PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
7066921-3	1982	The phenotypic profile of ACR cells chronically exposed to TPA, although effecting a change toward a more transformed phenotype (e.g., growth in agar), was in large measure neither stable nor uniform during consecutive passages or for a given cell strain during different periods of TPA application.	Tetradecanoylphorbol Acetate	59-62	acrosin	Homo sapiens	26-29	
7066921-3	1982	The phenotypic profile of ACR cells chronically exposed to TPA, although effecting a change toward a more transformed phenotype (e.g., growth in agar), was in large measure neither stable nor uniform during consecutive passages or for a given cell strain during different periods of TPA application.	Tetradecanoylphorbol Acetate	283-286	acrosin	Homo sapiens	26-29	
7066921-5	1982	We speculated that TPA-induced aneuploidy in these cells, coupled with DNA instability and aberrant chromosomal segregation, may conceivably be consistent with neoplasia in initiated ACR cells.	Tetradecanoylphorbol Acetate	19-22	acrosin	Homo sapiens	183-186	
7066921-6	1982	Finally, the apparent susceptibility of ACR cells to further transformation by TPA and N-methyl-N1-nitro-N-nitrosoguanidine (MNNG) (34,48) and by ocongenic viruses (37,45) indicates that genetic information residing within these cells, probably in the form of an ACR mutation, renders them more sensitive to these two distinct classes of carcinogens.	Tetradecanoylphorbol Acetate	79-82	acrosin	Homo sapiens	40-43