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Effective cost optimization approach in Healthcare to Minimize the treatment cost of Brain-tumor Patients

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Now in its sixth edition, this highly-regarded book is designed as an introductory text on the principles of diagnosis, staging and treatment of tumours. The new edition: • Includes up-to-date information on the most recent techniques and therapies available • Emphasises the importance of multidisciplinary teamwork in the care of cancer patients • Highlights frequent dilemmas and difficulties encountered during cancer management • Features the important contributions of a new author Professor Daniel Hochhauser • Contains a brand-new two-colour design. As with previous editions, the first part of the book is devoted to the mechanisms of tumour development and cancer treatment. This is followed by a systematic account of the current management of individual major cancers. For each tumour there are details of the pathology, mode of spread, clinical presentation, staging and treatment with radiotherapy and chemotherapy. This accessible and practical resource will be invaluable to trainees in oncology, palliative care and general medicine, as well as specialist nurses, general practitioners, medical students, and professions allied to medicine. © 2005, 2003, 1998, 1995, reprinted 1987 & 1988, 1986 by R. Souhami and J. Tobias, 2010 J. Tobias and D. Hochhauser. All rights reserved.
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Almost without fail, one of the first questions a patient with a meningioma asks is, “What caused my tumor?” Many possible etiologic factors have been proposed during the last century. Solid epidemiologic evidence for most of these factors has proven fleeting. The availability and application of molecular biology techniques to investigate meningioma tumorigenesis, however, has revealed many insights into how these tumors develop and progress on the cellular level. Not only will further understanding of meningioma tumorigenesis answer the patient's “first” question, it may also lead to a better molecular classification to complement the current morphologic classification of meningiomas (see Chapter 5) and, of course, hopefully lead to novel therapeutic approaches to treat these tenacious tumors. Somewhat confounding efforts to elucidate the cause of meningioma is a lack of universal agreement on the cell of origin for all meningiomas. Most meningiomas likely arise from mesodermal arachnoid cap cells normally found at the apex of arachnoid granulations.1,2 Cleland, in 1846, is credited with first correlating these cells to meningioma formation.3 They are found adjacent to major venous sinuses where the majority of meningiomas occur, and the normal arachnoid cap cells histologically resemble meningothelial meningiomas. However, meningiomas may occur at unusual sites such as choroid plexus,4,5 within bone,6,7 or, very rarely, outside the neural axis.8 For these tumors a different cell of origin may be possible, or they may arise from heterotopic meningothelial rests.
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Li-Fraumeni syndrome (LFS) is a classic cancer predisposition disorder that is commonly associated with germline mutations of the p53 tumor suppressor gene. Examination of the wide spectrum of adult-onset and childhood cancers and the distribution of p53 mutations has led to a greater understanding of cancer genotype-phenotype correlations. However, the complex LFS phenotype is not readily explained by the simple identification of germline p53 mutations in affected individuals. Recent work has identified genetic events that modify the LFS phenotype. These include intragenic polymorphisms, mutations/polymorphisms of genes in the p53 regulatory pathway, as well as more global events such as aberrant copy number variation and telomere attrition. These genetic events may, in part, explain the breadth of tumor histiotypes within and across LFS families, the apparent accelerated age of onset within families, and the range of clinical outcomes among affected family members. This review will examine the clinical and genetic definitions of LFS and offer insight into how lessons learned from the study of this rare disorder may inform similar questions in other familial cancer syndromes.
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Malignant brain tumours continue to be the cause of a disproportionate level of morbidity and mortality across a wide range of individuals. The most common variants in the adult and paediatric populations - malignant glioma and medulloblastoma, respectively - have been the subject of increasingly intensive research over the past two decades that has led to considerable advances in the understanding of their basic biology and pathogenesis. This Review summarizes these developments in the context of the evolving notion of molecular pathology and discusses the implications that this work has on the design of new treatment regimens.
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Cancer stem cells (CSCs) have been identified in a growing number of hematopoietic and solid tissue malignancies and are typically recognized by virtue of the expression of cell surface markers. CD133, a stem cell marker, is now extensively used as a surface marker to identify and isolate brain tumor stem cells (BTSCs) in malignant brain tumors. However, CD133 as the marker to sort BTSCs suffered some controversies. In this review, we reviewed the rise of CD133, analyzed the efficiency of CD133 on identification and isolation of BTSCs, explained some controversial study results and summed up the role of CD133 and other effective CSCs markers in sorting CSCs in other tumors. We analyzed current limited reports and found that the expression of CD133 was correlated with poor clinical prognosis in brain tumors. Finally, we summarized the mechanisms of chemo- and radio- resistance of CD133+ brain tumor cell, especially emphasized that the aberrant activation of development pathways in BTSCs can be potential targets to BTSCs, and outlined current preclinical studies on killing BTSCs or sensitizing BTSCs to chemo- and radio-therapies.
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Four types of cancer of the thyroid gland occur, each different in biological behaviour and in associated factors affecting prognosis. Knowledge of these differences makes it possible to determine appropriate treatment for each case and reduces the chance of undertreatment or overtreatment. Fortunately, most cancers of the thyroid gland are well differentiated and can be treated by conservative surgical measures; the results are low mortality, minimal morbidity, and good prognosis.
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