Background: CK2, a serine/threonine, protein kinase, targets over and above300 substrates including c-Myc. CK2 expression is elevated in human cancers includingbreast cancer and prostate cancer. c-Myc protooncogene expression is also up-regulated inthese cancers. Objectives: To evaluate the co expression and correlation of CK2 and c-Mycin prostate cancer as compared to their correlation in breast cancer. Study Design: Crosssectional analytical study. Setting: Army Medical College and AFIP, Duration: Two years.Methods: A retrospective study of immunohistochemical analysis, approved by Armed ForcesInstitute of Pathology Ethical Committee. Paraffin embedded tissues of diagnosed prostatecancer, 30 in number, 30 cases of Benign Prostatic Hypertrophy (BPH) and 30 cases of breastadenocarcinoma, were included in the study. We stained tissue sections for CK2 and c-Mycand measured staining intensity for each protein expression. Data analysis was done by SPSSversion 20. Pearson correlation coefficient was used for correlating the expression of bothproteins. P-value was calculated. Results: A strong correlation of CK2 with c-Myc was seen inprostate cancer tissue, in comparison to BPH. There was a very significant correlation presentbetween CK2 and c-Myc, especially in invasive cases of breast cancer. Conclusion: CK2 andc-Myc expressions are highly and significantly correlated in prostate cancer and breast cancerespecially in invasive cases. CK2 has influence over c-Myc and both can be used for forecastingthe cancer phenotype and aggression of disease.

Objective: To find out whether Casein Kinase 2 (CK2) and Survivin co-express and correlate in prostate as well as in breast cancer. Study Design: A cross sectional analytical study. Place and Duration of Study: Study was done at Army Medical College and in collaboration with Armed Forces Institute of Pathology (AFIP). The duration of this research was two years. Material and Methods: The research was authorized by the Ethical Committee of AFIP. CK2 expression was determined by immunohistochemistry in paraffin embedded tissues from established patients of prostate cancer (n=30) and breast adenocarcinoma (n=30). Correlation of CK2 with Survivin was evaluated. Data were analyzed through SPSS version 20. For studying the correlation between the two proteins, pearson correlation coefficient was calculated. Data was considered at p-value ≤0.05. Results: An expressively strong and affirmative correlation was found among expression of total CK2 and total Survivin in invasive along with non-invasive cases of both prostate and breast cancers. A significantly strong and positive correlation was found between nuclear CK2 and Survivin expression in non-invasive cases of prostate cancer and invasive as well as non-invasive cases of breast cancer. A significantly strong and positive correlation was found only between cytoplasmic CK2 and Survivin expression in non-invasive cases of prostate cancer. Conclusion: CK2 and Survivin expressions have strong and positive correlation in both prostate and breast cancer particularly in non-invasive stage of the cancer.

Objective: To check the co-expression of survivin and CK2 in prostate cancer patients as compared to the Benign Prostatic Hyperplasia (BPH) patients. Study Design: Cross-sectional analytical study. Place and Duration of Study: This study was conducted at Armed Forces Institute of Pathology, Army Medical College Rawalpindi, from Dec 2012 to April 2014. Material and Methods: The study was designed as a cross-sectional analytical study and conducted at Armed Forces Institute of Pathology, Army Medical College Rawalpindi, from Dec 2012 to April 2014, after approval from institutional ethical committee. Expression of survivin was analyzed by immunostaining in paraffinembedded sections from 30 diagnosed cases of resected prostate cancer and 30 BPH cases that were also immune stained for CK2. Results: The CK2 and survivin were found to overexpress in prostate cancer as compared to BPH. Total score of CK2 survivin were strongly positive and significantly correlated in non-invasive cases as compared to BPH. Conclusion: There is a strong positive correlation between survivin and CK2 over-expression in prostate cancerpatients specifically non-invasive cases suggesting the coordination between the two proteins in early stages ofprostate cancer progression.

