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Introduction/Objective Beta catenin plays an important role in cancer tumorigenesis and have been found to be associated with metastasis in a variety of tumors. Analyzing TCGA data, we found that 30% of endometrial endometrioid carcinoma cases have beta-catenin mutations. We hypothesize that beta-catenin mutation may be associated with metastasis of endometrial endometrioid carcinoma. ER and PR expression was also compared to determine any changes after metastasis. Methods Retrospective institutional review of all endometrial endometrioid carcinoma (192 cases) between 2011 to 2018 was performed, including 149 cases of FIGO grade I, 38 cases of FIGO grade II and 5 cases of FIGO grade III. 19 cases with paired primary and metastatic specimen were identified. Immunohistochemistry staining (IHC) was carried out for ER, PR and beta-catenin. Results Median patient age was 56 years. The most common metastatic site was vagina, accounting for 68% of metastasis (14/19), followed by bladder (3/19), lung (2/19) and rectum (1/19). The primary and metastatic carcinoma of all 19 cases exhibit very similar morphology. All of those cases were positive and concordant for ER and PR in primary and metastatic endometrioid carcinoma. On the other hand, nuclear beta-catenin staining caused by mutation was positive in 5 metastatic carcinoma but not in primary carcinoma. Conclusion IHC expression of ER and PR remains unchanged between primary and metastatic carcinoma, demonstrating the reliability of ER and PR to confirm the origin of metastatic carcinoma. 26% of the metastatic carcinoma (5/19) exhibit nuclear beta-catenin staining but not in primary carcinoma, suggesting the possible role of beta-catenin in metastasis of endometrial endometrioid carcinoma.

Objectives The most common genetic alterations in prostate cancer are fusions of ERG and other members of the E26 transformation-specific (ETS) family of transcription factors, including ETV1, ETV4, and FLI1. Analyzing TCGA data, we found that similar to ERG fusion, FLI1 fusion-associated FLI1 mRNA level increases. ERG IHC stain has been a surrogate test for ERG fusion. Therefore, we hypothesize that FLI IHC stain could also be used to detect FLI1 fusion in prostate cancer. Methods In total, 111 primary prostate adenocarcinoma (>10% by volume) cases from our institute were selected for tissue microarray (TMA) construction. The regular full section slides and TMA slides were subject to IHC stain of ERG and FLI1 (Santa Cruz, SC-113). The criteria for positive FLI1 are (1) nuclear staining; (2) only in tumor cells, not in nontumor cells; and (3) FLI1-positive cells should be negative for ERG IHC staining. Results For prostate TMA slides, ~50% of cases were positive for ERG; ~30% of cases were weakly positive for FLI1. However, all of the FLI1 weakly positive cases were positive for ERG as well possibly due to cross-reactivity between ERG and FLI1, which was demonstrated in other studies. Conclusion Overall, we conclude that the cross-reactivity between FL1 and ERG precluded the detection of FLI1 fusion in prostatic adenocarcinoma under current conditions. We are in the process of selecting some cases to detect FLI1 fusion by next-generation sequencing (NGS) and FISH.

Objectives: Renal cell carcinoma (RCC) is a heterogeneous neoplasm with different morphology and molecular changes. Recently, a study investigated panmetabolomic profiles and metabolic genes of more than 600 clear cell RCC (ccRCC) tumors showed the rate-limiting gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP-1) was inhibited in almost 100% of ccRCCs. Here, we …