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Titlebook: Genetic Mechanisms in Multiple Endocrine Neoplasia Type 2; Barry D. Nelkin Book 1996 Springer-Verlag Berlin Heidelberg 1996 biology.cell.g

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书目名称Genetic Mechanisms in Multiple Endocrine Neoplasia Type 2
编辑Barry D. Nelkin
视频video
丛书名称Medical Intelligence Unit
图书封面Titlebook: Genetic Mechanisms in Multiple Endocrine Neoplasia Type 2;  Barry D. Nelkin Book 1996 Springer-Verlag Berlin Heidelberg 1996 biology.cell.g
描述This book examines what is known about the molecular biology of multiple endocrine neoplasia, type 2 (MEN2). Mutations and alterations in gene expressions and signal transduction are placed in the context of their effects on the biology of the thyroid and adrenal cells which generate cancers in MEN2. Thus, this volume addresses the ret mutations, the effects these mutations may have on signal transduction, and developmental and neurobiological aspects of the cells affected of MEN2, and provides the basic researcher - in genetics, signal transduction, cell transformation, developmental or neurobiology - with a better understanding of how the knowledge generated by each of these fields intercalates within the overall biology of MEN2.
出版日期Book 1996
关键词biology; cell; gene; gene expression; genetics; molecular biology; mutation
版次1
doihttps://doi.org/10.1007/978-3-662-21948-5
isbn_softcover978-3-662-21950-8
isbn_ebook978-3-662-21948-5Series ISSN 1080-3645
issn_series 1080-3645
copyrightSpringer-Verlag Berlin Heidelberg 1996
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Mutations in Ret in MEN 2,e. This genetic information coupled with a basic understanding of the ways in which the different types of mutation may affect the activity of the ret protein, has already provided interesting insights into the biology of receptor tyrosine kinases. A more detailed elucidation of the genotype: phenot
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Origin of Adrenal Chromaffin Cells from the Neural Crest,istological techniques based on catecholamine biochemistry allowed early researchers to identify the precursors for adrenal chromaffin cells as they migrate from the primary sympathetic chains into the adrenal primordia. Subsequent production of antisera that recognize catecholamine-synthesizing enz
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Neuronal Properties of Thyroid C-Cell Tumor Lines,ntrast to the primarily endocrine nature of the parental C-cells. What can account for this transdifferentiation? In this chapter, we will try to answer that question by comparing the neuronal features of C-cell lines with those of normal C-cells treated with nerve growth factor. From that perspecti
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Conclusion,w therapeutic targets for MTC, pheochromocytoma and biologically related cancers. Here, I would like to point out some of the questions which have been raised in the text, and which seem to me to be of special interest for future study. Of course, these choices reflect my bias; and others might emph
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https://doi.org/10.1007/978-3-322-93658-5s has been reviewed extensively by Foulds.. Based on observations of karyotypic progression in hematopoietic and other neoplasms, Nowell. proposed a clonal evolution model for tumor progression. In this model, variant cell clones which possess some growth advantage overgrow the other cells in the tumor.
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