HTML Microdata document

This HTML5 document contains 486 embedded RDF statements represented using HTML+Microdata notation.

The embedded RDF content will be recognized by any processor of HTML5 Microdata.

Namespace Prefixes

Prefix	IRI
bibo	http://purl.org/ontology/bibo/
rdf	http://www.w3.org/1999/02/22-rdf-syntax-ns#
n3	http://purl.jp/bio/10/colil/ontology/201303#
n7	http://dx.doi.org/
n2	http://purl.jp/bio/10/colil/id/
n10	http://pubannotation.org/docs/sourcedb/PMC/sourceid/
n5	http://purl.org/spar/doco/
rdfs	http://www.w3.org/2000/01/rdf-schema#
dc	http://purl.org/dc/elements/1.1/
n9	http://togows.dbcls.jp/entry/pubmed/
n11	http://www.ncbi.nlm.nih.gov/pmc/articles/
xsdh	http://www.w3.org/2001/XMLSchema#

Statements

Subject Item: n2:27144340
rdf:type: n3:RelevantPaper n3:ReferencePaper n3:CitationPaper
rdfs:seeAlso: n7:10.18632%2Foncotarget.9120 n9:27144340 n10:0 n11:0
bibo:cites: n2:26341687 n2:20979473 n2:25470694 n2:26075077 n2:24722149 n2:21502504 n2:23695170 n2:18089725 n2:17625570 n2:24199682 n2:25955608 n2:10839993 n2:21795450 n2:15110491 n2:24644001 n2:22215748 n2:15849206 n2:25576294 n2:22701483 n2:25601484 n2:21791641 n2:20458531 n2:22235099 n2:19029956 n2:25228590 n2:24556908 n2:25941796 n2:21474455 n2:22038047 n2:23993685
n3:cocitationWith: n2:26622674 n2:24473757 n2:20573926 n2:22038047 n2:23797762 n2:17473213 n2:25522257 n2:26341687 n2:23362830 n2:27488947 n2:19221498 n2:21415163 n2:23695170 n2:23228696 n2:18439900 n2:25386929 n2:24920786 n2:19822355 n2:26019170 n2:26992204 n2:19508387 n2:29978950 n2:23526220 n2:24898303 n2:26847819 n2:24675041 n2:24644001 n2:24393785 n2:26503334 n2:19949011 n2:11846609 n2:25169538 n2:28586279 n2:23632475 n2:28126333 n2:23470965 n2:20947488 n2:29563138 n2:25352553 n2:24278407 n2:26984042 n2:22500211 n2:23936520 n2:27573756 n2:24351837 n2:25375092 n2:18006825 n2:28045889 n2:24100792 n2:23991948 n2:25504439 n2:15050914 n2:17047074 n2:26630530 n2:22576795 n2:18212742 n2:25624476 n2:26992917 n2:27004404 n2:27432227 n2:25470694
n3:hasRelevantBibliographicResourceOf: _:vb604921136 _:vb604921137 _:vb604921138 _:vb604921139 _:vb604921140 _:vb604921141 _:vb604921142 _:vb604921143 _:vb604921144 _:vb604921145 _:vb604921146 _:vb604921147 _:vb604921148 _:vb604921149 _:vb604921150 _:vb604921151 _:vb604921120 _:vb604921121 _:vb604921122 _:vb604921123 _:vb604921124 _:vb604921125 _:vb604921126 _:vb604921127 _:vb604921128 _:vb604921129 _:vb604921130 _:vb604921131 _:vb604921132 _:vb604921133 _:vb604921134 _:vb604921135 _:vb604921111 _:vb604921112 _:vb604921113 _:vb604921114 _:vb604921115 _:vb604921116 _:vb604921117 _:vb604921118 _:vb604921119 _:vb604921168 _:vb604921169 _:vb604921170 _:vb604921171 _:vb604921152 _:vb604921153 _:vb604921154 _:vb604921155 _:vb604921156 _:vb604921157 _:vb604921158 _:vb604921159 _:vb604921160 _:vb604921161 _:vb604921162 _:vb604921163 _:vb604921164 _:vb604921165 _:vb604921166 _:vb604921167
n3:pmcid: PMC0
bibo:doi: 10.18632%2Foncotarget.9120
n5:contains: _:vb51322663 _:vb51322667 _:vb51322669 _:vb51322646

