Datasets:

clinicalnlplab

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HoC_train

like 0

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: BACKGROUND Colorectal cancer is one of the main cancers in the Western world . About 90% of the deaths arise from formation of distant metastasis . The expression of the newly identified gene metastasis associated in colon cancer 1 ( MACC1 ) is a prognostic indicator for colon cancer metastasis . Here , we analyzed for the first time the impact of single nucleotide polymorphisms ( SNPs ) in the coding region of MACC1 for clinical outcome of colorectal cancer patients . Additionally , we screened met proto-oncogene ( Met ) , the transcriptional target gene of MACC1 , for mutations . METHODS We sequenced the coding exons of MACC1 in 154 colorectal tumors ( stages I , II and III ) and the crucial exons of Met in 60 colorectal tumors ( stages I , II and III ) . We analyzed the association of MACC1 polymorphisms with clinical data , including metachronous metastasis , UICC stages , tumor invasion , lymph node metastasis and patients ' survival ( n = 154 , stages I , II and III ) . Furthermore , we performed biological assays in order to evaluate the functional impact of MACC1 SNPs on the motility of colorectal cancer cells . RESULTS We genotyped three MACC1 SNPs in the coding region . Thirteen % of the tumors had the genotype cg ( rs4721888 , L31V ) , 48% a ct genotype ( rs975263 , S515L ) and 84% a gc or cc genotype ( rs3735615 , R804T ) . We found no association of these SNPs with clinicopathological parameters or with patients ' survival , when analyzing the entire patients ' cohort . An increased risk for a shorter metastasis-free survival of patients with a ct genotype ( rs975263 ) was observed in younger colon cancer patients with stage I or II ( P = 0.041 , n = 18 ) . In cell culture , MACC1 SNPs did not affect MACC1-induced cell motility and proliferation . CONCLUSION In summary , the identification of coding MACC1 SNPs in primary colorectal tumors does not improve the prediction for metastasis formation or for patients ' survival compared to MACC1 expression analysis alone . The ct genotype ( rs975263 ) might be associated with a reduced survival for younger colon cancer patients in early stages . However , further studies with larger sample sizes are needed .\n OUTPUT:\n" }, { "from": "agent", "value": "activating invasion and metastasis" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Polycylic aromatic hydrocarbons ( PAHs ) are ubiquitous contaminants in the marine environment . Their toxicity is mainly linked to the ability of marine species to biotransform them into reactive metabolites . PAHs are thus often detected at trace levels in animal tissues . For biomonitoring purposes , this findings have two main consequences , ( i ) the determination of the PAH tissue concentration is not suitable for the evaluation of individual exposure to PAHs ( ii ) it can explain sometimes the lack of correlations obtained with relevant markers of toxicity such as genotoxicity biomarkers . The aim of the present study was to better investigate the link between PAH exposure and genotoxicity in marine flatfish . During a laboratory experiment , juvenile soles were exposed for four weeks to a mixture of three PAHs , namely benzo[a]pyrene , fluoranthene and pyrene , followed by one week of depuration . Fish were exposed via the trophic route to a daily PAH concentration of 120 μg/g food . Fish were sampled at different time points . The bioavailability and the biotransformation of PAHs were assessed by the measurement of biliary metabolites using a sensitive UPLC MS/MS method . The 7-ethoxyresorufine-O-deethylase was also measured in liver subcellular fractions as a biomarker of phase I biotransformation activities . Genotoxicity was assessed in parallel by the measurement of DNA strand breaks in fish erythrocytes by the alkaline comet assay . During this study , the high amount of PAH metabolites produced in sole demonstrated the bioavailability of PAHs and their biotransformation by fish enzymes . A positive correlation was observed between the level of hydroxylated PAH metabolites and genotoxicity as measured by the alkaline comet assay .\n OUTPUT:\n" }, { "from": "agent", "value": "genomic instability and mutation" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: In the present study , post-treatment effects of dietary turmeric on markers related to apoptosis , cell proliferation , and inflammation in 7,12-dimethylbenz(a)anthracene ( DMBA)-induced hamster buccal pouch ( HBP ) tumors were investigated . Tumors were induced by applying 0.5% DMBA topically to the HBP three times per week for 12 weeks . After tumor development , half of the animals continued on the control diet and the other half were shifted to a 1% turmeric diet for 4 weeks . To rule out DMBA discontinuation as a cause of inhibition in tumor growth , DMBA treatment was continued during dietary exposure of turmeric in another set of animals until the end of the experiment . The turmeric diet inhibited tumor growth in animals with or without DMBA carcinogen treatment compared to the animals on the control diet . When compared to hamsters bearing tumors that remained on the control diet , the buccal pouches of hamsters bearing tumors receiving turmeric showed the following results : ( 1 ) decreased cell proliferation ( diminished PCNA , cyclin D1 , and Bcl-2 ) and PCNA labelling index , ( 2 ) enhanced apoptosis ( increased Bax , caspase-3 , caspase-9 , and cytochrome c , and decreased survivin ) and apoptotic index , ( 3 ) decreased inflammation ( decreased Cox-2 ) , and ( 4 ) decreased MAPK activation ( p-ERK and p-p38 ) . These data indicate that tumor growth decreased due to the modulation of cellular pathways associated with cell proliferation and apoptosis .