By Icon Health Publications
This can be a 3-in-1 reference e-book. It provides an entire clinical dictionary overlaying countless numbers of phrases and expressions with regards to arsenic. It additionally provides large lists of bibliographic citations. eventually, it presents details to clients on how you can replace their wisdom utilizing a variety of web assets. The booklet is designed for physicians, scientific scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to get to grips with examine devoted to arsenic. in case your time is efficacious, this ebook is for you. First, you won't waste time looking out the web whereas lacking loads of correct details. moment, the e-book additionally saves you time indexing and defining entries. eventually, you won't waste money and time printing hundreds of thousands of websites.
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Extra resources for Arsenic - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Cheif, Division of Oncology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 19-SEP-2003; Project End 31-AUG-2007 Summary: The long-term goal of this project is to identify the genetic events that contribute to the development of relapsed and resistant acute promyelocytic leukemia (APL). We hypothesize that relapsed/resistant AML is associated with specific genetic events that can be defined with high throughput genome-wide scans for mutations.
It is becoming clear however that this approach is associated with development, several years later, of myelodysplastic syndromes and AML. The demonstration of the effectiveness of arsenic trioxide (ATO) in APL makes it feasible to assess, in newly diagnosed APL, whether the combination of ATO + ATRA will enable elimination of myelotoxic therapy. To test this hypothesis (SA#1) we will conduct a trial of ATO + ATRA, with myelotoxic therapy added only if minimal residual disease (MRD), as judged by the standard manual PCR assay, persists or recurs.
One of the main difficulties in studying mechanisms of arsenic carcinogenesis is the lack of a suitable human cell model whereby the various tumorigenic stages can be dissected and the molecular changes associated with each stage examined. While preliminary data obtained by the applicant has shown that arsenic can induce malignant transformation of papillomavirus-immortalized human bronchial epithelial (BEP2D) cells, this model is not ideal due to the presence of viral oncoproteins. The newly established telomerase (hTERT) -immortalized human bronchial epithelial (IMNHBE) cell transformation model that has normal p53 and p16 functions represents an attractive alternative to further ascertain the mechanism involved in arsenic-induced bronchial carcinogenesis.