PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23868065-0	2013	Glucose starvation induces cell death in K-ras-transformed cells by interfering with the hexosamine biosynthesis pathway and activating the unfolded protein response.	Hexosamines	89-99	KRAS proto-oncogene, GTPase	Homo sapiens	41-46	
32300895-6	2020	RESULTS: CRC cells carrying distinct KRAS mutations exhibited differential metabolic remodelling, including differences in glycolysis, glutamine utilization and in amino acid, nucleotide and hexosamine metabolism.	Hexosamines	191-201	KRAS proto-oncogene, GTPase	Homo sapiens	37-41	
35011738-2	2022	In a previous study, we showed that murine KRAS/LKB1 co-mutant tumors and human co-mutant cancer cells have an enhanced dependence on glutamine-fructose-6-phosphate transaminase 2 (GFPT2), a rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP), which could be targeted to reduce survival of KRAS/LKB1 co-mutants.	Hexosamines	219-229	KRAS proto-oncogene, GTPase	Homo sapiens	304-308	
33257855-4	2020	Metabolomics and gene expression profiling pointed towards activation of the hexosamine biosynthesis pathway (HBP), another nitrogen-related metabolic pathway, in both mouse and human KRAS/LKB1 co-mutant tumours.	Hexosamines	77-87	KRAS proto-oncogene, GTPase	Homo sapiens	184-188