Madhu Kollareddy Email & Phone Number

Bristol, Gb

Bristol, England, United Kingdom

Transcriptional regulation of autophagy in Cancer

Bristol, United Kingdom

Finding new ways to destabilize MYCN, which is a main genetic abnormality in Neuroblastoma. MYCN protien which is a main oncogenic modality in neuroblastoma and several other cancers in undruggable. I identified its partners which modify MYCN posttranslationally. My idea is to target MYCN modifications thorugh inhibiting its arginine methylation and thereby repressing its transcriptional activity. In collaboration with GSK I am currently evaluating preclinical effects of argininge methytransferase inhibitors. I am also involved in developing new PROTACs in collaboration with Tocris Biosciences, UK. During my period in Bristol, as a Co-PI I procured two grants to study drug resistance in neuroblastoma and evaluating PRMT5 inhibitors in Rhabdomyosarcoma.Whilst at the University of Bristol, I am involved in giving lectures to third year undergraduate students (Developmental Genetics & Embryonal Cancers). I am also responsible for taking tutorials for first and second-year undergraduate students (4-8 hours per year). I have taken tutorials on the Normal and Tumour cells, Cellular and Molecular Pathology, and Disease and Defence units. I assess the presentation skills of the students and give written feedback. I am regularly involved in supervision of research projects of undergraduate, postgraduate taught and PhD students. My AFHEA training helped in designing innovative methods of teaching. For example, I implemented and engaged students with hands-on experience right from the start of the project. Also I effectively engage students in their projects by giving small problems and encourage to come up with solutions on their own.

Jackson, Mississippi Area

Mutant p53 is involved in promoting several oncogenic activities through regulating several genes involved in various oncogenic phenotypes. My main project is to delineate molecular mechanism of mtp53 mediated transcriptional regulation and associated cancer hallmarks. We identified several metabolic pathway altered in a mtp53 dependent manner. We identified several druggable targets within the metabolome.

Institue Of Molecualr And Translational Medicine

Worked on Tumor cell resistance mechanisms towards anticancer drugs that act in mitosis.Aurora kinase inhibitors are new anticancer drugs, which showed significant antitumor activity in preclinical studies and clinical trials. Tumor cell resistance mechanisms towards these drugs are not well understood. We used state of the art techniques to identify potential drug resistance mechanisms. These results we got help predict clinical response and aid in further development

Screening of anticancer drugs discovered in Cyclacel and studies on their modes of action. Became familiar witht the classical Animal tissue cultures studies in Cyclacel. Also became familiar with protein studies and flowcytometry studies.

Worked as microbiologist, quality control. Involved in pathogens identification and confirmation. Sucessfully faced FDA,UKMHRA, and WHO international audits. This success made the company to sell its own drugs in international markets. Became familiar with routine microbiological studies including environmental monitoring, water quality monitoring and raw materials monitoring.

Associate-Fellow-Higher Education Academy, Teaching, Gained Qualification

To develop my professional teaching and learning skills, I enrolled for the UKPSF-Higher Education Academy course. In June 2019, I was.

Doctor Of Philosophy (Ph.D.), Cancer Therapeutics, Pass

Identitification of cancer cell drug resistance mechanims towards Aurora kinase inhibitors. Identified and valied resistance mechanisms.

Ms, Biotechnology

Activities and Societies: Only studiesDuring the last semester, I got an opportunity to do my project in Cyclacel Ltd, which I consider it.

Msc, Biotechnology

Masters in Biotechnology

Bachelor’S Degree, Life Sciences And Chemistry, A