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Another limitation of the current study pertains to the absent inclusion of a variety of molecular markers that appear to play a significant role in driving malignant behavior or in producing drug resistance. These include P53 and PIK3CA mutation, cMET, NOTCH, and FOXM1. To the extent that pathways that cause che motherapeutic resistance were not assayed, the report of op timal protein expression for a given patient could over estimate the chance for benefit from the associated agent. Conclusion We observed that a majority of patients with serous histology demonstrated protein expression associated with resistance to one or more chemotherapeutic agents. Furthermore, the resistance pattern in each individual cancer was unpredictable.

Future studies could include clinical benefit analysis of MP in ovarian cancer patients in prospective trials or analysis of MA gene expression in ovarian tumors. Given the high proportion of ad vanced stage at diagnosis and the proclivity of ovarian cancer recurrence, efforts such as MP have the potential to make a large impact on survival of this disease. Background Choroid plexuses form the main interface between the blood and cerebrospinal fluid and participate in the control of brain homeostasis. In the rat, choroid plexuses of the fourth, lateral, and third ventricles ap pear in embryos on day 12, 13 and 16, respectively. In human, choroid plexuses develop around week 6 7 of gestation. Selective influx transport and secretion mechanisms confer on the choroidal epithelium an im portant role in supply of nutrient and bioactive mole cules to the developing brain.

The choroid plexuses also produce and secrete most of the CSF through the combined activity of various enzymes, transporters and ion channels located in the epithelial cells. The rate of CSF secretion increases around birth in most mam mals. In addition to these secreting and supplying activities, the choroid plexuses fulfill neuroprotective functions both as a physical and as a biochemical barrier between the blood and the nascent CSF. Transmis sion electron microscopy combined with the use of electron dense tracers and freeze fracture electron microscopy demonstrated that the tight junctions, which link adjacent epithelial cells, constitute the anatomical basis of this barrier. This physical barrier ap pears efficient in preventing the paracellular leakage of low molecular weight molecules from the earliest stages of plexus development. The molecular compos ition of choroidal TJs is regulated during development, as exemplified by the coordinated up or down regula tion of specific pore forming and tightening claudins that make up the core of the junctional complex.