 Good morning, myself, Monica Tyagi. I am a postdoc in the Department of General Surgery School of Medicine at Stanford University. I'll be talking about the recent publication that is being accepted to be published in Onko Target Journal. It is entitled as GATA 3 and Epobag 3B are the prognostic markers in Adrenocortical Carcinoma. And Epobag 3B is directly transcriptionally regulated by GATA 3. Adrenocortical Carcinoma, it is a rare and aggressive endocrine malignancy. Given there are no well-established exogenous factors which are associated with ACC, we postulated whether Epobag 3B could be an endogenous mechanism of genomic stability, mutations in ACC, and thereby be investigated at functions in vitro and in vivo. To begin with, we analyzed Epobag 3B gene expression in 21 normal adrenal cortices, 69 benign adrenal tumors, and 38 around primary ACC samples. And we found that the Epobag 3B mRNAs, they were significantly over-expressed in ACC, as we have shown in figure 1A of the paper. Including that, we have also analyzed two publicly available databases from GEU and EMBL for the expression of Epobag 3B and observed that in both the cohort, there was 5 to 6 fold increase in the expression of in Epobag 3B in ACC compared to the normal and adenocortical tube tissue samples, with no difference in expression between the benign and the normal ones. Now, since Epobag 3B is known to induce DNA damage, a critical molecular event in multiple cancers, we investigated the level of phospho-H2A-X, which is an indicator of DNA double strand break. We observed there's a high level of gamma-H2A-X in ACC as compared to the normal adrenal cortex and benign, which we have shown in figure 3A of the paper. We also performed a comprehensive genomic hybridization array in the ACC cohort and analyzed the association of Epobag 3B gene expression with gene copy number. We found that ACC with a higher Epobag 3B gene expression had high rate of chromosomal gain loss, particularly in chromosome number 4 and 8, as compared to the samples with lower Epobag 3B gene expression, which we have shown in figure 4A. Now, in order to decipher the mechanism by which Epobag 3B gene expression is upregulated in ACC, we analyzed a copy number change, microRNA, CPG methylation data in the same ACC sample that were available in our prior studies from where on we went ahead to work on this current project, which we are publishing now. We found in that study that there was no significant copy number difference or differentially expressed microRNA that target Epobag 3B and no differential CPG methylation in the Epobag 3B promoter or enhancer. Therefore, we performed a functional knockdown screen of 92 cancer associated transcription factor and identified GATA 3 as one of the key candidate as a transcriptional regulator of Epobag 3B gene expression, and this we have shown in figure 5A of this paper. We hear in this article shows that GATA 3 directly binds to the promoter region of Epobag 3B and transcriptionally regulates its gene expression in ACC. Lastly, we show that the expression level of Epobag 3B and GATA 3 are prognostic markers in the patients and in ACC. So what is the translational significance of this study? We all are aware of the genetic mutations that account for significant advancement for ACC prognition and the DMNA's activity of Epobag 3B enzyme is crucial contributor somatic mutation and genomic stability. In addition, it induces detectable DNA damage and activation of DNA repair machinery. Interestingly, high rate of T53 mutations associate with high level of Epobag 3B in ACC and we show that a high copy number alterations. We also demonstrate that GATA 3 regulates the expression of Epobag 3 and might be a promising prognostic marker in ACC and these findings provide a novel target for ACC and prognosis of the patient and this which we would be taking forward in future to work on and have a better perspective. For this work, we would like to thank our funding from NIH. I would also like to thank Dr. Electron Kebabu for giving this opportunity to work on this project. Thank you so much.