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Sareena Rana

As seen in: Science Magazine, BioRxiv, Cell Press
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Articles

Covalent inhibitors of the PI3Kα RAS binding domain impair tumor growth driven by RAS and HER2

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By Joseph E. Klebba, Nilotpal Roy, Steffen M. Bernard, Stephanie Grabow, Melissa Hoffman, Hui Miao, Jinwei Wang, Cynthia L. Berry, Richard Y Lin, Yongsheng Liu, Marie Pariollaud, Holly Parker, Sareena Rana, Junko Tamiya, Antonio Esparza-Oros, Igor Mochalkin
| Science Magazine Verified
Abstract Genetic disruption of the RAS binding domain (RBD) of Phosphoinositide 3-kinase alpha(PI3Kα) impairs the growth of tumors driven by the small guanosine triphosphatase RAS in mice and does not impact PI3Kα’s role in insulin mediated control of glucose homeostasis. Selectively blocking the RAS-PI3Kα interaction may represent a strategy for treating RAS-dependent cancers as it would avoid the toxicity associated with inhibitors of PI3Kα lipid kinase activity.
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Combining RASG12C(ON) inhibitor with SHP2 inhibition sensitises immune excluded lung tumours to immune checkpoint blockade: a strategy for turning cold tumours hot

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By Christopher Moore, Sareena Rana, Andrea de Castro, Panayiotis Anastasiou
| BioRxiv
Abstract Mutant selective drugs targeting the inactive, GDP-bound form of KRASG12C have been approved for use in lung cancer, but responses are short-lived due to rapid development of resistance. In this study we use a novel covalent tri-complex inhibitor, RMC-4998, that targets RASG12C in its active, GTP-bound form to investigate treatment of KRAS mutant lung cancer in various immune competent mouse models.
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Development of combination therapies to maximize the impact of KRAS-G12C inhibitors in lung cancer

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By Oncogene Biology, Christopher Moore, Sareena Rana, Miriam Molina-Arcas
| Science Magazine Verified
Research ArticleCancer Miriam Molina-Arcas1,2, Christopher Moore1, Sareena Rana1,2, Febe van Maldegem1, Edurne Mugarza1, Pablo Romero-Clavijo1, Eleanor Herbert3,4, Stuart Horswell5, Lian-Sheng Li6, Matthew R. Janes6, David C. Hancock1 and Julian Downward1,2,* 1Oncogene Biology, Francis Crick Institute, London NW1 1AT, UK. 2Lung Cancer Group, Institute of Cancer Research, London SW3 6JB, UK. 3Experimental Histopathology, Francis Crick Institute, London NW1 1AT, UK.
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