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Boston, MA, United States

Genesys Research Institute | Date: 2011-08-24

The invention features compositions comprising microRNAs that are differentially regulated in dormant versus fast growing neoplasias, and related methods of using the microRNAs for inducing or prolonging dormancy in a neoplastic cell or otherwise inhibiting the growth of a neoplastic cell.

Genesys Research Institute | Date: 2013-10-04

The invention generally features isolated platelets, compositions, methods, and kits useful for targeted delivery of one or more therapeutic agents to a site of injury, inflammation, disease, or disorder. Also featured are methods and kits for producing a platelet loaded with one or more therapeutic agents. Platelets loaded with one or more therapeutic agents are useful for treating neoplasia, hemophilia, wounds, and other pathologies or conditions involving sites of injury, inflammation, disease, or disorder where platelets are able to localize.

Genesys Research Institute | Date: 2014-01-31

Provided herein are an isolated or enriched population of tumor initiating cells derived from normal cells, cells susceptible to neoplasia, or neoplastic cells. Methods of use of the cells for screening for anti-hyperproliferative agents, and use of the cells for animal models of hyperproliferative disorders including metastatic cancer, diagnostic methods, and therapeutic methods are provided.

The invention features methods and compositions feature lapatinib and/or rapamycin for treating or preventing a cardiac condition induced by anthracycline treatment.

Sasi S.P.,GeneSys Research Institute | Bae S.,GeneSys Research Institute | Bae S.,Steward St Elizabeth Medical Center | Song J.,GeneSys Research Institute | And 12 more authors.
PLoS ONE | Year: 2014

Tumor necrosis factor-alpha (TNF) binds to two receptors: TNFR1/p55-cytotoxic and TNFR2/p75-pro-survival. We have shown that tumor growth in p75 knockout (KO) mice was decreased more than 2-fold in Lewis lung carcinoma (LLCs). We hypothesized that selective blocking of TNFR2/p75 LLCs may sensitize them to TNF-induced apoptosis and affect the tumor growth. We implanted intact and p75 knockdown (KD)-LLCs (>90%, using shRNA) into wild type (WT) mice flanks. On day 8 post-inoculation, recombinant murine (rm) TNF-α (12.5 ng/gr of body weight) or saline was injected twice daily for 6 days. Tumor volumes (tV) were measured daily and tumor weights (tW) on day 15, when study was terminated due to large tumors in LLC+TNF group. Tubular bones, spleens and peripheral blood (PB) were examined to determine possible TNF toxicity. There was no significant difference in tV or tW between LLC minus (-) TNF and p75KD/LLC-TNF tumors. Compared to 3 control groups, p75KD/LLC+TNF showed >2-5-fold decreases in tV (p<0.001) and tW (p<0.0001). There was no difference in tV or tW end of study vs. before injections in p75KD/LLC+TNF group. In 3 other groups tV and tW were increased 2.7-4.5-fold (p<0.01, p<0.0002 and p<0.0001). Pathological examination revealed that 1/3 of p75KD/LLC+rmTNF tumors were 100% necrotic, the remaining revealed 40-60% necrosis. No toxicity was detected in bone marrow, spleen and peripheral blood. We concluded that blocking TNFR2/p75 in LLCs combined with intra-tumoral rmTNF injections inhibit LLC tumor growth. This could represent a novel and effective therapy against lung neoplasms and a new paradigm in cancer therapeutics. © 2014 P Sasi et al.

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