I joined Imperial College following a PhD from University of Cambridge in DNA damage and repair mechanisms followed by a post-doctoral stint in DNA replication checkpoint pathways at the Clare Hall Labs, Cancer Research UK (now Francis Crick Institute).
Lung cancer is the most common Cancer in UK and presently I have been actively involved in understanding the biology and design novel strategies to target key drivers of this killer disease. One of the main aims of my research has been to understand the cellular signalling mechanisms downstream of Tyrosine Kinase family of receptors such as FGFR and EGFR. My research has broadly focused on understanding how the downstream players interact and orchestrates various mechanisms to evade directed therapy leading to resistance to chemotherapeutic drugs. I am currently involved in leading research in 4 major avenues:
- Elucidating the role of FGF2 mediated signalling in promoting chemo-resistance in Lung cancer models
- Role of p90 Ribosomal S6 kinases (RSK) downstream of MEK/ERK signalling in regulating tumorigenesis.
- Role of p90RSKs in regulation of cellular energetics.
- Drivers of Erlotinib resistance in downstream of EGFR (T790M) mutation
et al., 2018, Resistance to tyrosine kinase-targeted therapy in lung cancer: Autophagy and metabolic changes, Meta Gene
et al., 2018, Targeting autophagy sensitises lung cancer cells to Src family kinase inhibitors, Oncotarget, Vol:9, ISSN:1949-2553, Pages:27346-27362
et al., 2017, Emerging roles of hnRNPA1 inmodulating malignanttransformation, Wiley Interdisciplinary Reviews: Rna, Vol:8, ISSN:1757-7004
et al., 2017, Oncogene-Selective Sensitivity to Synchronous Cell Death following Modulation of the Amino Acid Nutrient Cystine, Cell Reports, Vol:18, ISSN:2211-1247, Pages:2547-2556
et al., 2016, Decreased glutathione biosynthesis contributes to EGFR T790M-driven erlotinib resistance in non-small cell lung cancer, Cell Discovery, Vol:2, ISSN:2056-5968