Osteoarthritic disease and Regenerative Medicine at the Rizzoli Research Institute (Bologna, Italy):
-NF-kB signaling and impact in lung cancer development: http://www.bioacademy.gr/faculty-details/HMqO/kenneth
Research Projects (USA and Europe)
As of January 1, 2016, I will be retiring from my full time Professorial position and thereafter will be Emeritus Professor at Stony Brook University. Thus as of January 1, 2016 I no longer have my own laboratory or research group at Stony Brook and will also no be an active member of any graduate programs (thus for these obvious reasons I can no longer take on students, technicians or postdoctoral fellows to work under my mentorship at Stony Brook University). However, in my retirement my research projects at Stony Brook University will be continuing in the laboratory of my collaborator Dr. Richard Kew in the Pathology Department; and I will also continue to give my block of lectures on B Lymphocyte development and function in immunity each September in Prof. Howard Fleit’s graduate immunology course (HBP 533) also in the Pathology Dept. In my retirement I will be living in Bologna, Italy and will only be returning to the USA ~4 times each year, which are spread out ~2-4 months apart (each ~7-12 days in duration). In addition, I will also continue to direct and co-direct basic biomedical research projects at other research institutes and Universities in the USA and Europe (where I also hold either Adjunct or Affiliated Appointments) on a year round basis including: (1) The Hospital for Special Surgery in Manhattan, NY with my colleagues Drs. Miguel Otero, Kirsty Culley and Mary Goldring, and also in collaboration with Dr. Eleonora Olivotto at the Rizzoli Orthopedic Research Institute (affiliated with the University of Bologna in Bologna, Italy); (2) The IMBB-FORTH Biomedical Research Institute. IMBB-FORTH (Ioannina Univ. Medical School, Ioannina, Greece) with my colleague Prof. Vagelis Kolettas; (3) The Biomedical Research Foundation Academy of Athens (BRFAA) in Athens. Greece with my colleagues Drs. Elia Chavdoula, Apostolos Klinakis and Dimitris Thanos; (4) San Diego State University’s Biology Dept with my colleague Prof. Roland Wolkowicz on the impact of NF-kappaB signaling in infectious viral disease. Overall, my research will continue to involve the regulation and mechanisms of action of the inhibitor of NF-kB kinase (IKK) complex. The IKK signaling complex is essential for the activation of the NF-kB transcription factor family. Moreover, the IKKb and IKKa serine threonine kinases in the IKK signalsome also functionally impact on a number of other NF-kB independent growth and differentiation pathways in various cell types. Thus IKKb and IKKa are orchestrators of developmental and inflammatory processes including all stress-like responses, innate and adaptive immunity and the survival and growth of normal and malignant cells. My research will continue to be focused on elucidating novel in vivo mechanism(s) of action of IKKa and how IKKa’s functions collaborate with or differ from with those of its homologous partner kinase IKKb. Together with colleagues and collaborators in the States and Europe I have been exploring the functional roles and mechanisms of action of IKKa and IKKb in different disease-related biological contexts including: (1) novel cell migration responses specifically elicited in response to tissue damage initially invoking a pronounced inflammatory reaction that can eventually give way to tissue repair in part via the recruitment of progenitor, stem cells, (2) gene expression and epigenomic regulation associated with the maintenance of articular chondrocyte homeostasis and/or differentiation programming and mechanical and pro-inflammatory stress that can lead to osteoarthritic disease, (3) alterations in gene expression programming in response to specific forms of extracellular stress including pro-inflammatory oncogenic events leading to DNA damage and premature cellular senescence and (4) specific alterations in cellular physiology that occur in cancer cell genesis and progression using a murine model of human lung cancer onset and progression.