000			03595nam a22004815i 4500
001			u373076
003			SIRSI
005			20160812084129.0
007			cr nn 008mamaa
008			100603s2010 au | s |||| 0|eng d
020			_a9783211798928 _9978-3-211-79892-8
040			_cMX-MeUAM
050		4	_aRC254-282
082	0	4	_a616.994 _223
100	1		_aGreil, Richard. _eeditor.
245	1	0	_aChronic Myeloid Neoplasias and Clonal Overlap Syndromes _h[recurso electrónico] : _bEpidemiology, Pathophysiology and Treatment Options / _cedited by Richard Greil, Lisa Pleyer, Viktoria Faber, Daniel Neureiter.
264		1	_aVienna : _bSpringer Vienna, _c2010.
300			_aXI, 295 p. _bonline resource.
336			_atext _btxt _2rdacontent
337			_acomputer _bc _2rdamedia
338			_aonline resource _bcr _2rdacarrier
347			_atext file _bPDF _2rda
505	0		_ato “Classic” Chronic Myeloproliferative Disorders (CMPDs) — Molecular and Cellular Biology -- Essential Thrombocythemia (ET) -- Polycythemia Vera (PV) -- Primary Myelofibrosis (PMF) [Previously Chronic Idiopathic Myelofibrosid (CIMF), Myelofibrosis with Myeloid Metaplasia (MMM), Agnogenic Myeloid Metaplasia (AMM)] -- Chronic myelogenous leukemia (CML) -- Myelodysplastic Syndromes (MDS) -- Chronic Myelomonocytic Leukemia (CMML) -- Rare Clonal Myeloid Diseases -- De novo “Classic” Paroxysmal Nocturnal Hemoglobinuria (PNH) (Marchiafava-Micheli Syndrome) -- Clonal Bone Marrow Failure Overlap Syndromes.
520			_aIntroduction The understanding of the genetic, epigenetic, immuno- well as for practicing hematologists or oncologists. logical and biological causes of myeloproliferative dis- Each chapter follows a similar architecture and leads orders has substantially improved in the last few years. through epidemiology, genetic and molecular causes, Together with refined tools in pathology, the successful hematological and clinical findings, prognostic factors establishment of mouse models mimicking at least some and current treatment approaches of the diseases. of the myeloproliferative disorders, and murine models Effort has been made to point out the evolving field of novel drugs in this arena but simultaneously diff- allowing to carefully dissect the role of mutations and gene dosage effects of, for example JAK2, this has led to entiate between standard and experimental treatment ever increasing numbers of modified classification approaches. schemes. It is therefore important for the heamtologist Together with the co-editors and all the authors of or oncologist to keep up with this rapid change in classi- the various chapters I hope that the readers of the book fication language, the upcoming of new entities or differ- will enjoy reading and benefit from the information entiation between, or subclassification of, rare diseases provided.
650		0	_aMedicine.
650		0	_aInternal medicine.
650		0	_aBlood transfusion.
650		0	_aOncology.
650	1	4	_aMedicine & Public Health.
650	2	4	_aOncology.
650	2	4	_aInternal Medicine.
650	2	4	_aBlood Transfusion Medicine.
700	1		_aPleyer, Lisa. _eeditor.
700	1		_aFaber, Viktoria. _eeditor.
700	1		_aNeureiter, Daniel. _eeditor.
710	2		_aSpringerLink (Online service)
773	0		_tSpringer eBooks
776	0	8	_iPrinted edition: _z9783211798911
856	4	0	_zLibro electrónico _uhttp://148.231.10.114:2048/login?url=http://link.springer.com/book/10.1007/978-3-211-79892-8
596			_a19
942			_cLIBRO_ELEC
999			_c200956 _d200956