIEW OF LITERATURE Maryam Shamassi and Sophie Bittinger Department of Anatomical Pathology, Royal Women’s Hospital, Melbourne, Vic, Australia Immature ovarian teratomas are rare tumours occurring most commonly in the first two decades of life. These tumours differ from their mature counterparts both histologically by the presence of immature tissue, and clinically by their more malignant behaviour. Microscopic examination reveals tissue from all three germ layers with at least one of the components having an immature appearance. The grade is based on the proportion of immature neuroepithelium and highly correlates with the tumour grade and hence prognosis. These tumours usually are confined to the ovary and are typically chemo- and radiosensitive. They may metastasise to peritoneum, liver or lung. We present a case of bilateral teratomas in a 25-year-old nulliparous woman who was found to have immature elements including neuroectodermal tissue, mesenchymal nodules, immature fat and cartilage within the left sided tumour. She is currently undergoing chemotherapy.
PRIMARY INTRAVASCULAR LARGE B-CELL LYMPHOMA OF THE CENTRAL NERVOUS SYSTEM – ANTEMORTEM DIAGNOSIS AND REVIEW OF LITERATURE Alka Sinha and Benhur Amanuel Anatomical Pathology, PathWest Laboratory Medicine, QEII Medical Centre, Nedlands, WA, Australia Intravascular large B-cell lymphoma (IVLBCL) is a rare type of extranodal large B-cell lymphoma occurring in adults, characterised by growth of neoplastic lymphoid cells within the lumina of blood vessels, particularly capillaries. The clinical presentations are non-specific and histological features are often subtle. We report a case of a 60-year-old male who presented with a several week history of headaches, general malaise and fluctuating visual disturbances followed by sudden onset of confusion. Neurological deficits included disorientation, nominal aphasia, left-right disorientation and left sided homonomous hemianopia. MRI of the brain revealed diffuse leptomeningeal enhancement and digital subtraction angiography showed an abnormality of a branch of the left of middle cerebral artery consistent with CNS vasculopathy. The differential diagnosis included vasculitis, stroke and atypical migraine necessitating an open biopsy. The histological sections revealed an intravascular infiltrate of large neoplastic B-cells that express CD20 within leptomeningeal vessels and small intraparencymal vessels with no involvement of the brain parenchyma. The case illustrates the protean clinical manifestations of CNS IVLBCL and the subtleties of its histological diagnosis. Correct diagnosis is important as treatment regimes drastically differ between IVLBCL and its clinical mimics. RENAL TUBULAR DYSGENESIS: AN UNUSUAL CAUSE OF ANHYDRAMNIOS Lisa Squires, Rohan Lourie, Jane Armes and Leo Francis Anatomical Pathology, Mater Pathology Services, South Brisbane, Qld, Australia
Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.