The present invention describes an association between genetic polymorphisms in the FAM13A1 (family with sequence similarity 13, member A1) gene and a predisposition to prolongation of the QT interval, and provides related methods for the prediction of such a predisposition, the administration of QT interval-prolonging compounds to individuals having such a predisposition, and determining whether a compound is capable of inducing QT prolongation.

A splice variant of bcr-abl mRNA that produces BCR-ABL protein with a truncated C-terminus and its role in resistance to treatment with kinase inhibitors is disclosed. Vectors for expressing the truncated gene product are provided as well as recombinant cells that express the truncated gene product from a cDNA construct. Also provided are methods compositions and kits for detecting the BCR-ABL splice variant. Additionally, methods for screening BCR-ABL kinase domain inhibitors which rely on the recombinant cells and methods of predicting likelihood for resistance of a CML patient with a BCR/ABL translocation respond to treatment with one or more BCR-ABL kinase inhibitors are also disclosed.

The present invention describes an association between genetic polymorphisms in the ABCC2 gene and a predisposition to prolongation of the QT interval, and provides related methods for the prediction of such a predisposition, the administration of QT interval-prolonging compounds to individuals having such a predisposition, and determining whether a compound is capable of inducing QT prolongation.

The present invention describes an association between genetic polymorphisms in the BAI3 gene and a predisposition to prolongation of the QT interval, and provides related methods for the prediction of such a predisposition, the administration of QT interval-prolonging compounds to individuals having such a predisposition, and determining whether a compound is capable of inducing QT prolongation.

The invention provides methods for the administration of compounds capable of prolonging a QTc interval and methods for predicting whether an individual is predisposed to such QTc prolongation.

Single nucleotide polymorphic sites of the bovine MAP1B, PPP1R11, and DDX4 genes are associated with improved bull fertility as measured by e.g. sire conception rates. Nucleic acid molecules, arrays, kits, methods of genotyping and marker-assisted bovine breeding methods based on these SNPs are disclosed.

The present invention provides a method for treating a human subject afflicted with multiple sclerosis or a single clinical attack consistent with multiple sclerosis with a pharmaceutical composition comprising glatiramer acetate and a pharmaceutically acceptable carrier, comprising the steps of: (i) determining a genotype of the subject at a location corresponding to the location of one or more single nucleotide polymorphisms (SNPs) selected from the group consisting of: Group 1, (ii) identifying the subject as a predicted responder to glatiramer acetate if the genotype of the subject contains one or more A alleles at the location of Group 2, one or more C alleles at the location of Group 3, one or more G alleles at the location of Group 4, or one or more T alleles at the location of kgp18432055, kgp279772, kgp3991733 or kgp7242489; and (iii) administering the pharmaceutical composition comprising glatiramer acetate and a pharmaceutically acceptable carrier to the subject only if the subject is identified as a predicted responder to glatiramer acetate.

The present disclosure encompasses methods of error corrected sequencing (ECS) that enable detection of very rare mutations well below the error rate of convention next generation sequencing (NGS). Further, the methods disclosed herein enable multiplex targeting of genomic DNA.

The present disclosure provides a molecular marker linked to Fusarium wilt resistance gene in tomato, and a method for obtaining the molecular marker linked to Fusarium wilt resistance gene in tomato. The molecular marker according to the present disclosure has a high specificity, and can be used to identify the resistance to Fusarium oxysporum f. sp. Physiological race 3 quickly and improve the breeding efficiency of the seeds resistant to Fusarium oxysporum f. sp. Physiological race 3. The molecular marker linked to Fusarium wilt resistance gene in tomato according to the present disclosure is prepared simply and has a low production cost. The molecular marker according to the present disclosure can be used to identify the resistance to Fusarium oxysporum f. sp. Physiological race 3, screen the tomato single plant which is resistant to Fusarium oxysporum f. sp. Physiological race 3, and/or determine the purity of hybrid seeds derived from hybridization of the tomato which is resistant to Fusarium oxysporum f. sp. Physiological race 3 and the tomato which is susceptible to Fusarium oxysporum f. sp. Physiological race 3. The molecular marker according to the present disclosure can be also used to prepare a kit, which has the same uses as that of the molecular marker according to the present disclosure.

Disclosed herein are methods for determining whether a PAR4 inhibitor should be administered to a human subject, the methods comprising administering a PAR4 inhibitor to a subject determined to have a “G” allele for a single-nucleotide polymorphism (SNP) at rs773902, and not administering a PAR4 inhibitor to a subject determined to have an “A” allele for the SNP at rs773902. A genotyping assay can be used to determine the SNP.