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Titlebook: CURED I - LENT Late Effects of Cancer Treatment on Normal Tissues; Philip Rubin (Professor Emeritus, Chair Emeritus), Book 2008 Springer-V

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Moyed Miften PhD,Olivier Gayou PhD,David S. Parda MD,Robert Prosnitz MD,Lawrence B. Marks MDnslocations that produce fusion proteins which activate . occur more frequently in ECD than in LCH. The presence of some of these activating mutations in circulating cells or in CD34+ bone marrow cells suggests that these diseases may arise from transforming events in early myeloid precursors. ICH c
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Gary R. Morrow PhD, MS,Joseph A. Roscoe PhD,Maralyn E. Kaufman PhD,Christopher Bole MA,Colmar Figuers associated with hypomorphic and/or monoallelic mutations in genes encoding effectors of the lymphocyte cytotoxicity, has changed our view of HLH’s pathophysiology, in which the disease develops after the progressive accumulation of genetic and environmental factors exceeds a critical threshold.
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Philip Rubin MDnation. Biopsies of such lesions are rare. In the few published cases biopsied, variable pathologies are described with perivascular inflammatory changes, variable neuronal loss, demyelination, and gliosis, but are nondiagnostic for CD1a+/CD207+ LCH cells. Granulomatous LCH can be responsive to chem
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