Publications by authors named "Alyssa M Bagadion"

Article Synopsis
  • Scientists are studying how some prostate cancer treatments stop working over time, leading to a more serious type of cancer called neuroendocrine prostate cancer (NEPC).
  • The research involved creating a special mouse model to see how certain genetic changes, like losing a gene called Rb1, help cancer become harder to treat and spread more easily.
  • They discovered that during this cancer change, there are new types of cells formed, and some important genetic information in the cells is altered, helping to understand how prostate cancer evolves.
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Despite recent therapeutic advances, prostate cancer remains a leading cause of cancer-related death. A subset of castration resistant prostate cancers become androgen receptor (AR) signaling-independent and develop neuroendocrine prostate cancer (NEPC) features through lineage plasticity. These NEPC tumors, associated with aggressive disease and poor prognosis, are driven, in part, by aberrant expression of N-Myc, through mechanisms that remain unclear.

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Positional cloning in maize (Zea mays) requires development of markers in the region of interest. We found that primers designed to amplify annotated insertion-deletion polymorphisms of seven base pairs or greater between B73 and Mo17 produce polymorphic markers at a 97% frequency with 49% of the products showing co-dominant fragment length polymorphisms. When the same polymorphisms are used to develop markers for B73 and W22 or Mo17 and W22 mapping populations, 22% and 31% of markers are co-dominant, respectively.

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