\n OUTPUT:\n" }, { "from": "agent", "value": "resisting cell death;sustaining proliferative signaling;tumor promoting inflammation" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Curcumin , a well-known chemopreventive agent from turmeric , inhibits the expression of several oncogenes and cell proliferation genes in tumor cells . This study aims to understand the precise molecular mechanism by which curcumin exerts its effects on retinoblastoma cells , by performing whole genome microarray analysis to determine the gene expression profiles altered by curcumin treatment . Curcumin suppressed cell viability and altered the cell cycle of retinoblastoma cells . We identified 903 downregulated genes and 1,319 upregulated genes when compared with the control cells after treatment with 20 μM curcumin concentration for 48 h . These genes were grouped into respective functional categories according to their biological function . We found that curcumin regulated the expression of genes that are involved in the regulation of apoptosis , tumor suppressor , cell-cycle arrest , transcription factor , and angiogenesis . Quantitative real-time polymerase chain reaction ( qRT-PCR ) analysis was used to validate the results of genome array , and the results were consistent with the obtained data . In conclusion , treatment of curcumin affects the expression of genes involved in various cellular functions and plays an important role in tumor metastasis and apoptosis . Thus , curcumin might be an effective chemopreventive agent for retinoblastoma cancer .\n OUTPUT:\n" }, { "from": "agent", "value": "inducing angiogenesis;resisting cell death;sustaining proliferative signaling;activating invasion and metastasis" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: The ATM/ATR DNA damage checkpoint functions in the maintenance of genetic stability and some missense variants of the ATM gene have been shown to confer a moderate increased risk of prostate cancer . However , whether inactivation of this checkpoint contributes directly to prostate specific cancer predisposition is still unknown . Here , we show that exposure of non-malignant prostate epithelial cells ( HPr-1AR ) to androgen led to activation of the ATM/ATR DNA damage response and induction of cellular senescence . Notably , knockdown of the ATM gene expression in HPr-1AR cells can promote androgen-induced TMPRSS2 : ERG rearrangement , a prostate-specific chromosome translocation frequently found in prostate cancer cells . Intriguingly , unlike the non-malignant prostate epithelial cells , the ATM/ATR DNA damage checkpoint appears to be defective in prostate cancer cells , since androgen treatment only induced a partial activation of the DNA damage response . This mechanism appears to preserve androgen induced autophosphorylation of ATM and phosphorylation of H2AX , lesion processing and repair pathway yet restrain ATM/CHK1/CHK2 and p53 signaling pathway . Our findings demonstrate that ATM/ATR inactivation is a crucial step in promoting androgen-induced genomic instability and prostate carcinogenesis .\n OUTPUT:\n" }, { "from": "agent", "value": "enabling replicative immortality;genomic instability and mutation" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Trinucleotide repeat ( TNR ) expansions and deletions are associated with human neurodegenerative diseases and prostate cancer . Recent studies have pointed to a linkage between oxidative DNA damage , base excision repair ( BER ) and TNR expansion , which is demonstrated by the observation that DNA polymerase β ( pol β ) gap-filling synthesis acts in concert with alternate flap cleavage by flap endonuclease 1 ( FEN1 ) to mediate CAG repeat expansions . In this study , we provide the first evidence that the repair of a DNA base lesion can also contribute to CAG repeat deletions that were initiated by the formation of hairpins on both the template and the damaged strand of a continuous run of ( CAG)(20 ) or ( CAG)(25 ) repeats . Most important , we found that pol β not only bypassed one part of the large template hairpin but also managed to pass through almost the entire length of small hairpin . The unique hairpin bypass of pol β resulted in large and small deletions in coordination with FEN1 alternate flap cleavage . Our results provide new insight into the role of BER in modulating genome stability that is associated with human diseases .\n OUTPUT:\n" }, { "from": "agent", "value": "genomic instability and mutation" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: Diets rich in fruits and vegetables are associated with lower risk of cancer which may be conferred in part by the antioxidant properties of these foods . However , antioxidant supplementation or increased consumption of antioxidant-rich foods has been reported to have inconsistent effects on DNA damage . The present work ( the DART study ) investigated the extent of inter-individual variation in DNA damage , the capacity for base excision repair ( BER ) and the responses of both variables to supplementation with an antioxidant supplement for 6 weeks . There was a wide inter-individual variation in endogenous lymphocyte DNA strand breaks ( 8-fold variation ) , in damage after a challenge with H2O2 ( 16-fold variation ) and in DNA repair ( 41-fold variation ) measured using the comet assay . When stratified into tertiles according to the pre-supplementation level of endogenous DNA damage , there was a statistically significant decrease in DNA damage after supplementation in the tertile with the highest pre-supplementation level of damage . There was no effect of supplementation on BER . Endogenous DNA damage level before supplementation was significantly different ( P = 0.037 ) between the three genotypes for the Val16Ala single nucleotide polymorphism in manganese superoxide dismutase ( rs4880 ) with individuals homozygous/wild type showing less damage than those carrying the alanine variant .\n OUTPUT:\n" }, { "from": "agent", "value": "genomic instability and mutation" } ]

