SummaryMore than one neoplastic founder clone can exist in benign epithelial tumours. Although theories of clonal selection make pluriclonality appear unlikely in carcinomas, published data do not exclude this possibility. This study looked for evidence of multiclonal X inactivation in ovarian carcinoma using AR methylation as a marker. Fifteen unifocal ovarian carcinomas and 14 multifocal carcinomas all in Scottish patients were studied. One representative formalin-fixed paraffin-embedded tumour block was chosen for each of the former and two for the latter. From each of these 43 tumour blocks three samples each of *10 4 carcinoma cells were obtained by microdissection (129 in all). DNA released by proteinase K digestion was subjected to PCR amplification of the androgen receptor gene AR exon I CAG repeat polymorphism with and without prior digestion with methylation-sensitive restriction enzymes HpaII and HhaI. Complex amplification patterns were consistent with mosaic X inactivation in some ovarian carcinomas but acquired anomalies of AR methylation cannot be excluded. Parallel analysis of other Xlinked polymorphic loci would strengthen the inference of clonality status from DNA methylation data in tumour X studies. Strikingly, the number of CAG repeats in the 29 ovarian tumour patients (median 16, range 11 -20) was substantially fewer than in 34 previously studied breast cancer patients from the same scottish population (median 21, range 14 -26; P 5 0.0001), and women homozygous for the AR CAG repeat were over-represented in the ovarian cancer patients but not in the breast cancer series. These findings reinforce recent suggestions that AR may have a role in ovarian carcinogenesis.
KeynoTe sPeaKer: Mary ellen Jeans lecTure undersTanding huMan Pain PercePTion and analgesia Through advanced neuroiMaging invited speaker: irene Tracey nuffield Professor anaesthetic science & director, oxford centre for fMri of Brain, nuffield department of clinical neurosciences, (head, nuffield division anaesthetics), oxford university, england, uK The ability to experience pain is old and shared across species. It confers an evolutionary advantage and provides a warning of harm or impending threat. As far back as Hippocrates, it was understood that the brain was key to a person experiencing pain. Fortunately, these days we now have many techniques available to explore the human central nervous system in vivo from a functional, structural and chemical perspective in both patients and healthy subjects. Relating specific neurophysiologic measures to perceptual or non-perceptual changes induced by peripheral or central sensitisation, behavioural, psychological or pharmacological mechanisms and identifying their site of action within the CNS has both value and has been a major goal for scientists, clinicians and the pharmaceutical industry. Identifying non-invasively where functional and structural plasticity, sensitisation and other amplification or attenuation processes occur along the pain neuraxis for an individual and relating these neural mechanisms to specific pain experiences, measures of pain relief, persistence of pain states, degree of injury and the subject's underlying genetics, has neuroscientific relevance and potential diagnostic value. Learning Objectives: 1. Better knowledge of the range of physiological measures available using advanced neuroimaging that give novel insights into central pain mechanisms 2. To understand the importance of the descending pain modulatory system in acute and chronic pain 3. To learn how current theories regarding how the brain generates perception can inform the pain field.
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