You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["AnatomicalEntity"].

Please return the output as a JSON object of the format: {"AnatomicalEntity": ["tumor cells", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

1,4-phenylenebis(methylene)selenocyanate, but not selenomethionine, inhibits androgen receptor and Akt signaling in human prostate cancer cells. 
The lack of treatment for worried-well patients with high-grade prostatic intraepithelial neoplasia combined with issues of recurrence and hormone resistance in prostate cancer survivors remains a major public health obstacle. The long latency of prostate cancer development provides an opportunity to intervene with agents of known mechanisms at various stages of disease progression. A number of signaling cascades have been shown to play important roles in prostate cancer development and progression, including the androgen receptor (AR) and phosphatidylinositol 3-kinase/Akt signaling pathways. Crosstalk between these two pathways is also thought to contribute to progression and hormone-refractory prostate disease. Our initial investigations show that the naturally occurring organoselenium compound selenomethionine (SM) and the synthetic 1,4-phenylenebis(methylene)selenocyanate (p-XSC) can inhibit human prostate cancer cell viability; however, in contrast to SM, p-XSC is active at physiologically relevant doses. In the current investigation, we show that p-XSC, but not an equivalent dose of SM, alters molecular targets and induces apoptosis in androgen-responsive LNCaP and androgen-independent LNCaP C4-2 human prostate cancer cells. p-XSC effectively inhibits AR expression and transcriptional activity in both cell lines. p-XSC also decreases Akt phosphorylation as well as Akt-specific phosphorylation of the AR. Inhibition of Akt, however, does not fully attenuate p-XSC-mediated downregulation of AR activity, suggesting that inhibition of AR signaling by p-XSC does not occur solely through alterations in the phosphatidylinositol 3-kinase/Akt survival pathway. Our data suggest that p-XSC inhibits multiple signaling pathways in prostate cancer, likely accounting for the downstream effects on proliferation and apoptosis.
{"AnatomicalEntity": ["prostate cancer cells", "high-grade prostatic intraepithelial neoplasia", "LNCaP", "cell lines", "prostate cancer", "LNCaP C4-2 human prostate cancer cells", "prostate cancer cell", "prostate disease"]}