[ { "from": "human", "value": "The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.\n ###\n INPUT: We found that the human colon cancer cell line SW480 consists of two distinct subpopulations which we have designated E-type ( epithelial ) and R-type ( round ) . Pure cultures of each type were obtained by subcloning , and both have maintained their characteristic phenotypes for at least 1 year ( 40 passages ) . E-type cells are the major ( &gt ; 98% ) type in the parental SW480 cell line . They form flat epithelial-like colonies . In contrast , R-type cells , which constitute a minor fraction ( &lt ; 2% ) of the parental cell line , have a rounded shape and grow in clusters of piled-up cells . Compared to E-type cells or the parental SW480 cells , isolated R-type cells display decreased doubling time , loss of contact inhibition , less adhesiveness to culture plates , higher anchorage-independent growth in soft agar , and a much more aneuploid karyotype . When injected s.c. into nude mice , R-type cells produce much larger tumors within the same period of time than E-type cells , and the tumors are less differentiated than those produced by the E-type cells . Cell fusion experiments between R-type and E-type cells revealed that the R-type phenotype is dominant , and the results suggest that this is due to one or a few genetic changes . Taken together , these findings suggest that the R-type cells represent a more malignant variant of the E-type cells . They may be useful , therefore , for studying mechanisms involved in tumor progression .\n OUTPUT:\n" }, { "from": "agent", "value": "evading growth suppressors" } ]