Subject Item: _:vb51322646
rdf:type: n5:Section
dc:title: introduction
n5:contains: _:vb51322660 _:vb51322661 _:vb51322662 _:vb51322656 _:vb51322657 _:vb51322658 _:vb51322659 _:vb51322652 _:vb51322653 _:vb51322654 _:vb51322655 _:vb51322648 _:vb51322649 _:vb51322650 _:vb51322651 _:vb51322647

Subject Item: _:vb51322647
rdf:type: n3:Context
rdf:value: Genomic alterations in the anaplastic lymphoma kinase (ALK) gene are found in numerous malignancies [>>1<<]. ALK rearrangements, first discovered by Soda et al. in 2007 [2], are either inversions or translocations of the ALK-tyrosine kinase (-TK) receptor gene with other fusion partners.
n3:mentions: n2:21474455

Subject Item: _:vb51322648
rdf:type: n3:Context
rdf:value: ALK rearrangements, first discovered by Soda et al. in 2007 [>>2<<], are either inversions or translocations of the ALK-tyrosine kinase (-TK) receptor gene with other fusion partners.
n3:mentions: n2:17625570

Subject Item: _:vb51322649
rdf:type: n3:Context
rdf:value: The expression of the echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion oncogene, which is caused by a small inversion within chromosome 2p, was found in non-small cell lung cancer (NSCLC) [>>2<<]. The product of the ALK rearrangement consists of a constitutively activated receptor TK with pro-oncogenic effects [3]. Consequently, tumors with ALK rearrangements are associated with ALK signaling, thus being effectively inhibited by
n3:mentions: n2:17625570

Subject Item: _:vb51322650
rdf:type: n3:Context
rdf:value: The product of the ALK rearrangement consists of a constitutively activated receptor TK with pro-oncogenic effects [>>3<<]. Consequently, tumors with ALK rearrangements are associated with ALK signaling, thus being effectively inhibited by small molecules ALK-TK inhibitors (-TKIs).
n3:mentions: n2:24722149

Subject Item: _:vb51322651
rdf:type: n3:Context
rdf:value: Crizotinib is a multitargeted TKI with activity against MET, ALK, and ROS1 [>>4<<, 5]. This active substance has been found to greatly outperform the best chemotherapy agents in NSCLC patients with ALK rearrangements [6, 7].
n3:mentions: n2:22215748

Subject Item: _:vb51322652
rdf:type: n3:Context
rdf:value: Crizotinib is a multitargeted TKI with activity against MET, ALK, and ROS1 [4, >>5<<]. This active substance has been found to greatly outperform the best chemotherapy agents in NSCLC patients with ALK rearrangements [6, 7].
n3:mentions: n2:18089725

Subject Item: _:vb51322653
rdf:type: n3:Context
rdf:value: This active substance has been found to greatly outperform the best chemotherapy agents in NSCLC patients with ALK rearrangements [>>6<<, 7]. Recently, the PROFILE 1014 study demonstrated that crizotinib significantly improved PFS and ORR in the first-line treatment for ALK-positive NSCLC patients, with an acceptable safety profile, thus establishing crizotinib as a
n3:mentions: n2:25576294

Subject Item: _:vb51322654
rdf:type: n3:Context
rdf:value: This active substance has been found to greatly outperform the best chemotherapy agents in NSCLC patients with ALK rearrangements [6, >>7<<]. Recently, the PROFILE 1014 study demonstrated that crizotinib significantly improved PFS and ORR in the first-line treatment for ALK-positive NSCLC patients, with an acceptable safety profile, thus establishing crizotinib as a standard
n3:mentions: n2:25601484

Subject Item: _:vb51322655
rdf:type: n3:Context
rdf:value: significantly improved PFS and ORR in the first-line treatment for ALK-positive NSCLC patients, with an acceptable safety profile, thus establishing crizotinib as a standard of care for previously untreated ALK-positive patients [>>8<<]. However, acquired resistance eventually develops in most patients. Two main mechanisms of crizotinib resistance have been reported.
n3:mentions: n2:25470694

Subject Item: _:vb51322656
rdf:type: n3:Context
rdf:value: The other mechanism is activation of alternative signaling pathways, including the development of EGFR mutations or activation of the wild-type EGFR, HER2-, or KIT-receptors [>>9<<–12]. Thus, innovative treatment strategies are urgently needed to overcome therapeutic resistance to crizotinib to improve the survival of NSCLC patients.
n3:mentions: n2:21791641 n2:25941796 n2:22235099

