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.
    ###
    INPUT: Class switch recombination ( CSR ) in B lymphocytes is initiated by introduction of multiple DNA double-strand breaks ( DSBs ) into switch ( S ) regions that flank immunoglobulin heavy chain ( IgH ) constant region exons . CSR is completed by joining a DSB in the donor S mu to a DSB in a downstream acceptor S region ( e.g. , S gamma1 ) by end-joining . In normal cells , many CSR junctions are mediated by classical nonhomologous end-joining ( C-NHEJ ) , which employs the Ku70/80 complex for DSB recognition and XRCC4/DNA ligase 4 for ligation . Alternative end-joining ( A-EJ ) mediates CSR , at reduced levels , in the absence of C-NHEJ , even in combined absence of Ku70 and ligase 4 , demonstrating an A-EJ pathway totally distinct from C-NHEJ . Multiple DSBs are introduced into S mu during CSR , with some being rejoined or joined to each other to generate internal switch deletions ( ISDs ) . In addition , S-region DSBs can be joined to other chromosomes to generate translocations , the level of which is increased by absence of a single C-NHEJ component ( e.g. , XRCC4 ) . We asked whether ISD and S-region translocations occur in the complete absence of C-NHEJ ( e.g. , in Ku70/ligase 4 double-deficient B cells ) . We found , unexpectedly , that B-cell activation for CSR generates substantial ISD in both S mu and S gamma1 and that ISD in both is greatly increased by the absence of C-NHEJ . IgH chromosomal translocations to the c-myc oncogene also are augmented in the combined absence of Ku70 and ligase 4 . We discuss the implications of these findings for A-EJ in normal and abnormal DSB repair .
    OUTPUT:

agent
genomic instability and mutation
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: Class switch recombination ( CSR ) in B lymphocytes is initiated by introduction of multiple DNA double-strand breaks ( DSBs ) into switch ( S ) regions that flank immunoglobulin heavy chain ( IgH ) constant region exons . CSR is completed by joining a DSB in the donor S mu to a DSB in a downstream acceptor S region ( e.g. , S gamma1 ) by end-joining . In normal cells , many CSR junctions are mediated by classical nonhomologous end-joining ( C-NHEJ ) , which employs the Ku70/80 complex for DSB recognition and XRCC4/DNA ligase 4 for ligation . Alternative end-joining ( A-EJ ) mediates CSR , at reduced levels , in the absence of C-NHEJ , even in combined absence of Ku70 and ligase 4 , demonstrating an A-EJ pathway totally distinct from C-NHEJ . Multiple DSBs are introduced into S mu during CSR , with some being rejoined or joined to each other to generate internal switch deletions ( ISDs ) . In addition , S-region DSBs can be joined to other chromosomes to generate translocations , the level of which is increased by absence of a single C-NHEJ component ( e.g. , XRCC4 ) . We asked whether ISD and S-region translocations occur in the complete absence of C-NHEJ ( e.g. , in Ku70/ligase 4 double-deficient B cells ) . We found , unexpectedly , that B-cell activation for CSR generates substantial ISD in both S mu and S gamma1 and that ISD in both is greatly increased by the absence of C-NHEJ . IgH chromosomal translocations to the c-myc oncogene also are augmented in the combined absence of Ku70 and ligase 4 . We discuss the implications of these findings for A-EJ in normal and abnormal DSB repair .
    OUTPUT:
