Abstract: Disclosed herein are methods of treatment by administering SRA737 as a monotherapy or in a combination therapy that is useful for treating patients with cancer.

Abstract: The invention relates to a computer readable medium including software instructions, which when executed by a scaling parameters for processor perform a method. The method includes obtaining a first and a second pre-calculated history, wherein the first and the second pre-calculated history corresponds to a first and a second path of particles through a reference material. The method further includes obtaining a first and a second plurality of phase space points and performing a first and a second set of simulations in parallel on a first and a second GPU. Each simulation uses a distinct one of the first and second plurality of phase space points, the geometry information, and the first and second pre-calculated history. The sets of simulations are performed on the GPU's to obtain a set of simulated histories. The method further includes calculating an absorbed dose of energy in the target using the set of simulated histories.

Abstract: The present invention provides compositions and methods of use thereof to prevent and/or treat pathogenic infection. In particular, the present invention provides the use of kinase inhibitors to inhibit kinases that involve in pathogen-host cell interactions that are associated with or cause pathogenic infections, therefore, to effectively prevent and/or treat pathogenic infections with far less likely to engender resistance as compared to conventional antibiotics and anti-viral drugs. The present invention further provides the use of kinase inhibitors for the treatment of acute pathogenic infections for a short period of time to avoid toxicities that may caused by long term use of these kinase inhibitors.

Abstract: The present invention provides compositions and methods of use thereof to prevent and/or treat pathogenic infection. In particular, the present invention provides the use of kinase inhibitors to inhibit kinases that involve in pathogen-host cell interactions that are associated with or cause pathogenic infections, therefore, to effectively prevent and/or treat pathogenic infections with far less likely to engender resistance as compared to conventional antibiotics and anti-viral drugs. The present invention further provides the use of kinase inhibitors for the treatment of acute pathogenic infections for a short period of time to avoid toxicities that may caused by long term use of these kinase inhibitors.

Abstract: The concurrent administration of chemotherapy and immunotherapy has been considered a contraindication because of the concern that the induced lymphopenia would ablate therapeutic efficacy of immunotherapy. Temozolomide has been shown to be an effective chemotherapeutic for patients with malignant gliomas and to deprive patients with glioblastoma (GBM) patients of this agent in order to treat with immunotherapy is controversial. Despite conventional dogma, we demonstrate that both chemotherapy and immunotherapy can be delivered concurrently without negating the effects of immunotherapy, in fact, the temozolomide induced lymphopenia may actually be synergistic with a peptide vaccine.

Abstract: The invention relates to compositions, kits, and methods for detecting, characterizing, preventing, and treating human breast cancers. A variety of newly identified markers are provided, wherein changes in the levels of expression of one or more of the markers is correlated with the presence of breast cancer.

Abstract: The present invention discloses MmRad51-deficient transgenic mice and mouse cells, as well as MmRad51/p53-deficient transgenic mice and mouse cells. Also described is a method of screening for proteins that rescue the senescence phenotype in MmRad51/p53-deficient cells.

Abstract: Ku deficient cells and transgenic animals are described that comprise at least one allele of the XRCC5 gene that has been mutated by targeted disruption. Fibroblasts derived from XRCC5 mutant embryos and mice were found to prematurely age. These cells displayed decreased growth, slow entry into S phase, altered colony size distribution that favored small colonies, short life span and morphology characteristic of terminal differentiation. Mutant cells were also hypersensitive to .gamma.-radiation. The tissue culture data was at least partly reproduced in vivo because mutant mice grew slower than control littermates. The XRCC5 mutation, designated xrcc5.sup.M1, was a deletion of nucleotides 701-964 that shifted the reading frame. xrcc5.sup.M1 is expected to be null because the deleted allele produced no detectable transcript and because lymphocyte development and V(D)J recombination was severely disrupted.