Abstract: The disclosure relates to methods of identifying subjects at risk of developing bevacizumab-induced toxicities such as proteinuria and/or hypertension involving measuring nucleic acid or gene mutations in a sample obtained from the subject.

Abstract: The disclosure relates to methods of identifying subjects at risk of developing bevacizumab-induced toxicities such as proteinuria and/or hypertension involving measuring nucleic acid or gene mutations in a sample obtained from the subject.

Abstract: The disclosure relates to methods of identifying subjects at risk of developing bevacizumab-induced toxicities such as proteinuria and/or hypertension involving measuring nucleic acid or gene mutations in a sample obtained from the subject.

Abstract: The present invention concerns the methods and compositions for evaluating the risk of ironotecan toxicity in a cancer patient based on the genotype of the patient at position ?3156 of the UGT1A1 gene or at any position in linkage disequilibrium with the ?3156 variant.

Abstract: The present invention is directed to methods and compositions for determining the presence or absence of polymorphisms within an ABCC2, UGT1A1, and/or SLCO1B1 gene and correlating these polymorphisms with activity levels of their gene products and making evaluations regarding the effect on their substrates, particularly those substrates that are drugs. In addition, there are methods and compositions of evaluating the risk of an individual for developing toxicity or adverse event(s) to an ABCC2, UGT1A1, and/or SLCO1B1 substrate. In some embodiments, the invention concerns methods and compositions for determining the presence or absence of ABCC2 3972C>T variant and predicting or anticipating the level of activity of ABCC2 and determining dosages of an ABCC2 drug substrate, such as irinotecan, in a patient.

Abstract: The present invention concerns polymorphisms in the epidermal growth factor receptor (EGFR), gene. In some embodiments, the present invention is directed at compositions and methods involving single nucleotide polymorphisms (SNPs) in the promoter of the EGFR gene that affect EGFR expression. The identification of polymorphisms associated with EGFR expression or activity enables novel methods and compositions for evaluating the potential efficacy and toxicity of an EGFR-targeting therapeutic agent, predicting a patient's clinical prognosis, and evaluating a patient's risk of developing a disease that is associated with EGFR dysregulation.

Abstract: Various embodiments of the invention include methods and compositions for evaluating the risk of irinotecan toxicity in a patient. In certain embodiments, the methods include detecting a promoter polymorphism in one or both UGT1A1 genes of the patient. In particular embodiments the promoter polymorphism is a single nucleotide polymorphism and may be in linkage disequilibrium with a UGT1A1 (TA)n repeat. The methods may include obtaining a nucleic acid sample from the patient and detecting the presence or absence of a promoter polymorphism. The promoter polymorphism may be at nucleotide position −3440, −3401, −3279, −3177, −3175, or −3156 from the UGT1A1 gene transcriptional start site. The number of TA repeats can be 5, 6, 7, 8 more TA repeats. In particular embodiments, the promoter polymorphism is a −3440C>A, −3401T>C, −3279G>T, −3177C>G, −3175A>G, −3156G>A polymorphism or any combination thereof.

Abstract: This invention concerns UGT2B7 and its ability to glucuronidate various drugs, including epirubicin. It concerns methods and compositions for determining the level of UGT2B7 activity based on genetic composition, and consequently, allows dosing of UTG2B7-glucuronidated drugs to be improved or optimized based on a patient's level of predicted UGT2B7 activity. It further concerns methods of treatment in which UGT2B7 substrates are administered to patients as part of a treatment regimen.

Abstract: This invention provides methods, formulations and kits to reduce the toxicity of flavopiridol and analogs thereof. Disclosed are therapeutics and treatment methods employing such drugs in combination with agents that increase conjugative enzyme activity or glucuronosyltransferase activity, and agents that decrease biliary transport protein activity, such as cyclosporine A, the resultant effects of which are to decrease the significant side effects previously associated with treatment using these drugs. The invention also characterizes specific isoforms of glucuronyltransferase enzymes involved in glucuronidation of flavopiridols and their analogs.