American-Eurasian Journal of Toxicological Sciences 7 (4): 311-315, 2015 ISSN 2079-2050 © IDOSI Publications, 2015 DOI: 10.5829/idosi.aejts.2015.7.4.10148 Corresponding Author: Sarah Sadiq, Department of Biochemistry and Molecular Biology Army Medical College, National University of Sciences and Technology, Abid Majeed Road, Rawalpindi, Pakistan. 311 c-Myc and CK2 Correlation: A Passageway to Human Breast Cancer Sarah Sadiq, Abdul Khaliq Naveed, Fatima Qaiser, 1 2 3 Shahid Jamal, Shoaib N. Hashmi and Aiza Sadia 4 5 4 Department of Biochemistry and Molecular Biology Army Medical College, 1 National University of Sciences and Technology, Abid Majeed Road, Rawalpindi, Pakistan Department of Biochemistry, Islamic International Medical College, 2 Riphah International University, Rawalpindi, Pakistan Army Medical College, National University of Sciences and Technology, 3 Abid Majeed Road, Rawalpindi, Pakistan Department of Pathology, Army Medical College, 4 National University of SciencesTechnology, Abid Majeed Road, Rawalpindi, Pakistan Armed Forces Institute of Pathology,Rawalpindi, Pakistan 5 Abstract: c-Myc transcription factor is a protooncogene and a substrate of Casein Kinase 2 enzyme, both of these are upregulated in breast cancer. A Cross Sectional Analytical study with breast cancer paraffin embedded tissue sections (N=30) was conducted using Immunohistochemistry, cytoplasmic and nuclear expression of c-Myc and CK2 enzyme was determined and correlation between the two was found out. Scoring was performed by three histopathologists, blindly, any incongruity in results, corrected by using nearest readings. A high expression of Total CK2 in invasive cases was seen as compared to non-invasive. Nuclear and cytoplasmic localization was also higher in invasive group as compared to non- invasive.Total c-Myc expression was high in the invasive group, in comparison with non- invasive. In invasive cases, there was very strong and significant correlation between c-Myc and CK2 total, between c-Myc and CK2 cytoplasm and between c-Myc and CK2 nucleus. c-Myc and CK2 as biomarkers can help predicting the cancer phenotype and aggression. Key words: c-Myc CK2 Ca Breast Correlation INTRODUCTION are protected by CK2, from degradation by caspases. This Breast cancer is the commonest among women, under in cancers, support to tumorigenesis in transgenic mice, developed and developed world, causing death of over makes it a prospective candidate for molecular targeted 508000 females in 2011 [1]. CK2 has over 100 substrates, therapy [7]. One of the substrates of CK2 is c-Myc. It is a many of which are connected with signal transduction recognized proto-oncogene. c-Myc is necessary for and cell division [2]. Up-regulated in cancers, protein normal development but in cancers, it is upregulated. The kinase CK2 supports neoplastic phenotype [3]. A reason for the upregulation in cancer is not known but is ubiquitous serine / threonine kinase, particularly thought to take part in development of tumor [8]. c-Myc conserved, having a regulatory subunit (28 kDa ), the is a nuclear transcription factor that is essential for catalytic subunits (42 kDa and 38 kDa ') and 2 2, mammalian development [9]. Tissues with increased '2 2, ' 2 tetramers [4]. The finding that CK2 displays proliferation have been found to over express c-Myc [10]. dual specificity kinase action, has opened new venues for In lymphomas including Burkitt lymphoma, translocation research its cellular activities [5]. CK2 is consistently of c-Myc to immunoglobulin or locus on T cell receptor deregulated in different cancers [6]. Regulatory proteins can cause deregulated expression and transformation in activity can lead to tumorigenesis [5]. CK2 elevated levels