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HAMILTON, NJ, United States

The present invention is directed to novel haplotype tagging single nucleotide polymorphisms (SNPs) in specific regions outside the HFE gene that serve as a reliable biomarker for a decreased risk for childhood lymphoblastic leukemia (ALL) in a child. There is provided herein methods and reagents for assessing the haplotype tagging SNPs selected from the group consisting of rs807212, rs198853, rs9467664, rs2213284, rs2230655 and rs12346. The method useful in applying these SNPs in predicting a decreased risk of childhood lymphobastic leukemia (ALL) is also disclosed.

Disclosed are methods of attenuating activity of the gene promoter of CIP2A. siRNAs are used to target against Ets1 and Elk1 transcriptional factors, thereby blocking the binding of Ets1 and Elk1 to the CIP2A gene promoter. It is disclosed that the siRNAs targeted against Ets1 and Elk1 attenuate the gene expression of CIP2A. A kit containing siRNA reagents for attenuating the CIP2A gene expression is also disclosed.

Disclosed are diagnostic methods for determining a subtype of methicillin-resistant

The present invention is directed to the identification of a novel repressor located between 1.2 kb to 1.6 kb from the translation start site of the IFN-1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-1 (i.e., increases the production of IFN-1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-1 protein that promotes an anti-viral response as well as treats asthma diseases and colon diseases.

The present invention provides a method of determining if a tumor cell is susceptible to killing by a chemotherapeutic agent, comprising: (a) providing a tumor cell; (b) infecting said tumor cell with a herpes simplex virus or a herpes simplex virus defective in an immediate early gene selected from the group consisting of ICP27, ICP4, and ICP22; and (c) determining the presence of apoptotic killing of said tumor cell, wherein the presence of apoptotic killing is indicative of susceptibility to said chemotherapeutic agent. Chemotherapeutic agent may include doxorubicin, etoposide, paclitaxel, cisplatin, or 5-fluororuacil. The present invention also provides a herpes simplex virus promoter construct having a lacZ gene to assess tumor resistance to chemotherapeutic agents.

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