Mudasir Rashid

My dedication to cancer research has allowed me to develop a deeper understanding of the disease process and has given me the opportunity to take part in research projects that focus on developing innovative treatments. During my Doctoral degree (PhD), I engaged in elucidating the molecular profiles of histone H3 isoforms and variants in gastric adenocarcinoma, utilizing various techniques such as cell culture and epigenetic methods. Notably, I reported on the transcriptional regulation of the H3C14 gene, highlighting a novel axis involving EGF-EGFR-FOXC1-KAT2A-H3C14. Additionally, I observed isoform-specific posttranslational modification (H3.2K9me2) and its correlation with global chromatin condensation via the H3.2K9me2-HP1-lamin axis in gastric adenocarcinoma. Furthermore, I noted a reversal of heterochromatin organization, manifested as a decrease in H3K9me2 levels and an increase in H3K9Ac levels, upon treatment with HDAC class I inhibitors, leading to programmed cell death with time-dependent kinetics. The prevalence of H3.2 in heterochromatin formation may prevent DNA damage, promote chemotherapy resistance, and regulate gene expression, offering potential therapeutic avenues. During my postdoctoral research (PDF) in Dr. Ashkthorab's laboratory, we performed exome next-generation sequencing (NGS) on African American (AA) colorectal cancer (CRC) patients. Our findings revealed six novel non-synonymous mutations within the mismatch repair genes, occurring in different domains with varying mutation frequencies. These AA-CRC MSH3 missense mutations were identified as novel and deleterious through multiple algorithms and methods. Some of these mutations were located within the ATPase site of the MSH3 protein, while others affected the MSH3-MSH2 interacting domains. Molecular Dynamics Simulation (MDS) demonstrated that these mutations altered the overall protein features compared to wild-type MSH3 proteins. Further investigations involved mimicking these mutations using CRISPR-Cas9 techniques to comprehend their biological significance within the CRC model system. Our data suggested that these mutations could be crucial events in AA-CRC pathogenesis. Additionally, I have worked on diverse projects, such as studying the anti-inflammatory and antioxidant properties of saffron's bioactive compounds as a protective agent in animal models, known as the saffron project. Also, I am involved in reviewing peer-reviewed research articles and am involved as a guest and associate editor in highly reputed journals, which makes me aware of current research and deepens my knowledge in the cancer field. Moreover, I possess a comprehensive understanding of the ethical guidelines and protocols essential for conducting research (certification from Howard University). Lastly, with my resolute drive, determination, and extensive academic and research background, I am confident in my capacity to create a significant impact as a cancer researcher. My research journey has been an invaluable learning experience, equipping me with the necessary skills to thrive as an independent investigator.