Subject Item: _:vb51322657
rdf:type: n3:Context
rdf:value: Gatekeeper mutations, such as L1196M, L1152R, C1156Y, and F1174L hinder drug binding and are frequently detected in crizotinib-resistant samples [>>13<<, 14]. Besides, the IGF-1R signaling pathway is involved in crizotinib resistance. In a previous study, the addition of IGF-1 induced resistance to the inhibitory effects of crizotinib on growth. Chronic ALK inhibition was associated with
n3:mentions: n2:20979473

Subject Item: _:vb51322658
rdf:type: n3:Context
rdf:value: Gatekeeper mutations, such as L1196M, L1152R, C1156Y, and F1174L hinder drug binding and are frequently detected in crizotinib-resistant samples [13, >>14<<]. Besides, the IGF-1R signaling pathway is involved in crizotinib resistance. In a previous study, the addition of IGF-1 induced resistance to the inhibitory effects of crizotinib on growth. Chronic ALK inhibition was associated with
n3:mentions: n2:21502504

Subject Item: _:vb51322659
rdf:type: n3:Context
rdf:value: Metformin has aroused keen interest as a potential anticancer agent ever since the report was published of the clinical evidence that the cancer risk and mortality were reduced in diabetics who received metformin [>>16<<]. Previously, we reported that metformin in combination with gefitinib or erlotinib had a synergistic inhibitory effect on the proliferation, migration, and invasion of cell lines resistant to EGFR-TKIs (epidermal growth factor
n3:mentions: n2:15849206

Subject Item: _:vb51322660
rdf:type: n3:Context
rdf:value: metformin in combination with gefitinib or erlotinib had a synergistic inhibitory effect on the proliferation, migration, and invasion of cell lines resistant to EGFR-TKIs (epidermal growth factor receptor-tyrosine kinase inhibitors) [>>17<<]. However, it remains unknown whether metformin may overcome crizotinib resistance.
n3:mentions: n2:24644001

Subject Item: _:vb51322661
rdf:type: n3:Context
rdf:value: Interestingly, metformin has been found to exert an inhibitory effect on IGF-1R signaling [>>18<<, 19], which encouraged us to perform the present study aimed at investigating whether metformin could restore crizotinib sensitivity in crizotinib-resistant cells through inhibition of the IGF-1R signaling pathway.
n3:mentions: n2:19029956

Subject Item: _:vb51322662
rdf:type: n3:Context
rdf:value: Interestingly, metformin has been found to exert an inhibitory effect on IGF-1R signaling [18, >>19<<], which encouraged us to perform the present study aimed at investigating whether metformin could restore crizotinib sensitivity in crizotinib-resistant cells through inhibition of the IGF-1R signaling pathway.
n3:mentions: n2:22038047

Subject Item: _:vb51322663
rdf:type: n5:Section
dc:title: materials and methods
n5:contains: _:vb51322664 _:vb51322665 _:vb51322666

Subject Item: _:vb51322664
rdf:type: n3:Context
rdf:value: Crizotinib-resistant cell lines were generated as previously reported [>>33<<]. Generally, parental cells were cultured with increasing concentrations of crizotinib.
n3:mentions: n2:23993685

Subject Item: _:vb51322665
rdf:type: n3:Context
rdf:value: The relative cell invasion index was calculated as reported previously [>>17<<]. Triplicate samples of 2 × 104 cells treated as indicated were seeded into the upper well in serum-free medium and incubated with 10% FBS in the lower chambers.
n3:mentions: n2:24644001

Subject Item: _:vb51322666
rdf:type: n3:Context
rdf:value: The detailed procedures of colony formation assay were described previously [>>34<<]. Briefly, 500 cells were resuspended in culture medium and seeded in six-well plates.
n3:mentions: n2:25955608

Subject Item: _:vb51322667
rdf:type: n5:Section
dc:title: results
n5:contains: _:vb51322668

Subject Item: _:vb51322668
rdf:type: n3:Context
rdf:value: It was reported that metformin disrupted mitochondrial respiration, which then increased the intracellular ratio of AMP: ATP and induced activation of AMPK [>>20<<]. We thus analyzed the activation of AMPK caused by the metformin treatment. The results showed that metformin alone or in combination significantly stimulated the activation of AMPK (Figure 3). Taken together, these data suggest that
n3:mentions: n2:10839993

