I'm Luzeena, postdoctoral fellow at the Elsässer laboratory at SciLifeLab, Sweden. My research interests primarily lie in uncovering novel microproteins thar drive drug resistance in severe malignancies like pancreatic cancer.
During my doctoral training, I assessed the role epigenetic regulators MLL/KMT2 histone methyltransferases played in mediating differential gene expression in pancreatic cancer, particularly in the context of mechanisms potentially driving drug resistance. KMT2s are mutated in about 15% of pancreatic cancer patients, and preliminary results from our lab demonstrated that KMT2D in particular had tumour-suppressive activity in PDAC. Through my 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. With this model, I aimed to better understand the interactions between heterogeneous cell populations present within the tumour microenvironment. Specifically, I was interested in how the tumour as a whole, and cells present within, evolve over time, in response to factors like applied therapy, space, 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.
During my doctoral training, I assessed the role epigenetic regulators MLL/KMT2 histone methyltransferases played in mediating differential gene expression in pancreatic cancer, particularly in the context of mechanisms potentially driving drug resistance. KMT2s are mutated in about 15% of pancreatic cancer patients, and preliminary results from our lab demonstrated that KMT2D in particular had tumour-suppressive activity in PDAC. Through my 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. With this model, I aimed to better understand the interactions between heterogeneous cell populations present within the tumour microenvironment. Specifically, I was interested in how the tumour as a whole, and cells present within, evolve over time, in response to factors like applied therapy, space, 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.
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