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  • Hepatoid adenocarcinoma closely resembles HCC and in some ca

    2024-04-02

    Hepatoid adenocarcinoma closely resembles HCC and in some cases can be indistinguishable morphologically. Hepatoid adenocarcinoma is an aggressive neoplasm, and metastasis to the liver is common [12]. Gastric metastasis from HCC has also been reported [27]. Distinguishing hepatoid adenocarcinoma from HCC is important for treatment purposes and improving patient outcome. Arginase-1 is considered a very sensitive and specific marker for HCC. However, our results show that a majority of hepatoid adenocarcinomas are also positive for arginase-1, and hence arginase-1 is not useful in distinguishing hepatoid adenocarcinoma from HCC. A recent study by Shahid et al [28] had shown that arginase-1 was negative in all their 3 cases of hepatoid adenocarcinoma. However, another recent study by Reis et al [29] showed that 4 (31%) of 13 hepatoid adenocarcinomas were positive for arginase-1. As proposed by others, arginase-1 puromycin selection concentration in hepatoid adenocarcinomas also supports the view that hepatoid morphology may represent true hepatocellular differentiation [22], [25]. Hepatoid adenocarcinomas have a tendency to metastasize to the liver, and the results of our study show that the mere demonstration of arginase-1 positivity in a liver tumor should not be considered as a definite indicator of HCC. Likewise, our results also show that arginase-1 positivity within an extrahepatic neoplasm (such as within the stomach or lung) that resembles HCC is also not diagnostic of metastatic HCC. All 8 cases of hepatoid adenocarcinoma in our study were positive for Hepar-1, and 4 of them (50%) were also positive for glypican-3. These results are supported by other similar observations in the literature [12], [13], [22], [30], [31], [32]. AFP expression was seen in 4 cases (50%), and 3 of these cases also had elevated serum AFP level ,while the serum AFP level in the fourth case was unknown. A negative AFP stain in our study was concordant with a normal serum AFP level. These results indicate that positive AFP staining in hepatoid adenocarcinoma usually correlates with elevated serum AFP levels, as reported by others [11], [13], [19], [33]. Other studies have also reported albumin ISH positivity in hepatoid adenocarcinomas [28], [34]. Likewise, in our study we found that the majority of hepatoid adenocarcinomas were positive for albumin ISH. The canalicular staining pattern on p-CEA, which is regarded by some as a marker for HCC, is also frequently seen in hepatoid adenocarcinomas, as 3 of the 8 cases in our study showed a canalicular pattern of staining with p-CEA. This result has also been reported by one prior study [11].
    Introduction Myeloid malignancies are clonal disorders originating from hematopoietic stem or progenitor cells. [1] Myelodysplastic syndromes (MDS) are characterized by cytopenias, dysplasia affecting one or more myeloid lineage, dysfunctional hematopoeisis and an increased risk of progression to acute myeloid leukemia (AML) [2]. Chronic myelomonocytic leukemia (CMML) falls into the MDS/myeloproliferative neoplasm (MPN) category, with patients displaying persistent monocytosis, fewer than 20% blasts in peripheral blood (PB) and bone marrow (BM), and dysplasia in one or more myeloid lineage [2]. It has become evident that dysregulation of the BM microenvironment contributes to the etiology of these diseases [3]. This phenomenon is better characterized in MDS, as abnormal cytokine expression is a well-described feature of the MDS BM microenvironment, especially early in disease development. For example, M-CSF, TNFα, TGFβ, IL-1α, IL-6, IL-8 and VEGF have all been found to be elevated in MDS patient BM samples [4]. Increased rates of apoptosis have also been observed within this inflammatory niche [5]. More recently, inflammatory cell death or “pyroptosis” has also been implicated in the development of MDS [6], [7]. Abnormalities within the BM lead to suppression of hematopoiesis and perturbation of processes such as angiogenesis and extracellular matrix deposition, both of which are important to maintaining an environment conducive to hematopoiesis [8]. Within this environment, immunosuppressive cell types such as myeloid-derived suppressor cells (MDSCs) and regulatory T cells are expanded while natural killer cells exhibit impaired function and CD8+ T cell populations are increased [9], [10], [11], [12]. Despite the knowledge that these diseases have an inflammatory component, the mechanisms behind these observed phenomena and the specific consequences of immune dysregulation in the BM microenvironment remain to be elucidated.