Abstract:
:We have previously identified amplification at 4q12 in testicular germ cell tumors of adolescents and adults centered around the KIT gene encoding a tyrosine kinase transmembrane receptor. Analysis of primary testicular germ cell tumors totaling 190 cases revealed 21% of the seminoma subtype with an increased copy number of KIT whereas this change was rarely found in the nonseminomas. In most cases, gain of KIT did not include the immediately flanking noncoding DNA or the flanking genes KDR and PDGFRA. Increased copy number of KIT was not found in the putative precursor lesion, carcinoma in situ (CIS), adjacent to tumor with this change. KIT overexpression was found independent of gain and KIT immunostaining was stronger in selected cases with gain of KIT compared to those without. Taken together with activating mutations of KIT in exon 17 identified in 13% of seminomas, this suggests that the KIT gene product plays a role in the progression of CIS towards seminoma, the further understanding of which may lead to novel less toxic therapeutic approaches.
journal_name
Cancer Resjournal_title
Cancer researchauthors
McIntyre A,Summersgill B,Grygalewicz B,Gillis AJ,Stoop J,van Gurp RJ,Dennis N,Fisher C,Huddart R,Cooper C,Clark J,Oosterhuis JW,Looijenga LH,Shipley Jdoi
10.1158/0008-5472.CAN-05-0471subject
Has Abstractpub_date
2005-09-15 00:00:00pages
8085-9issue
18eissn
0008-5472issn
1538-7445pii
65/18/8085journal_volume
65pub_type
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