Subject Item: _:vb51322669
rdf:type: n5:Section
dc:title: discussion
n5:contains: _:vb51322672 _:vb51322673 _:vb51322674 _:vb51322675 _:vb51322676 _:vb51322677 _:vb51322678 _:vb51322679 _:vb51322680 _:vb51322681 _:vb51322670 _:vb51322671

Subject Item: _:vb51322670
rdf:type: n3:Context
rdf:value: A combination of crizotinib with pemetrexed, or a targeted agent, such as an Hsp90 inhibitor, is currently being tested in clinical trials in ALK-positive advanced NSCLCs [>>7<<]. In the present study, we also adopted this approach, by using metformin in combination with crizotinib. As expected, the addition of metformin enhanced the sensitivity of H2228 and H3122 cells to crizotinib. Moreover, in the
n3:mentions: n2:25601484

Subject Item: _:vb51322671
rdf:type: n3:Context
rdf:value: In lung cancer patients with diabetes, meta-analysis showed that the use of metformin improved survival [>>22<<]. A retrospective study from our group showed that in advanced NSCLC patients with type 2 diabetes, metformin together with EGFR-TKI resulted in longer PFS and OS [23]. Metformin can target cancer stem cells, which are hypothesized to be
n3:mentions: n2:26075077

Subject Item: _:vb51322672
rdf:type: n3:Context
rdf:value: A retrospective study from our group showed that in advanced NSCLC patients with type 2 diabetes, metformin together with EGFR-TKI resulted in longer PFS and OS [>>23<<]. Metformin can target cancer stem cells, which are hypothesized to be critical initiators of cancers [24]. In HER2-positive carcinomas, metformin in combination with the anti-HER2 monoclonal antibody trastuzumab could synergistically
n3:mentions: n2:26341687

Subject Item: _:vb51322673
rdf:type: n3:Context
rdf:value: Metformin can target cancer stem cells, which are hypothesized to be critical initiators of cancers [>>24<<]. In HER2-positive carcinomas, metformin in combination with the anti-HER2 monoclonal antibody trastuzumab could synergistically suppress the self-renewal and proliferation of cancer stem/progenitor cells [25]. Metformin is also involved
n3:mentions: n2:22701483

Subject Item: _:vb51322674
rdf:type: n3:Context
rdf:value: In HER2-positive carcinomas, metformin in combination with the anti-HER2 monoclonal antibody trastuzumab could synergistically suppress the self-renewal and proliferation of cancer stem/progenitor cells [>>25<<]. Metformin is also involved in the targeted therapy of NSCLCs. Previously, we and other researchers reported that metformin in combination with EGFR-TKIs erlotinib or gefitinib had a synergistic inhibitory effect on the proliferation,
n3:mentions: n2:20458531

Subject Item: _:vb51322675
rdf:type: n3:Context
rdf:value: Previously, we and other researchers reported that metformin in combination with EGFR-TKIs erlotinib or gefitinib had a synergistic inhibitory effect on the proliferation, migration, and invasion of cell lines resistant to TKIs [>>17<<, 26]. Taken together, data from the current study suggest that metformin, in combination with crizotinib, has the promising potential of turning into a novel anti-cancer agent that enhances the effect of crizotinib.
n3:mentions: n2:24644001

Subject Item: _:vb51322676
rdf:type: n3:Context
rdf:value: Previously, we and other researchers reported that metformin in combination with EGFR-TKIs erlotinib or gefitinib had a synergistic inhibitory effect on the proliferation, migration, and invasion of cell lines resistant to TKIs [17, >>26<<]. Taken together, data from the current study suggest that metformin, in combination with crizotinib, has the promising potential of turning into a novel anti-cancer agent that enhances the effect of crizotinib.
n3:mentions: n2:23695170

Subject Item: _:vb51322677
rdf:type: n3:Context
rdf:value: The levels of IGF-1 appear to correlate with cancer risk in human populations [>>27<<], and the high contents of IGF-1 are associated with increased mortality in the general population [28].
n3:mentions: n2:15110491

Subject Item: _:vb51322678
rdf:type: n3:Context
rdf:value: The levels of IGF-1 appear to correlate with cancer risk in human populations [27], and the high contents of IGF-1 are associated with increased mortality in the general population [>>28<<]. Elevated IGF-1 concentrations were observed in patients who had taken crizotinib [29]. The amounts of IGF-1R were greater in tumor biopsies taken at the time of acquired resistance when compared to those obtained from the respective
n3:mentions: n2:21795450

