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Michael R Green






UMassMed Faculty Page


Title: Identification of Epigenetic Modifiers of the Silenced FMR1 Gene: Potential Targets for Fragile X Syndrome Therapeutics. UMMS16-03; Patent Pending. 

Title: New XCI Inhibitors as Potential Rett Syndrome Therapeutics. UMMS15-53; Patent Pending. 

Title: A Method to Treat Chronic Myelogenous Leukemia (CML) Patients who have Developed BCR-ABL-Independent Imatinib Resistance and to Eradicate CML Stem Cells. UMMS14-47; Patent Pending.

  • This new innovation addresses the issues associated drug resistance of chronic myeloid leukiemia (CML) cells to imatinib mesylate (IM). IM improves patient survival and are used widely to treat early stages of CML, but the efficacy is known to drop when drug resistance is developed. This new invention builds on the finding that in IM resistant CML cells, RAF/MEK/ERK pathway is activated that is not subjected to IM targeting. Remarkably, when FDA approved MEK inhibitor, trametinib is treated in conjunction with IM, they synergistically kill CML cells and improve survival in mouse models. more info.

Title: SRPX FOR TREATMENT OF CANCER. UMMS 12-08; Patent 9,290,744

  •  This technology provides compositions and methods of treatment for lung cancer. The invention is based on a discovery the tumor suppressor, SRPX is found at low levels of expression in solid human tumors compared to normal tissue. When SRPX is introduced at sufficient levels to tumor cells, SRPX can induce apoptosis and senescence to inhibit cellular proliferation. SRPX can easily be administered using the AAV gene therapy method and markedly suppresses lung cancer in mice. more info.

Title: Identification of Genes Preferentially Required for Growth of p53-Deficient Human Cancer Cells. UMMS09-56; Patent Pending. 

  • This invention discloses a novel cluster of genes discovered through a RNAi screen which could be a potential target of cancer treatment in p53 mutation cancers. p53 gene is mutated in numerous cancer therefore the newly discovered genes have potential for becoming a therapeutic target in wide range of cancers. The inventors performed a bias screen using p53 mutant cancer cells, p53-/- and +/- colorectal HCT116 cell lines and shRNA library. This screening yielded a selection of genes that are preferentially required for viability in p53 mutant cancer cells.  The verification experiments showed that a 24 gene-knockdown preferentially impaired growth of the p53 cell line. Using mice xenograft, 4 required genes were identified and show high potential for clinical use. 


Innovation TopicsRNAi/micro-RNA TherapySmall MoleculesFragile X syndrome/Fragile X-associated tremor/ataxia syndromePolycystic ovarian syndromePremature ovarian agingRett SyndromeHypophosphatemiaIncontinentia pigmentiAicardiCHILD syndromeDermal hypoplasiaLujan-Fryns syndromeNephritisFragile X syndrome/Fragile X-associated tremor/ataxia syndromeCharcot-Marie-Tooth diseaseMyopathyDysplasiaCancerChronic myeloid leukiemia (CML)Gene TherapyBiologicsAAVLung cancerp53 mutant cancer