By Icon Health Publications
It is a 3-in-1 reference booklet. It offers an entire scientific dictionary overlaying hundreds of thousands of phrases and expressions on the subject of acute myeloid leukemia. It additionally offers broad lists of bibliographic citations. ultimately, it presents info to clients on how one can replace their wisdom utilizing a number of net assets. The booklet is designed for physicians, scientific scholars getting ready for Board examinations, scientific researchers, and sufferers who are looking to get to grips with examine devoted to acute myeloid leukemia. in the event that your time is efficacious, this e-book is for you. First, you won't waste time looking the net whereas lacking loads of appropriate info. moment, the ebook additionally saves you time indexing and defining entries. eventually, you won't waste time and cash printing enormous quantities of websites.
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Additional info for Acute Myeloid Leukemia - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
HMRP8bcl-2 mice develop a massive buildup of stem cells, myelomonocytic progenitors, and monocytes in a syndrome that mimics human chronic myelomonocytic leukemia (CMML). Despite the development of CMML, hMRP8bcl-2 mice rarely progress to acute myeloid leukemia (AML). Primitive myeloid blast cells from hMRP8bcl-2 mice express the Fas receptor and, despite overexpression of Bcl-2, are induced to die by Fas ligation. To provide a further block in PCD in the myeloid lineage, he crossed hMRP8bcl-2 mice with Fas-deficient Fas lpr/lpr mice.
A cDNA clone of rno was obtained from a normal leukocyte library. The predicted sequence of rno shows that 28 Acute Myeloid Leukemia it belongs to the family of leucine rich repeat proteins and has a high degree of homology to the human ribonuclease inhibitor. PCR and sequencing also revealed that there are at least 3 isoforms of rno. Expression of rno in AML cells inhibits growth, and induces differentiation and apoptosis. The HYPOTHESIS for this proposal is that NO affects the growth and differentiation of AML cells by modulating the expression of specific genes.
Associate Professor; Pharmacology and Cancer Biology; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 15-MAY-1996; Project End 30-JUN-2005 Summary: (Adapted from the investigator's abstract) The long term objective of this research is to elucidate the biological role of the c-Able proto-oncogene. Mutant forms of c-Abl are associated with the development of murine, feline and human leukemias. Elucidation of a biological role for the c-Abl tyrosine kinase has been hampered for nearly 20 years due to a lack of knowledge regarding the signals that lead to c-Abl activation and definition of the physiological relevance of the activated c-Abl tyrosine kinase in mammalian cells.