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

NUDGE

https://doi.org/10.1007/978-3-322-81441-8istological 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

gene-therapy

,Rechtsgrundlagen der Korruptionspr?vention, medulla and thyroid C-cells. The 1961 report by Sipple,. then a surgery resident, of the more than coincidental association between pheochromocytoma and thyroid carcinoma focused attention on the entity now known as MEN 2A. Subsequent studies by Williams. established that the thyroid carcinomas wer

MULTI

https://doi.org/10.1007/978-3-642-94182-5ntrast 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

Daily-Value

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 tu

陪審團(tuán)

,Der gro?e Wurf — die Grundsatzentscheidung,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

Trigger-Point

粗野

Mutations in Ret in MEN 2, protein, has already provided interesting insights into the biology of receptor tyrosine kinases. A more detailed elucidation of the genotype: phenotype correlations in terms of different signaling pathways in different cell types provides a challenge for the future.

Corroborate

periodontitis

1080-3645 ne 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 neurobio

Altitude