<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">London, C A</style></author><author><style face="normal" font="default" size="100%">Galli, S J</style></author><author><style face="normal" font="default" size="100%">Yuuki, T</style></author><author><style face="normal" font="default" size="100%">Hu, Z Q</style></author><author><style face="normal" font="default" size="100%">Helfand, S C</style></author><author><style face="normal" font="default" size="100%">Geissler, E N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Spontaneous canine mast cell tumors express tandem duplications in the proto-oncogene c-kit.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental hematology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Exp. Hematol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amino Acid Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Binding Sites</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Dog Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Dogs</style></keyword><keyword><style  face="normal" font="default" size="100%">Exons</style></keyword><keyword><style  face="normal" font="default" size="100%">Mast-Cell Sarcoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphorylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Point Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Proto-Oncogene Proteins c-kit</style></keyword><keyword><style  face="normal" font="default" size="100%">Reverse Transcriptase Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Homology, Amino Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Stem Cell Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Tandem Repeat Sequences</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Tyrosine</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">1999 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">27</style></volume><pages><style face="normal" font="default" size="100%">689-97</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Spontaneous mast cell tumors (MCT) are the most common malignant neoplasm in the dog, representing between 7% and 21% of all canine tumors, an incidence much higher than that found in humans. These tumors often behave in an aggressive manner, metastasizing to local lymph nodes, liver, spleen, and bone marrow. The proto-oncogene c-kit is known to play a critical role in the development and function of mast cells. Point mutations in the kinase domain of c-kit leading to tyrosine phosphorylation in the absence of ligand binding have been identified in three mastocytoma lines, (P815, RBL, and HMC-1), and some human patients with various forms of mastocytosis. We now demonstrate that although c-kit derived from canine MCT did not contain the previously described activating point mutations, 5 of the 11 tumors analyzed possessed novel mutations consisting of tandem duplications involving exons 11 and 12. We also show that one such duplication, detected in a canine mastocytoma cell line, was associated with constitutive phosphorylation of c-kit protein (KIT), suggesting that these mutations may contribute to the development or progression of canine MCT.</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/10210327?dopt=Abstract</style></custom1></record></records></xml>