Subject Item: _:vb51322679
rdf:type: n3:Context
rdf:value: The downstream signaling pathway, Akt/mTOR/S6 kinase pathway, was also associated with crizotinib resistance [>>30<<]. The activation of the mTOR pathway was related to increased autophagy of the ALK receptor, leading to a weakened response to crizotinib treatment [31]. A synergistic in vitro growth inhibitory effect was established when an ALK
n3:mentions: n2:25228590

Subject Item: _:vb51322680
rdf:type: n3:Context
rdf:value: The activation of the mTOR pathway was related to increased autophagy of the ALK receptor, leading to a weakened response to crizotinib treatment [>>31<<]. A synergistic in vitro growth inhibitory effect was established when an ALK inhibitor was combined with an mTOR inhibitor [32]. Thus, we investigated whether metformin overcomes crizotinib resistance through the inhibition of the IGF-1R
n3:mentions: n2:24556908

Subject Item: _:vb51322681
rdf:type: n3:Context
rdf:value: A synergistic in vitro growth inhibitory effect was established when an ALK inhibitor was combined with an mTOR inhibitor [>>32<<]. Thus, we investigated whether metformin overcomes crizotinib resistance through the inhibition of the IGF-1R signaling pathway.
n3:mentions: n2:24199682

Subject Item: _:vb604921111
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 6
n3:hasRelevantPaperId: n2:24644001

Subject Item: _:vb604921112
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 4
n3:hasRelevantPaperId: n2:24473757

Subject Item: _:vb604921113
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:27432227

Subject Item: _:vb604921114
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:23526220

Subject Item: _:vb604921115
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:22038047

Subject Item: _:vb604921116
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:23695170

Subject Item: _:vb604921117
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:28586279

Subject Item: _:vb604921118
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:25375092

Subject Item: _:vb604921119
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 3
n3:hasRelevantPaperId: n2:25470694

Subject Item: _:vb604921120
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:11846609

Subject Item: _:vb604921121
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26992917

Subject Item: _:vb604921122
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:15050914

Subject Item: _:vb604921123
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26622674

Subject Item: _:vb604921124
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26847819

Subject Item: _:vb604921125
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:17473213

Subject Item: _:vb604921126
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:25386929

Subject Item: _:vb604921127
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:25504439

Subject Item: _:vb604921128
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23797762

Subject Item: _:vb604921129
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:19822355

Subject Item: _:vb604921130
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:27004404

Subject Item: _:vb604921131
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:18006825

Subject Item: _:vb604921132
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:25522257

Subject Item: _:vb604921133
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26503334

Subject Item: _:vb604921134
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:25624476

Subject Item: _:vb604921135
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23228696

Subject Item: _:vb604921136
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23936520

Subject Item: _:vb604921137
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24393785

Subject Item: _:vb604921138
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24898303

Subject Item: _:vb604921139
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26341687

Subject Item: _:vb604921140
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26630530

Subject Item: _:vb604921141
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:22576795

Subject Item: _:vb604921142
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23632475

Subject Item: _:vb604921143
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:17047074

Subject Item: _:vb604921144
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:20947488

Subject Item: _:vb604921145
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23362830

Subject Item: _:vb604921146
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24100792

Subject Item: _:vb604921147
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:27488947

Subject Item: _:vb604921148
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23470965

Subject Item: _:vb604921149
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24278407

Subject Item: _:vb604921150
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:27573756

Subject Item: _:vb604921151
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:25169538

Subject Item: _:vb604921152
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:28045889

Subject Item: _:vb604921153
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:29978950

Subject Item: _:vb604921154
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24920786

Subject Item: _:vb604921155
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26019170

Subject Item: _:vb604921156
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:19949011

Subject Item: _:vb604921157
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:18439900

Subject Item: _:vb604921158
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:21415163

Subject Item: _:vb604921159
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:23991948

Subject Item: _:vb604921160
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:22500211

Subject Item: _:vb604921161
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:28126333

Subject Item: _:vb604921162
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:19221498

Subject Item: _:vb604921163
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:25352553

Subject Item: _:vb604921164
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26984042

Subject Item: _:vb604921165
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:18212742

Subject Item: _:vb604921166
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:19508387

Subject Item: _:vb604921167
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24675041

Subject Item: _:vb604921168
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:29563138

Subject Item: _:vb604921169
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:20573926

Subject Item: _:vb604921170
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:24351837

Subject Item: _:vb604921171
rdf:type: n3:RelevantBibliographicResource
n3:RelevantScore: 2
n3:hasRelevantPaperId: n2:26992204