I'm Luzeena, postdoctoral fellow with the Elsässer laboratory at Karolinska Institutet. My research interests primarily lie in uncovering novel microproteins and their role in cancer, particularly with respect to how they could regulate oncogenic mechanisms such as cell viability, ER stress, and drug resistance. At the Elsässer lab, I leverage chemical and synthetic biology, and proteomic methods developed in-house, with my expertise in cancer and molecular biology, to develop innovative projects to investigate cancer microproteins.
During my doctoral training, I investigated how epigenetic regulators MLL/KMT2 histone methyltransferases (HMT) mediated differential gene expression in pancreatic cancer, particularly in the context of mechanisms driving drug resistance. KMT2s are mutated in about 15% of pancreatic cancer patients, making them a clinically significant mutation. Over the course of our investigation, we discovered that HMT KMT2D in particular displayed tumour-suppressive activity in PDAC. Through my doctoral thesis, we further demonstrated that loss of KMT2D altered response to chemotherapeutic agents used for PDAC treatment, in particular, response to 5-fluorouracil.
I am also interested in cancer evolution, using colorectal cancer spheroids as a disease model to better understand cancer cell dynamics over time and space. With this model, I aimed to better understand the interactions between heterogeneous cell populations present within the tumour microenvironment over time and in the context of applied pressure (such as drug treatment). Specifically, I was interested in how the tumour as a whole, and subcellular populations contained within, evolve over time, in response to factors like applied therapy, space, competition, and nutrient availability. I developed methods to model treatment strategies derived from these principles, such as adaptive therapy, in gastrointestinal malignancies like pancreatic and colorectal cancer.
My undergraduate research involved investigating how gestational exposure to endocrine disruptors (Bisphenol-A, Methylparaben) led to diseases and disorders in adult life. My focus was on elucidating the sex-specific differences in the neurological outcomes of endocrine disruption, such as memory, learning, locomotion, and anxiety, using animal models like zebrafish, rats and mice.
I have had the opportunity to live, study, and work in several countries, through which I experienced different cultures, ethnicities, and diverse workspaces. I believe these experiences have shaped me to be an international scientist capable of adapting to and thriving in an increasingly global scientific community.
During my doctoral training, I investigated how epigenetic regulators MLL/KMT2 histone methyltransferases (HMT) mediated differential gene expression in pancreatic cancer, particularly in the context of mechanisms driving drug resistance. KMT2s are mutated in about 15% of pancreatic cancer patients, making them a clinically significant mutation. Over the course of our investigation, we discovered that HMT KMT2D in particular displayed tumour-suppressive activity in PDAC. Through my doctoral thesis, we further demonstrated that loss of KMT2D altered response to chemotherapeutic agents used for PDAC treatment, in particular, response to 5-fluorouracil.
I am also interested in cancer evolution, using colorectal cancer spheroids as a disease model to better understand cancer cell dynamics over time and space. With this model, I aimed to better understand the interactions between heterogeneous cell populations present within the tumour microenvironment over time and in the context of applied pressure (such as drug treatment). Specifically, I was interested in how the tumour as a whole, and subcellular populations contained within, evolve over time, in response to factors like applied therapy, space, competition, and nutrient availability. I developed methods to model treatment strategies derived from these principles, such as adaptive therapy, in gastrointestinal malignancies like pancreatic and colorectal cancer.
My undergraduate research involved investigating how gestational exposure to endocrine disruptors (Bisphenol-A, Methylparaben) led to diseases and disorders in adult life. My focus was on elucidating the sex-specific differences in the neurological outcomes of endocrine disruption, such as memory, learning, locomotion, and anxiety, using animal models like zebrafish, rats and mice.
I have had the opportunity to live, study, and work in several countries, through which I experienced different cultures, ethnicities, and diverse workspaces. I believe these experiences have shaped me to be an international scientist capable of adapting to and thriving in an increasingly global scientific community.
Contact
Luzeena Raja
Postdoctoral fellow, Elsässer Lab
Research Division of Genome Biology, Department of Medical Biochemistry and Biophysics
SciLifeLab, Karolinska Institutet
Tomtebodavagen 23A, 17165 Solna, Sweden