고려대학교 생명과학대학 생명과학부/ 대학원 분자생명과학과

Tumor hypoxia is known to occur via two mechanisms: chronic hypoxia where rapidly proliferating cancer cells are being pushed outside the oxygen diffusion distance thereby becoming hypoxic and eventually necrotic; or acute hypoxia whereby a rapid closure of tumor vasculature causing temporary cessation of the blood flow hence causing transient hypoxic environment.  Under these conditions, tumor cells can engage HIF (hypoxia-inducible factor) signaling, turning on multiple cellular pathways including angiogenesis, glycolytic metabolism, and metastases. 

Tumor hypoxia has been well established as a major contributing factor for failures in radiotherapy and chemotherapy. Although much attempt has been made to overcome tumor hypoxia, including hypoxic radiosensitizers and hypoxic cell cytotoxins it is still a major hurdle in today’s cancer treatment in the clinic.  One of those attempts, although not being used to treat cancer but rather to diagnose, is ¹⁸F-misonidazole, a PET tracer detecting tissue hypoxia in patients.

In this seminar, I will highlight the above tumor microenvironment, our recent unpublished data demonstrating how tumor-associated macrophages could contribute to this process, as well as our collaborative work where we’re developing quantum dot approach to detect the real-time tumor hypoxia.