HTML Microdata document

This HTML5 document contains 843 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
rdfs	http://www.w3.org/2000/01/rdf-schema#
bibo	http://purl.org/ontology/bibo/
n8	http://pubannotation.org/docs/sourcedb/PMC/sourceid/
n11	http://togows.dbcls.jp/entry/pubmed/
xsdh	http://www.w3.org/2001/XMLSchema#
n3	http://purl.jp/bio/10/colil/id/
n6	http://dx.doi.org/
n2	http://purl.jp/bio/10/colil/ontology/201303#
n10	http://purl.org/spar/doco/
n9	http://www.ncbi.nlm.nih.gov/pmc/articles/
dc	http://purl.org/dc/elements/1.1/
rdf	http://www.w3.org/1999/02/22-rdf-syntax-ns#

Statements

Subject Item: n3:21996748
rdf:type: n2:CitationPaper n2:RelevantPaper n2:ReferencePaper
rdfs:seeAlso: n6:10.1038%2Fonc.2011.430 n8:0 n9:0 n11:21996748
bibo:cites: n3:12062090 n3:12000726 n3:19732411 n3:11106655 n3:10593896 n3:16585505 n3:19460966 n3:21286374 n3:18245495 n3:14681207 n3:1705486 n3:10505759 n3:12719525 n3:12496364 n3:18064304 n3:16286510 n3:12605716 n3:17534898 n3:19047086 n3:11751630 n3:9802880 n3:16452201 n3:12490294 n3:17655922 n3:17639039 n3:18829522 n3:15150118 n3:3593682 n3:19028870 n3:11454708 n3:16869739 n3:9334313 n3:11710818 n3:21685461 n3:11555612 n3:12556241 n3:17903452 n3:14706336 n3:19412433 n3:12467210 n3:19147554 n3:10196157 n3:1698952
n2:cocitationWith: n3:19574223 n3:28440066 n3:21690215 n3:26289314 n3:20840587 n3:28233416 n3:27313791 n3:25118277 n3:29254156 n3:8252621 n3:15894267 n3:29721179 n3:12591930 n3:17126425 n3:23471984 n3:20824144 n3:26106858 n3:25727148 n3:21613822 n3:26482785 n3:25270552 n3:24496449 n3:15297422 n3:28739923 n3:23752186 n3:17016645 n3:23103869 n3:20966025 n3:24185138 n3:23846917 n3:12373287 n3:23270819 n3:22467855 n3:17337080 n3:23446997 n3:10505759 n3:29245923 n3:15249209 n3:23741253 n3:20981102 n3:20427809 n3:16789792 n3:18505598 n3:26021314 n3:9712917 n3:18064304 n3:18039136 n3:28848451 n3:26389634 n3:20610624 n3:27004211 n3:27310703 n3:22975374 n3:22975375 n3:1850375 n3:21586612 n3:24840647 n3:29672570 n3:17460664 n3:24412155 n3:9371521 n3:28602885 n3:9802880 n3:26057990 n3:16723715 n3:30352677 n3:21155971 n3:24736782 n3:24755488 n3:23951320 n3:10872425 n3:28575679 n3:11454708 n3:27461391 n3:30730015 n3:30358133 n3:16072037 n3:23592772 n3:23691363 n3:11555612 n3:11846609 n3:28510121 n3:16024626 n3:11518720 n3:31355137 n3:22402744 n3:14706336 n3:18772397 n3:24463821 n3:17249709 n3:23151657 n3:23624389 n3:16557279 n3:21625220 n3:28232049 n3:10402475 n3:30204432 n3:25595436 n3:24101524 n3:26332121 n3:16823988 n3:23726834 n3:10962434
n2:hasRelevantBibliographicResourceOf: _:vb475014660 _:vb475014661 _:vb475014662 _:vb475014663 _:vb475014656 _:vb475014657 _:vb475014658 _:vb475014659 _:vb475014668 _:vb475014669 _:vb475014670 _:vb475014671 _:vb475014664 _:vb475014665 _:vb475014666 _:vb475014667 _:vb475014676 _:vb475014677 _:vb475014678 _:vb475014679 _:vb475014672 _:vb475014673 _:vb475014674 _:vb475014675 _:vb475014684 _:vb475014685 _:vb475014686 _:vb475014687 _:vb475014680 _:vb475014681 _:vb475014682 _:vb475014683 _:vb475014692 _:vb475014693 _:vb475014694 _:vb475014695 _:vb475014688 _:vb475014689 _:vb475014690 _:vb475014691 _:vb475014700 _:vb475014701 _:vb475014702 _:vb475014703 _:vb475014696 _:vb475014697 _:vb475014698 _:vb475014699 _:vb475014708 _:vb475014709 _:vb475014710 _:vb475014711 _:vb475014704 _:vb475014705 _:vb475014706 _:vb475014707 _:vb475014716 _:vb475014717 _:vb475014718 _:vb475014719 _:vb475014712 _:vb475014713 _:vb475014714 _:vb475014715 _:vb475014724 _:vb475014725 _:vb475014726 _:vb475014727 _:vb475014720 _:vb475014721 _:vb475014722 _:vb475014723 _:vb475014732 _:vb475014733 _:vb475014734 _:vb475014735 _:vb475014728 _:vb475014729 _:vb475014730 _:vb475014731 _:vb475014740 _:vb475014741 _:vb475014742 _:vb475014743 _:vb475014736 _:vb475014737 _:vb475014738 _:vb475014739 _:vb475014748 _:vb475014749 _:vb475014750 _:vb475014751 _:vb475014744 _:vb475014745 _:vb475014746 _:vb475014747 _:vb475014652 _:vb475014653 _:vb475014654 _:vb475014655 _:vb475014649 _:vb475014650 _:vb475014651
n2:pmcid: PMC0
bibo:doi: 10.1038%2Fonc.2011.430
n10:contains: _:vb12915069 _:vb12915088 _:vb12915109 _:vb12915105

