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Dale L Greiner





UMassMed Faculty Page


Title: Genetically Modified Non-Human Animals and Methods Relating to Complement Dependent Cytotoxicity. UMMS16-63; Patent Pending. 

  • The present invention provides a genetically modified immunodeficient mouse, wherein the genome of the mouse comprises a repaired C5 complement component structural gene such that the 5 genetically modified immunodeficient mouse expresses the C5 complement component structural gene and is characterized by an intact complement system. The present invention relates to immunodeficient non-obese diabetic (NOD), A/J, A/He, AKR, DBA/2, NZB/B1N, BlO.D2/oSn and other mouse strains genetically modified to restore complement-dependent cytotoxicity which is lacking in the unmodified immunodeficient mice.

Title: Improving Efficacy of VEGF-Targeted Therapy in Prostate Cancer. UMMS16-02; Patent Pending. 

  • This invention discloses methods to improve the response to VEGF/VEGFR-targeted therapy in patients resistant to bevacizumab and sunitinib. Our critical finding is that inhibition of Rac1 activity using a commercially available compound renders resistant cells sensitive to bevacizumab and sunitinib and can therefore be used as an adjuvant to treat aggressive forms of prostate cancer. 

Title: Development of NOD.Cg-Prkdc<scid> Il2rg<tm1Wjl> Tlr4lps-del Sz/Sz ("NSG Tlr4 Mice"). UMMS13-61; Patent Pending. 

  • This invention provides a immunodeficient mouse model based on the NOD strain (referred to as NSG and NRG mice) that can be engrafted with functional human immune systems, including adaptive and innate immune systems. These mice completely lack adaptive immune cells such as T and B cells, as well as NK cells.  To study the response of human innate immune cells to the TLR agonist LPS in the absence of a murine innate immune response, these NSG mice completely lack TLR4 on their innate immune cells. 

Title: Transgenic Non-Human Animal and Methods for Stem Cell Engraftment. UMMS10-43; Patent Pending. 

  • A transgenic immunodeficient non-obese diabetic (NOD) mouse homozygous for the SCID mutation and having an IL2 receptor gamma chain deficiency. Administration of human stem cells to the mouse in the absence of conditioning by irradiation results in similar or greater levels of engraftment of human stem cells compared to a non-obese diabetic (NOD) mouse homozygous. 


Innovation Topics: Research ToolsAnimal ModelsImmunodeficient diseasesType I DiabetesType II DiabetesSmall MoleculesCancerProstate cancerCombination therapySunitinibBevacizumanImmunologyImmunodeficient diseasesMouse model