Hospital Research Teams
The Adriana Haimovitz-Friedman Lab
Research
Adriana Haimovitz-Friedman, PhD
The focus of my laboratory is to understand how SDRT can initiate an innate response in the local tumor and also contribute to initiation of a response in distant tumors (Abscopal/Adscopal like effects).
In addition, we use combination of SDRT and chemotherapeutic drugs with short acting anti-angiogenic agents, which result in improved tumor response with less overall toxicity.
People
Adriana Haimovitz-Friedman, PhD
- Optimizing the use of Single high Dose Radiation Therapy (SDRT) in pre-clinical studies to activate innate immune signaling pathways, potentially leading to adaptive immune responses within the local tumors and in distant ones, i.e eliciting Adscopal and/or Abscopal effects.
- haimovia@mskcc.org
- Email Address
- (646) 888-2172
- Office Phone
Members
Weill Cornell PhD Student
Lab Technician
Research Associate
Postdoctoral Research Fellow
Research Fellow
Visiting Associate Attending Radiation Oncologist from Seoul, Korea
Research Scholar
Lab Affiliations
Achievements
- Our Laboratory was the first to discover that radiation can induced damage to the plasma membrane of the endothelial cells, which resulted in a paradigm shift in the treatments of radiation and introduced the Single high Dose Radiation therapy, SDRT, in the clinic, which results in cures for those tumors that are otherwise non-responders to conventional fractionated radiation therapy.
- We found the optimal timing to combine SDRT with anti-angiogenics and with chemotherapy.
- For both prostate and breast cancers, ATM down regulation can radiosensitize via a specific signal transduction pathway involving de novo ceramide generation.
- Radiation-induced acute blood-brain barrier disruption is mediated by the acid sphingomyelinase (ASMase) pathway, a major contribution to the radiation and brain drug delivery field.
- Mice suffering from sepsis can be rescued by protecting the microvasculature.
Read more
- Mice are protected from Radiation-induced gastrointestinal syndrome by protecting the microvasculature via inhibition of the ASMase/Ceramide pathway.