Walker Gj
University of Southern California
9 Papers
345 Citations
Walker Gj is an academic researcher from University of Southern California. The author has contributed to research in topics: Melanoma & Tumor suppressor gene. The author has an hindex of 8, co-authored 9 publications. Previous affiliations of Walker Gj include QIMR Berghofer Medical Research Institute.
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Papers
Mutations of the CDKN2/p16INK4 gene in Australian melanoma kindreds
Walker Gj,C J Hussussian,Flores Jf,J M Glendening,Frank G. Haluska,Nicholas C. Dracopoli,Nicholas K. Hayward,Jane W. Fountain +7 more
TL;DR: In seven Australian melanoma kindreds, CDKN2 mutations were found to segregate with the putative melanoma chromosome previously assigned by 9p haplotype analysis, providing additional strong support that theCDKN2 gene is the chromosome 9p21 familial melanoma locus.
151
•Journal Article
Low frequency of p16/CDKN2A methylation in sporadic melanoma: comparative approaches for methylation analysis of primary tumors.
Mark L. Gonzalgo,Christina M. Bender,Edward H. You,J. Michael Glendening,Flores Jf,Walker Gj,Walker Gj,Nicholas K. Hayward,Peter A. Jones,Jane W. Fountain +9 more
TL;DR: PCR-based techniques can be reliably used for the accurate detection and quantitation of aberrant levels of DNA methylation in tumor specimens, and methylation-associated gene silencing does not represent a common mechanism for p16 inactivation in sporadic melanoma.
Analysis of the CDKN2A, CDKN2B and CDK4 genes in 48 Australian melanoma kindreds.
Flores Jf,Pamela M. Pollock,Walker Gj,Walker Gj,J M Glendening,Amy H. Lin,Jane M. Palmer,Marilyn K. Walters,Nicholas K. Hayward,Jane W. Fountain +9 more
TL;DR: Germline mutations within the cyclin-dependent kinase inhibitor 2A (CDKN2A) gene and one of its targets, the Cyclin dependent kinase 4 (CDK4), have been identified in a proportion of melanoma kindreds.
91
•Journal Article
Homozygous loss of the p15INK4B gene (and not the p16INK4 gene) during tumor progression in a sporadic melanoma patient.
TL;DR: It is suggested that hemizygous loss (or haplo-insufficiency) of the p16INK4 gene may be enough to place a melanocyte on a tumor pathway, and/or that the p 16ink4 gene is not the sole 9p21 locus targeted in sporadic melanoma.
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Localization of Multiple Melanoma Tumor–Suppressor Genes on Chromosome 11 by Use of Homozygosity Mapping-of-Deletions Analysis
Eleonora K. Goldberg,J. Michael Glendening,Zarir E Karanjawala,Anjali Sridhar,Walker Gj,Walker Gj,Nicholas K. Hayward,Andrew J. Rice,Devinda Kurera,Yasmine Tebha,Jane W. Fountain +10 more
TL;DR: It is proposed that HOMOD analysis can be used as an adjunct to LOH analysis in the localization of tumor-suppressor genes.
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