Protein kinase CK2 plays a critical role in cell growth, proliferation, and suppression of cell death. CK2 is overexpressed, especially in the nuclear compartment, in the majority of cancers, including prostate cancer (PCa). CK2-mediated activation of transcription factor nuclear factor kappa B (NF-κB) p65 is a key step in cellular proliferation, resulting in translocation of NF-κB p65 from the cytoplasm to the nucleus. As CK2 expression and activity are also elevated in benign prostatic hyperplasia (BPH), we sought to increase the knowledge of CK2 function in benign and malignant prostate by examination of the relationships between nuclear CK2 and nuclear NF-κB p65 protein expression. The expression level and localization of CK2α and NF-κB p65 proteins in PCa and BPH tissue specimens was determined. Nuclear CK2α and NF-κB p65 protein levels are significantly higher in PCa compared with BPH, and these proteins are positively correlated with each other in both diseases. Nuclear NF-κB p65 levels correlated with Ki-67 or with cytoplasmic NF-κB p65 expression in BPH, but not in PCa. The findings provide information that combined analysis of CK2α and NF-κB p65 expression in prostate specimens relates to the disease status. Increased nuclear NF-κB p65 expression levels in PCa specifically related to nuclear CK2α levels, indicating a possible CK2-dependent relationship in malignancy. In contrast, nuclear NF-κB p65 protein levels related to both Ki-67 and cytoplasmic NF-κB p65 levels exclusively in BPH, suggesting a potential separate impact for NF-κB p65 function in proliferation for benign disease as opposed to malignant disease.

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 noninvasive.Total c-Myc expression was high in the invasive group, in comparison with noninvasive. 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.

The CK2, a serine/threonine, protein kinase, targets over and above 300 substrates including c-Myc. CK2 expression is elevated in human cancers including prostate cancer. c-Myc expression is also up-regulated in the prostate cancer. The objective was to evaluate the co expression and correlation of CK2 and c-Myc in prostate cancer. Study Design: Cross Sectional Analytical Study. Duration: Study was conducted at Army Medical College and AFIP, duration was two years. Methods: a retrospective study of immunohistochemical analysis, approved by Armed Forces Institute of Pathology Ethical Committee. Paraffin embedded tissues of diagnosed prostate cancer, 30 in number and 30 cases of Benign Prostatic Hyperplasia (BPH) were included in the study. The tissue sections were subjected to immunostaining for CK2 and c-Myc and staining intensity was measured for each protein expression. Data was analysed through SPSS version 20. Pearson correlation coefficient was applied to correlate expressions of CK2 and c-Myc and p-value calculated.Results; significant expression observed in prostate cancer tissue as compared to BPH. Strong correlation was observed between the CK2 and c-Myc nucleus and amid the c-Myc and CK2 total, as compared to BPH. Conclusion.CK2 and cMyc expressions are highly and significantly correlated in prostate cancer in invasive as well as non-invasive stages as compared to BPH as control.

Protein kinase CK2 has emerged as a major signal involved in diverse cellular functions of health and disease. The nature of its broad of range of functions is underscored by the large number of potential substrates of CK2 present in various locales in the cell. CK2 has gained much attention for its role in cancer biology, which is attributed to its functions both in cell growth and proliferation as well as in the regulation of cell death. Indeed, it appears that CK2 impact on cell death may be one of its most important functions, especially in the context of cancer biology where both cell proliferation and cell death are dysregulated and elevated CK2 in cancer would have an effect on both of these activities. Just as CK2 has been proposed to have a global role in cell growth-related activities, it appears that it may have an analogous global role in the suppression of apoptosis when it is elevated and induce cell death when it is downregulated. In this review, we have highlighted the current status of CK2 involvement in the processes related to cell death with a focus on apoptosis. It is proposed that a newly identified mechanism of CK2 regulation of cell death relates to its impact on early intracellular dynamics of Ca2+ signaling which profoundly alter mitochondrial function and lead to cell death.

