Abstract: A method of purifying circulating tumor cells is disclosed. The method involves purifying a first buffy coat layer from a blood sample on a first density gradient. The blood sample comprises a circulating tumor cell. The first buffy coat layer is reconstituted in whole blood to yield an enriched sample. The volume of whole blood used to reconstitute the first buffy coat layer is less than 20% of the volume of the blood sample. Circulating tumor cell enrichment reagent is added to the enriched sample at a volume of less than 20% of the total volume of the enriched sample. The enriched sample is placed on a second density gradient and a second buffy coat layer is collected. The second buffy coat layer comprises the circulating tumor cell.

Abstract: Disclosed herein are methods of predicting whether or not a subject will benefit from treatment with a Src inhibitor on the basis of the expression of one or more of Von Hippel Lindau (VHL), Src, PTP1B, pFAK, HIF-1?, and/or CA-IX in a tumor sample from the subject.

Abstract: The invention disclosed herein provides methods for the examination and/or quantification of biochemical pathways that are disregukted in pathologies such as cancer and to reagents and kits adapted for performing such methods. For example a correlation between VHL loss and mTOR inhibitor sensitivity in human kidney cancer cells is disclosed, indicating that VHL loss confers autonomous and angiogenic competitive advantages to such cells.

Abstract: Disclosed herein are methods of predicting whether or not a subject will benefit from treatment with a Src inhibitor on the basis of the expression of one or more of Von Hippel Lindau (VHL), Src, PTP1B, pFAK, HIF-1?, and/or CA-IX in a tumor sample from the subject.

Abstract: The invention disclosed herein provides methods for the examination and/or quantification of biochemical pathways that are disregukted in pathologies such as cancer and to reagents and kits adapted for performing such methods. For example a correlation between VHL loss and mTOR inhibitor sensitivity in human kidney cancer cells is disclosed, indicating that VHL loss confers autonomous and angiogenic competitive advantages to such cells.

Abstract: The invention disclosed herein provides methods for the examination and/or quantification of the PI3K/Akt and Ras/MAPK biochemical pathways that are disregulated in pathologies such as cancers of the prostate and gliomas. The invention disclosed herein further provides reagents and kits adapted for performing such methods.