My main research interest is studying lung cancer development and progression as well as mechanisms of resistance to its treatment. One aspect of my laboratory research is interrogating the cancer stem cells theory in lung cancer. We have established the role of Notch activity in enriching a lung cancer stem cell population and inferring resistance to standard chemotherapy. The other major focus is understanding mechanisms of resistance to targeted therapy. Specifically, the development of resistant mutations to EGFR TKI agents. Our findings suggest that these mutation are not preexisting but rather actively acquired after exposure to EGFR TKIs. We delineated the mechanism underlying this process, showing that AICDA is activated through NFaB pathway causing cytosine deamination-based mutations. We are currently exploring the role of AICDA in resistance to new generation EGFR TKIs as well as other targeted inhibitors. Furthermore, we are working on developing AICDA inhibitors and assessing combination regimens to overcome EGFR resistance with the aim to translate our findings into clinical trials.
Dr. Khaled Hassan is a radiation oncologist and physician scientist with appointments in Cleveland Clinic's Lerner Research Institute and Taussig Cancer Institute.
Appointed
2019
Education & Fellowships
Fellowship - University of Michigan
Hematology/Medical Oncology
Ann Arbor, MI USA
2009
Residency - Good Samaritan Hospital of Maryland
Internal Medicine
Baltimore, MD USA
2006
Graduate School - American University of Beirut Medical Center
Riad El Soth, Beirut, Lebanon
1999
Medical Education - Kursk State Medical Institute
Kursk,
1998
Undergraduate - AMERICAN UNIVERSITY OF BEIRUT
BEIRUT,
1994
Certifications
My main research interest is studying lung cancer development and progression as well as mechanisms of resistance to its treatment. One aspect of my laboratory research is interrogating the cancer stem cells theory in lung cancer. We have established the role of Notch activity in enriching a lung cancer stem cell population and inferring resistance to standard chemotherapy. The other major focus is understanding mechanisms of resistance to targeted therapy. Specifically, the development of resistant mutations to EGFR TKI agents. Our findings suggest that these mutation are not preexisting but rather actively acquired after exposure to EGFR TKIs. We delineated the mechanism underlying this process, showing that AICDA is activated through NFaB pathway causing cytosine deamination-based mutations. We are currently exploring the role of AICDA in resistance to new generation EGFR TKIs as well as other targeted inhibitors. Furthermore, we are working on developing AICDA inhibitors and assessing combination regimens to overcome EGFR resistance with the aim to translate our findings into clinical trials.
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