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Pathological Heterogeneity (pathological + heterogeneity)
Selected AbstractsMixed metaplastic carcinoma of the breast associated with pregnancy: Diagnostic dilemmas in fine-needle aspiration cytologyDIAGNOSTIC CYTOPATHOLOGY, Issue 10 2009Lazaros Skagias M.D. Abstract Metaplastic carcinoma of the breast represents a rare entity characterized by the simultaneous presence of ductal, squamous, and/or mesenchymal components in several proportions. There are limitations in fine-needle aspiration diagnosis due to its pathological heterogeneity. When it develops under pregnancy and lactation influence, the cytologic evaluation appears to be more difficult and accurate diagnosis often proves challenging. We describe a case of mixed metaplastic carcinoma with dominant areas of squamous metaplasia, sarcomatoid stroma with spindle cells, and a minor component of cartilaginous metaplasia. We notify our experience in diagnostic approach of this entity focusing on differential diagnosis. Diagn. Cytopathol. 2009. © 2009 Wiley-Liss, Inc. [source] Early-onset Alzheimer's disease with presenilin-1 M139V mutation: clinical, neuropsychological and neuropathological studyEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2003A. J. Larner The clinical, neuropsychological and neuropathological features of a patient with early-onset Alzheimer's disease as a result of the M139V presenilin-1 (PSEN-1) mutation are presented, and compared with previous reports of patients with the same mutation. Similarities, such as the age at onset and the relative preservation of naming skills, and differences, such as the significant basal ganglia, thalamic and cerebellar pathology, are noted. This clinical and pathological heterogeneity in patients with the same PSEN-1 mutation suggests phenotype modulation by genetic and/or epigenetic factors. [source] Methotrexate-related leukoencephalopathy without radiation therapy: Distribution of brain lesions and pathological heterogeneity on two autopsy casesNEUROPATHOLOGY, Issue 2 2009Jun Matsubayashi This report concerns two rare autopsy cases of methotrexate (MTX)-related leukoencephalopathy without radiation therapy. In the first case, there were widespread necrotic foci with prominent spheroids, that is, disseminated necrotizing leukoencephalopathy (DNL), mainly in the cerebral white matter. In contrast, in the second case, there were widespread demyelinated foci without significant axonal changes, which we would like to name disseminated demyelinating leukoencephalopathy (DDL), mainly in the cerebral white matter. We emphasize that the pathology of pure MTX-related leukoencephalopathy is not uniform, and may show at least two kinds of histologic change. Furthermore, both cases did not develop significant vascular changes, which are usually induced by radiation therapy. The distribution of the lesions in two cases was examined by large specimens, including hemisphere specimens. The distribution of the lesions in the brain of our cases was also different. In the first case, the DNL lesions were predominantly distributed in the frontal and temporal lobes. In the second case, the DDL lesions were prominently localized in the occipital lobe. To our knowledge, this is the first report describing not only the pathological findings of MTX-related leukoencephalopathy without irradiation but also the precise distributions of the lesions. [source] The challenge of multiple sclerosis: How do we cure a chronic heterogeneous disease?,,ANNALS OF NEUROLOGY, Issue 3 2009Howard L. Weiner MD Multiple sclerosis is (MS) a T-cell autoimmune disease characterized by a relapsing-remitting followed by a progressive phase. Relapses are driven by the adaptive immune system and involve waves of T helper cell 1 (Th1), Th17, and CD8 cells that infiltrate the nervous system and provoke a attack. These cells are modulated by regulatory T and B cells. Infiltration of T cells into the nervous system initiates a complex immunological cascade consisting of epitope spreading, which triggers new attacks, and activation of the innate immune system (microglia, dendritic cells, astrocytes, B cells), which leads to chronic inflammation. The secondary progressive phase is due to neurodegeneration triggered by inflammation and is driven by the innate immune system. Why a shift to the progressive stage occurs and how to prevent it is a central question in MS. Effective treatment of MS must affect multiple disease pathways: suppression of proinflammatory T cells, induction of regulatory T cells, altering traffic of cells into the nervous system, protecting axons and myelin, and controlling innate immune responses. Without biomarkers, the clinical and pathological heterogeneity of MS makes treatment difficult. Treatment is further hampered by untoward adverse effects caused by immune suppression. Nonetheless, major progress has been made in the understanding and treatment of MS. There are three definitions of cure as it applies to MS: (1) halt progression of disease, (2) reverse neurological deficits, and (3) prevent MS. Although the pathways to each of these cures are linked, each requires a unique strategy. Ann Neurol 2009;65:239,248 [source] |