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: BACKGROUND To investigate the dynamics of inter- and intratumoral molecular alterations during tumor progression in recurrent gliomas . METHODOLOGY/PRINCIPAL FINDINGS To address intertumoral heterogeneity we investigated non-microdissected tumor tissue of 106 gliomas representing 51 recurrent tumors . To address intratumoral heterogeneity a set of 16 gliomas representing 7 tumor pairs with at least one recurrence , and 4 single mixed gliomas were investigated by microdissection of distinct oligodendroglial and astrocytic tumor components . All tumors and tumor components were analyzed for allelic loss of 1p/19q ( LOH 1p/19q ) , for TP53- mutations and for R132 mutations in the IDH1 gene . The investigation of non-microdissected tumor tissue revealed clonality in 75% ( 38/51 ) . Aberrant molecular alterations upon recurrence were detected in 25% ( 13/51). 64% ( 9/14 ) of these were novel and associated with tumor progression . Loss of previously detected alterations was observed in 36% ( 5/14 ) . One tumor pair ( 1/14 ; 7% ) was significant for both . Intratumoral clonality was detected in 57% ( 4/7 ) of the microdissected tumor pairs and in 75% ( 3/4 ) of single microdissected tumors. 43% ( 3/7 ) of tumor pairs and one single tumor ( 25% ) revealed intratumoral heterogeneity . While intratumoral heterogeneity affected both the TP53- mutational status and the LOH1p/19q status , all tumors with intratumoral heterogeneity shared the R132 IDH1- mutation as a common feature in both their microdissected components . CONCLUSIONS/SIGNIFICANCE The majority of recurrent gliomas are of monoclonal origin . However , the detection of divertive tumor cell clones in morphological distinct tumor components sharing IDH1- mutations as early event may provide insight into the tumorigenesis of true mixed gliomas .
    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: BACKGROUND To investigate the dynamics of inter- and intratumoral molecular alterations during tumor progression in recurrent gliomas . METHODOLOGY/PRINCIPAL FINDINGS To address intertumoral heterogeneity we investigated non-microdissected tumor tissue of 106 gliomas representing 51 recurrent tumors . To address intratumoral heterogeneity a set of 16 gliomas representing 7 tumor pairs with at least one recurrence , and 4 single mixed gliomas were investigated by microdissection of distinct oligodendroglial and astrocytic tumor components . All tumors and tumor components were analyzed for allelic loss of 1p/19q ( LOH 1p/19q ) , for TP53- mutations and for R132 mutations in the IDH1 gene . The investigation of non-microdissected tumor tissue revealed clonality in 75% ( 38/51 ) . Aberrant molecular alterations upon recurrence were detected in 25% ( 13/51). 64% ( 9/14 ) of these were novel and associated with tumor progression . Loss of previously detected alterations was observed in 36% ( 5/14 ) . One tumor pair ( 1/14 ; 7% ) was significant for both . Intratumoral clonality was detected in 57% ( 4/7 ) of the microdissected tumor pairs and in 75% ( 3/4 ) of single microdissected tumors. 43% ( 3/7 ) of tumor pairs and one single tumor ( 25% ) revealed intratumoral heterogeneity . While intratumoral heterogeneity affected both the TP53- mutational status and the LOH1p/19q status , all tumors with intratumoral heterogeneity shared the R132 IDH1- mutation as a common feature in both their microdissected components . CONCLUSIONS/SIGNIFICANCE The majority of recurrent gliomas are of monoclonal origin . However , the detection of divertive tumor cell clones in morphological distinct tumor components sharing IDH1- mutations as early event may provide insight into the tumorigenesis of true mixed gliomas .
    OUTPUT:
