Function Of Multiple Independent Tumor Foci

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for ERG and SPINK1 (Table 1). Given the presence of multiple independent tumor foci in a sample, ERG/SPINK1 screening identified mutually exclusive expression in independent tumor foci with additional tumor foci negative for ERG/SPINK1 (Figure 6-left panel). On a consecutive whole mount tissue slide from the same patient, we performed ETV1 RNA-ISH and identified a third independent tumor foci positive for ETV1 (Figure 6-right panel). Further on a third consecutive slide we performed PTEN IHC and found PTEN loss only in the tumor foci positive for ETV1 (image not shown). These results indicate the independent origin of each tumor foci with distinct driver molecular aberration. The designated dominant nodule (large size) was negative for…show more content…
Regarding racial disparity in the prevalence of ETS gene fusions and SPINK1 expression, we observed higher incidence of SPINK1+ in AA compared to CA. It is important to note that we have observed about 21.1% of the cases negative for ERG and SPINK1 in all tumor foci (Table 1). Moreover, we did not observe any patient sample that is positive for ERG or SPINK1 in all tumor foci indicating the extent of molecular heterogeneity and independent clonal origin of each tumor foci with distinct driver molecular aberrations. Therefore, we evaluated all the ERG/SPINK1- negative and positive cases for ETV1 by RNA-ISH and thus far, we have completed evaluation of 132 cases (78, CA, 33, AA and others-screening in progress) and observed 6.06% of the cases positive for ERG+/SPINK1+/ETV1+ (triple marker positive) in a mutually exclusive manner (Table 2; Figure 6). We also observed cases with ERG+ and SPINK1+ expression either in immediately adjacent tumor foci with different Gleason pattern (Figure 8) or at a distant tumor foci of varying size and Gleason pattern (Figure 10). Similar to ERG+ and SPINK1+ expression in adjacent tumor foci we observed cases with ERG+ and ETV1+ expression in immediately adjacent tumor foci (Figure 9). It is for the first time we have demonstrated the molecular heterogeneity of PCa using driver molecular aberrations by preserving the spatial tumor landscape for direct qualitative and quantitative assessment under
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