Translocation t(4;14)(p16.3;q32) Is a Recurrent Genetic Lesion in Primary Amyloidosis-Reference-Cited by-同舟云学术

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Translocation t(4;14)(p16.3;q32) Is a Recurrent Genetic Lesion in Primary Amyloidosis

Published:2001-05 Issue:5 Volume:158 Page:1599-1603
ISSN:0002-9440
Container-title:The American Journal of Pathology
language:en
Short-container-title:The American Journal of Pathology

Author:

Perfetti Vittorio,Coluccia Addolorata M.L.,Intini Daniela,Malgeri Ursula,Vignarelli Maurizio Colli,Casarini Simona,Merlini Giampaolo,Neri Antonino

Publisher

Elsevier BV

Subject

Pathology and Forensic Medicine

Reference15 articles.

1. Biological features of the clone involved in primary amyloidosis (AL);Perfetti;Leukemia,2001

2. Multiple myeloma: increasing evidence for a multistep transformation process;Hallek;Blood,1998

3. Molecular analysis of 11q13 breakpoints in multiple myeloma;Ronchetti;Blood,1999

4. Frequent translocation t(4;14)(p16.3;q32.3) in multiple myeloma is associated with increased expression and activating mutations of fibroblast growth factor receptor 3;Chesi;Nat Genet,1997

5. A novel chromosomal translocation t(4;14)(p16.3;q32) in multiple myeloma involves the fibroblast growth-factor receptor 3 gene;Richelda;Blood,1997

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