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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN Print: 0893-9675
ISSN Online: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v14.i1.30
pages 33-55

Tumor Protein D52 Overexpression and Gene Amplification in Cancers from a Mosaic of Microarrays

Mona Shehata
The University of Sydney Discipline of Paediatrics and Child Health, Molecular Oncology Laboratory, Oncology Research Unit, The Children's Hospital at Westmead,
Judith Weidenhofer
Molecular Oncology Laboratory, Oncology Research Unit, The Children's Hospital at Westmead, Locked Bag 4001, Westmead 2145, NSW, Australia
Keerthi Thamotharampillai
The University of Sydney Discipline of Paediatrics and Child Health, Molecular Oncology Laboratory, Oncology Research Unit, The Children's Hospital at Westmead, Locked Bag 4001, Westmead 2145, NSW, Australia
Jayne R. Hardy
Molecular Oncology Laboratory, Oncology Research Unit, The Children's Hospital at Westmead, Locked Bag 4001, Westmead 2145, NSW, Australia
Jennifer A. Byrne
The University of Sydney Discipline of Paediatrics and Child Health, Molecular Oncology Laboratory, Oncology Research Unit, The Children's Hospital at Westmead, Locked Bag 4001, Westmead 2145, NSW, Australia

ABSTRACT

The tumor protein D52 gene is increasingly recognized to be overexpressed in different cancer types, frequently through gain of the corresponding locus at chromosome 8q21.13. This review summarizes the literature identifying D52 overexpression and/or gene amplification in different cancers, as well as recent publications directly analyzing D52 functions. Since D52 overexpression is increasingly being identified in tumors of different cellular origins, this is likely to perturb fundamental cell properties common to different cell types. Furthermore,since increased D52 expression occurs at different stages of tumorigenesis and progression, this could contribute to these processes through multiple mechanisms. Although functions are beginning to emerge from targeted studies, the pathways through which D52 overexpression contributes to cell transformation and the molecular interactions required remain undefined. In summary, while targeting D52 overexpression could provide therapeutic benefits in many cancer types, this will require an improved understanding of D52's cellular and molecular functions.