Targeting HOX/PBX dimers in cancer
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Richard Morgan1, Mohamed El-Tanani1, Keith D. Hunter2, Kevin J. Harrington3 and Hardev S. Pandha4
1 Institute of Cancer Therapeutics, Faculty of Life Sciences, University of Bradford, Bradford, UK
2 Unit of Oral and Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, Sheffield, UK
3 Targeted Therapy Team, Chester Beatty Laboratories, The Institute of Cancer Research, London, UK
4 Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK
Richard Morgan, email:
Keywords: HOX, PBX, HXR9, targeted therapy, biomarker
Received: December 08, 2016 Accepted: February 23, 2017 Published: March 07, 2017
The HOX and PBX gene families encode transcription factors that have key roles in establishing the identity of cells and tissues in early development. Over the last 20 years it has become apparent that they are also dysregulated in a wide range of solid and haematological malignancies and have a predominantly pro-oncogenic function. A key mode of transcriptional regulation by HOX and PBX proteins is through their interaction as a heterodimer or larger complex that enhances their binding affinity and specificity for DNA, and there is growing evidence that this interaction is a potential therapeutic target in malignancies that include prostate, breast, renal, ovarian and lung cancer, melanoma, myeloma, and acute myeloid leukaemia. This review summarizes the roles of HOX and PBX genes in cancer and assesses the therapeutic potential of HOX/PBX dimer inhibition, including the availability of biomarkers for its application in precision medicine.
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