human
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.
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    INPUT: BACKGROUND : The p38Î± MAP kinase pathway is involved in inflammation , cell differentiation , growth , apoptosis and production of pro-inflammatory cytokines TNF-Î± and IL-1Î² . The overproduction of these cytokines plays an important role in cancer . The aim of this work was to design a peptide inhibitor on the basis of structural information of the active site of p38Î± . METHODS : A tetrapeptide , VWCS as p38Î± inhibitor was designed on the basis of structural information of the ATP binding site by molecular modeling . The inhibition study of peptide with p38Î± was performed by ELISA , binding study by Surface Plasmon Resonance and anti-proliferative assays by MTT and flow cytometry . RESULTS : The percentage inhibition of designed VWCS against pure p38Î± protein and serum of HNSCC patients was 70.30 and 71.5% , respectively . The biochemical assay demonstrated the K(D) and IC(50) of the selective peptide as 7.22ï¿½10(-9)M and 20.08nM , respectively . The VWCS as inhibitor significantly reduced viability of oral cancer KB cell line with an IC(50) value of 10Î¼M and induced apoptosis by activating Caspase 3 and 7 . CONCLUSIONS : VWCS efficiently interacted at the ATP binding pocket of p38Î± with high potency and can be used as a potent inhibitor in case of HNSCC . GENERAL SIGNIFICANCE : VWCS can act as an anticancer agent as it potentially inhibits the cell growth and induces apoptosis in oral cancer cell-line in a dose as well as time dependent manner . Hence , p38Î± MAP kinase inhibitor can be a potential therapeutic agent for human oral cancer .
    OUTPUT:

agent
resisting cell death
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.
    ###
    INPUT: BACKGROUND : The p38Î± MAP kinase pathway is involved in inflammation , cell differentiation , growth , apoptosis and production of pro-inflammatory cytokines TNF-Î± and IL-1Î² . The overproduction of these cytokines plays an important role in cancer . The aim of this work was to design a peptide inhibitor on the basis of structural information of the active site of p38Î± . METHODS : A tetrapeptide , VWCS as p38Î± inhibitor was designed on the basis of structural information of the ATP binding site by molecular modeling . The inhibition study of peptide with p38Î± was performed by ELISA , binding study by Surface Plasmon Resonance and anti-proliferative assays by MTT and flow cytometry . RESULTS : The percentage inhibition of designed VWCS against pure p38Î± protein and serum of HNSCC patients was 70.30 and 71.5% , respectively . The biochemical assay demonstrated the K(D) and IC(50) of the selective peptide as 7.22ï¿½10(-9)M and 20.08nM , respectively . The VWCS as inhibitor significantly reduced viability of oral cancer KB cell line with an IC(50) value of 10Î¼M and induced apoptosis by activating Caspase 3 and 7 . CONCLUSIONS : VWCS efficiently interacted at the ATP binding pocket of p38Î± with high potency and can be used as a potent inhibitor in case of HNSCC . GENERAL SIGNIFICANCE : VWCS can act as an anticancer agent as it potentially inhibits the cell growth and induces apoptosis in oral cancer cell-line in a dose as well as time dependent manner . Hence , p38Î± MAP kinase inhibitor can be a potential therapeutic agent for human oral cancer .
    OUTPUT:
