PMC:7426526 / 10771-12024 JSONTXT

{"project":"TEST0","denotations":[{"id":"32849491-156-162-3395799","span":{"begin":156,"end":158},"obj":"[\"30862050\"]"},{"id":"32849491-126-132-3395800","span":{"begin":287,"end":289},"obj":"[\"23807730\"]"},{"id":"32849491-154-160-3395801","span":{"begin":446,"end":448},"obj":"[\"30862050\"]"},{"id":"32849491-158-164-3395802","span":{"begin":450,"end":452},"obj":"[\"23807730\"]"},{"id":"32849491-107-113-3395803","span":{"begin":562,"end":564},"obj":"[\"9212098\"]"},{"id":"32849491-113-119-3395804","span":{"begin":720,"end":722},"obj":"[\"23807730\", \"21251617\", \"27377587\", \"31471945\", \"25621103\"]"},{"id":"32849491-234-239-3395805","span":{"begin":1044,"end":1045},"obj":"[\"11689955\"]"},{"id":"32849491-237-243-3395806","span":{"begin":1047,"end":1049},"obj":"[\"27611934\"]"},{"id":"32849491-194-199-3395807","span":{"begin":1246,"end":1247},"obj":"[\"11689955\"]"},{"id":"32849491-197-203-3395808","span":{"begin":1249,"end":1251},"obj":"[\"27611934\"]"}],"text":"Tumors generated on the basis of CSCs are believed to follow a unidirectional hierarchy, in which only the CSC population is able to initiate tumor growth (51). At the time point of tumor initiation, it is suggested that cancer stem cells divide asymmetrically to maintain the CSC pool (52). These asymmetric divisions generate transient amplifying cells, which are undergoing symmetric divisions; therefore having a high proliferative capacity (51, 52). Based on recent data from hematological cancers (AML), the hierarchical model proposed by Bonnet and Dick (43) is most likely a simplified description. It is now believed that the organization of CSCs (in solid as well as in hematological cancers) is more complex (52–56). In contrast to the CSC model in which only a small subpopulation of cells is able to promote tumor initiation and growth, the clonal evolution model states that genetically unstable cells accumulate genomic and genetic alterations over time causing an increase in tumor aggressiveness, resistance and heterogeneity (5, 57). Both models are not mutually exclusive, which can be explained by the cellular plasticity (plasticity model) that suggests, that different cellular states can interconvert (as explained later) (5, 57)."}

{"project":"MyTest","denotations":[{"id":"32849491-30862050-34970179","span":{"begin":156,"end":158},"obj":"30862050"},{"id":"32849491-23807730-34970180","span":{"begin":287,"end":289},"obj":"23807730"},{"id":"32849491-30862050-34970181","span":{"begin":446,"end":448},"obj":"30862050"},{"id":"32849491-23807730-34970182","span":{"begin":450,"end":452},"obj":"23807730"},{"id":"32849491-9212098-34970183","span":{"begin":562,"end":564},"obj":"9212098"},{"id":"32849491-23807730-34970184","span":{"begin":720,"end":722},"obj":"23807730"},{"id":"32849491-21251617-34970184","span":{"begin":720,"end":722},"obj":"21251617"},{"id":"32849491-27377587-34970184","span":{"begin":720,"end":722},"obj":"27377587"},{"id":"32849491-31471945-34970184","span":{"begin":720,"end":722},"obj":"31471945"},{"id":"32849491-25621103-34970184","span":{"begin":720,"end":722},"obj":"25621103"},{"id":"32849491-11689955-34970185","span":{"begin":1044,"end":1045},"obj":"11689955"},{"id":"32849491-27611934-34970186","span":{"begin":1047,"end":1049},"obj":"27611934"},{"id":"32849491-11689955-34970187","span":{"begin":1246,"end":1247},"obj":"11689955"},{"id":"32849491-27611934-34970188","span":{"begin":1249,"end":1251},"obj":"27611934"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Tumors generated on the basis of CSCs are believed to follow a unidirectional hierarchy, in which only the CSC population is able to initiate tumor growth (51). At the time point of tumor initiation, it is suggested that cancer stem cells divide asymmetrically to maintain the CSC pool (52). These asymmetric divisions generate transient amplifying cells, which are undergoing symmetric divisions; therefore having a high proliferative capacity (51, 52). Based on recent data from hematological cancers (AML), the hierarchical model proposed by Bonnet and Dick (43) is most likely a simplified description. It is now believed that the organization of CSCs (in solid as well as in hematological cancers) is more complex (52–56). In contrast to the CSC model in which only a small subpopulation of cells is able to promote tumor initiation and growth, the clonal evolution model states that genetically unstable cells accumulate genomic and genetic alterations over time causing an increase in tumor aggressiveness, resistance and heterogeneity (5, 57). Both models are not mutually exclusive, which can be explained by the cellular plasticity (plasticity model) that suggests, that different cellular states can interconvert (as explained later) (5, 57)."}

{"project":"2_test","denotations":[{"id":"32849491-30862050-34970179","span":{"begin":156,"end":158},"obj":"30862050"},{"id":"32849491-23807730-34970180","span":{"begin":287,"end":289},"obj":"23807730"},{"id":"32849491-30862050-34970181","span":{"begin":446,"end":448},"obj":"30862050"},{"id":"32849491-23807730-34970182","span":{"begin":450,"end":452},"obj":"23807730"},{"id":"32849491-9212098-34970183","span":{"begin":562,"end":564},"obj":"9212098"},{"id":"32849491-23807730-34970184","span":{"begin":720,"end":722},"obj":"23807730"},{"id":"32849491-21251617-34970184","span":{"begin":720,"end":722},"obj":"21251617"},{"id":"32849491-27377587-34970184","span":{"begin":720,"end":722},"obj":"27377587"},{"id":"32849491-31471945-34970184","span":{"begin":720,"end":722},"obj":"31471945"},{"id":"32849491-25621103-34970184","span":{"begin":720,"end":722},"obj":"25621103"},{"id":"32849491-11689955-34970185","span":{"begin":1044,"end":1045},"obj":"11689955"},{"id":"32849491-27611934-34970186","span":{"begin":1047,"end":1049},"obj":"27611934"},{"id":"32849491-11689955-34970187","span":{"begin":1246,"end":1247},"obj":"11689955"},{"id":"32849491-27611934-34970188","span":{"begin":1249,"end":1251},"obj":"27611934"}],"text":"Tumors generated on the basis of CSCs are believed to follow a unidirectional hierarchy, in which only the CSC population is able to initiate tumor growth (51). At the time point of tumor initiation, it is suggested that cancer stem cells divide asymmetrically to maintain the CSC pool (52). These asymmetric divisions generate transient amplifying cells, which are undergoing symmetric divisions; therefore having a high proliferative capacity (51, 52). Based on recent data from hematological cancers (AML), the hierarchical model proposed by Bonnet and Dick (43) is most likely a simplified description. It is now believed that the organization of CSCs (in solid as well as in hematological cancers) is more complex (52–56). In contrast to the CSC model in which only a small subpopulation of cells is able to promote tumor initiation and growth, the clonal evolution model states that genetically unstable cells accumulate genomic and genetic alterations over time causing an increase in tumor aggressiveness, resistance and heterogeneity (5, 57). Both models are not mutually exclusive, which can be explained by the cellular plasticity (plasticity model) that suggests, that different cellular states can interconvert (as explained later) (5, 57)."}