Objectives: The present study was designed to evaluate the role of CK2α; in prognosis of breast cancer patients diagnosed at the same stage of the disease, and to predict aggressiveness of the tumor. Methods: A retroprospective immunohistochemical analysis of CK2α was carried out in human breast cancer tissue specimens. All the cases included were diagnosed at stage II of disease. χ 2 tests and Regression analysis were carried out to determine the correlation between histopathological parameters and expression pattern of CK2α Results: There was a positive correlation between total as well as nuclear expression of CK2α with increasing Nottingham prognostic index (p<0.0001). CK2α was also found to be significantly associated with the lymph node metastasis (p<0.0001). Conclusion: Immunohistochemical expression of CK2α can be used as an indicator of poor prognosis of disease even if overall stage of the breast cancer is the same. CK2α can also serve to predict the aggressiveness of the breast cancer as well and can identify the sub set of patients at high risk of developing lymph node metastasis.

OBJECTIVES:Genetic analysis of two consanguineous Pakistani families with localized autosomal recessive hypotrichosis was performed with the goal to establish genotype-phenotype correlation.MATERIALS AND METHODS:Genomic DNA extraction had been done from peripheral blood samples. Extracted DNA was then subjected to PCR (polymerase chain reaction) for amplification. Linkage analysis was performed using 8% polyacrylamide gel. Candidate gene was sequenced after gene linkage supported at highly polymorphic microsatellite markers of the diseased region.RESULTS:Both families were initially tested for linkage to known genes, which were involved in human hereditary hypotrichosis, by genotyping Highly polymorphic microsatellite markers. Family B showed partial linkage at P2RY5 gene on chromosome 13q14.11-q21.32; hence, all exonic regions and their introns boundaries were subjected to DNA sequencing for any pathogenic mutation.CONCLUSION:Both families were tested for linkage by genotyping polymorphic microsatellite markers linked to known alopecia loci. Family A excluded all known diseased regions that is suggestive of some novel chromosomal disorder. However, sequencing of P2RY5 gene in family B showed no pathogenic mutation.

Journal of Cellular BiochemistryVolume 115, Issue 12 p. fm i-fm iii ContentsFree Access Table of Contents: Volume 115, Number 12 First published: 15 October 2014 https://doi.org/10.1002/jcb.24980AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume115, Issue12December 2014Pages fm i-fm iii RelatedInformation

ABSTRACTCK2 (official acronym for casein kinase 2 or II) is a potent suppressor of apoptosis in response to diverse apoptotic stimuli—thus its molecular downregulation or activity inhibition results in potent induction of cell death. CK2 downregulation is known to impact mitochondrial apoptotic circuitry but the underlying mechanism(s) remain unclear. Utilizing prostate cancer cell lines subjected to CK2‐specific inhibitors which cause loss of cell viability, we have found that CK2 inhibition in cells causes rapid early decrease in mitochondrial membrane potential (Δψm). Cells treated with the CK2 inhibitors TBB (4,5,6,7‐tetrabromobenzotriazole) or TBCA (tetrabromocinnamic acid) demonstrate changes in Δψm which become apparent within 2 h, that is, significantly prior to evidence of activation of other mitochondrial apoptotic signals whose temporal expression ensues subsequent to loss of Δψm. Further, we have demonstrated the presence of CK2 in purified mitochondria and it appears that the effect on Δψm evoked by inhibition of CK2 may involve mitochondrial localized CK2. Results also suggest that alterations in Ca2+ signaling may be involved in the CK2 mediated regulation of Δψm and mitochondrial permeability. Thus, we propose that a key mechanism of CK2 impact on mitochondrial apoptotic circuitry and cell death involves early loss of Δψm which may be a primary trigger for apoptotic signaling and cell death resulting from CK2 inhibition. J. Cell. Biochem. 115: 2103–2115, 2014. © 2014 Wiley Periodicals, Inc.