HOX genes: molecular genetics and effect of mutation | ||||
Egyptian Pharmaceutical Journal | ||||
Article 1, Volume 24, Issue 1, January 2025, Page 1-9 PDF (163.47 K) | ||||
DOI: 10.21608/epj.2025.402029 | ||||
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Authors | ||||
Hassan M. Rezka1; Hader I. Sakr2; Abeer O. Ismaile3; Alaa A. Almowallad3; Taif M. Almaqboule3; Abdulelah K. Alqawlaq3; Joud A. Albassame3; Abdulaziz A. Bukharie3; Hadi H. Almoshawar3 | ||||
1Department of Anatomy & Embryology, Mansoura University, Mansoura, | ||||
2Department of Medical Physiology, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo, Egypt | ||||
3General surgery Department, General Medicine Practice Program, Batterjee Medical College, Jeddah, Saudi Arabia | ||||
Abstract | ||||
In vertebrates, the axial skeleton, limbs, stomach, urogenital tract, and external genitalia all develop partly controlled by the homeobox-containing HOX gene families, which are deeply conserved throughout animal evolution. Much knowledge has been learned about the functions of HOX genes in many physiological and pathologic processes since their original discovery. There are 39 HOX genes in mammals, separated into the HOX A, B, C, and D clusters. Thirtynine homeobox genes in mammals are clustered into four clusters: HOX A–D, with a correlation between mutations of HOXB13, most often G84E, with breast, colorectal, and early-onset prostate cancer in humans. Here, we discuss the current knowledge of homeobox signaling in genitourinary development and cancer and the role of homeobox protein cofactors in both development and cancer | ||||
Keywords | ||||
Bosley–Salih–Alorainy syndrome; human HOX disorders; prostate cancer; synpolydactyly type II | ||||
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