Licht Lab Alumni
Aditya Bele, PhD
I graduated from University of Nebraska Medical Center and joined Dr.Jonathan Licht’s group as a Postdoctoral associate in June 2016. My graduate research was focused on understanding role of a novel protein “ecdysoneless” in regulation of cell cycle and breast oncogenesis. My current research focuses on identifying and characterizing novel mutations in Histone genes that can further lead to unstable nucleosome assembly, deregulation of transcription machinery, aberrant gene expression and eventually cancer.
Camille Jacques, PhD
I joined the Licht Laboratory in April 2017 as a Postdoc from the University of Nantes, in the western part of France. During my PhD I studied the epigenetic implications of miRNAs and the BET bromodomains proteins in chemoresistance and metastatic spreading of bone sarcomas. As a member of Dr. Licht’s team I will have the opportunity to focus my research in delineating how mutations of the histone methyltransferase KMT2C, as well as the ones frequently found in genes involved in the Cohesin complex, could collaborate with the oncogenic Ras/ERK pathway in disturbing chromatin structure/function in hematopoietic malignancies. A better understanding of these mechanisms is of paramount interest in an attempt to bring the proof of concept that the targeting of these factors may improve the clinical outcome of these pathologies.
I am a joint graduate student of the Licht lab and the Kelleher lab at Northwestern University. I study histone H3K27 and K36 methylation kinetics in MMSET overexpression and gain-of-function mutation systems targeted mass spectrometry. By measuring histone mark kinetics, we can better understand how overexpression of MMSET and E1099K gain-of-function mutation alter MMSET enzyme activity and affect epigenetic landscape. I also study MMSET interacting proteins by proximity-based labeling. BirA, a biotin ligase domain, is fused to MMSET and expressed in multiple myeloma cell line. Supplemented with biotin, proteins that are close to MMSET will be labeled and identified by mass spectrometry. The investigation of MMSET interacting partners will facilitate us better understanding of the biological functions of MMSET under normal and cancerous circumstances.
Sayantan Maji, PhD
My current research project is focused on the role of KDM6A/UTX, a H3K27me2/3 demethylase which is frequently mutated in Urothelial Bladder Carcinoma (UBC). Loss of KDM6A has been reported in over 12 cancers and it has been designated as a bona fide tumor suppressor. KDM6A mutations in bladder carcinoma associate with earlier grade and are inversely correlated with stage. Therefore, KDM6A inactivation may be a powerful driver and early event in bladder oncogenesis. However, information regarding the molecular pathogenesis of KDM6A loss in bladder cancer is sparse, especially, how somatic alterations in KDM6A along with other key oncogenic mutations contribute to UBC development. The overall goal of my project is to understand the underlying mechanism of bladder cancer pathogenesis and study if alterations of the chromatin regulator KDM6A levels may undermine the chromatin landscape to deregulate gene expression and amplify oncogenic signaling mutations including that of RAS and PIK3CA.
I joined the Licht Laboratory as a Laboratory Technician in March 2019. I studied Pre-professional Biology at the University of Florida and graduated in the Fall of 2017. I intend to pursue research in genetics and microbiology.