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:

8.2. Species Differences in PPARalpha-Associated Signaling
The PPARalpha isotype has prime importance for studies with animal models to predict the effects of hepatic PPs in humans, because PPARalpha agonists induce seemingly quite different actions in rodents and humans [53]. Originally, as the name indicates, PPARs were studied because of their ability to bind PPs and consequently induce PP-metabolizing enzymes. In rats and mice, but not in humans, PPs such as hypolipidemic drugs, industrial plasticizers, and herbicides are non-genotoxic carcinogens that cause liver tumors [54]. In humans, these drugs function to maintain lipid homeostasis and do not induce peroxisome proliferation. Thus, the toxicity and carcinogenicity of PPs are highly species specific [55]. The species differences may be attributable to lower PPAR mRNA expression levels in h-hepatocytes compared with rodent cells [56, 57]. Alternatively, or additionally, species differences may be the result of different sensitivities of the genes associated with the peroxisome proliferation response to low levels of PPs, owing to structural differences in PPARalpha [54]. There are both similarities and differences in responses to xenobiotics among not only different species (interspecies) but also individuals of the same species (intraspecies). Interspecific PPARalpha diversity between rodents and humans is well known and has been studied with respect to drug metabolism. NR subfamily 1 members have at least two functions in mammals. One is to regulate peroxisome proliferation through binding to PPAR response elements (PPREs) in the promoters of genes such as ACO [58, 59], bifunctional dehydrogenase/hydratase (BFE) [60], and microsomal CYP4A1 [61]. The other is to modulate the serum cholesterol level by targeting genes such as the lipoprotein lipase gene [62] and the apolipoprotein regulating genes AI, AII, and CII [63]. The former mechanism appears to function in rodents, but not in humans, and is responsible for the induction of peroxisome proliferation and hepatocarcinogenesis, whereas the latter mechanism controls basic lipid metabolism in both rodents and humans [56]. This species difference in xenobiotic receptor/ligand signaling may be attributable to differences in the expression level of a receptor, or to differences in receptor/ligand binding affinity, and causes difficulty in determining responses in humans based on rodent data [56].
{"AnatomicalEntity": ["peroxisome", "hepatic", "serum", "cells", "h-hepatocytes", "liver tumors"]}