Subject Item: _:vb12915069
rdf:type: n10:Section
dc:title: introduction
n10:contains: _:vb12915070 _:vb12915071 _:vb12915072 _:vb12915073 _:vb12915074 _:vb12915075 _:vb12915076 _:vb12915077 _:vb12915078 _:vb12915079 _:vb12915080 _:vb12915081 _:vb12915082 _:vb12915083 _:vb12915084 _:vb12915085 _:vb12915086 _:vb12915087

Subject Item: _:vb12915070
rdf:type: n2:Context
rdf:value: Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy that is the fourth leading cause of cancer death in the United States, with an overall five year survival rate of less than six percent (Siegel et al >>2011<<). PDAC exhibits a wide range of genetic and epigenetic alterations including a high frequency (90-95%) of activating Kras mutations, homozygous deletion (85%) and epigenetic silencing (15%) of the tumor suppressor genes p16INK4A/p14ARF
n2:mentions: n3:21685461

Subject Item: _:vb12915071
rdf:type: n2:Context
rdf:value: (90-95%) of activating Kras mutations, homozygous deletion (85%) and epigenetic silencing (15%) of the tumor suppressor genes p16INK4A/p14ARF (INK4A), as well as an over-abundance of heparin binding growth factors (HBGFs) (Korc >>2003<<, Schneider and Schmid 2003).
n2:mentions: n3:12556241

Subject Item: _:vb12915072
rdf:type: n2:Context
rdf:value: Kras mutations, homozygous deletion (85%) and epigenetic silencing (15%) of the tumor suppressor genes p16INK4A/p14ARF (INK4A), as well as an over-abundance of heparin binding growth factors (HBGFs) (Korc 2003, Schneider and Schmid >>2003<<). In spite of an improved understanding of these molecular alterations, there is a high incidence of treatment failure in PDAC, due, in part, to the resistance of pancreatic cancer cells to chemotherapy and radiotherapy (Kleeff et al
n2:mentions: n3:12605716

Subject Item: _:vb12915073
rdf:type: n2:Context
rdf:value: In spite of an improved understanding of these molecular alterations, there is a high incidence of treatment failure in PDAC, due, in part, to the resistance of pancreatic cancer cells to chemotherapy and radiotherapy (Kleeff et al >>2007<<, Korc 2007, Schneider and Schmid 2003).
n2:mentions: n3:17534898

Subject Item: _:vb12915074
rdf:type: n2:Context
rdf:value: of an improved understanding of these molecular alterations, there is a high incidence of treatment failure in PDAC, due, in part, to the resistance of pancreatic cancer cells to chemotherapy and radiotherapy (Kleeff et al 2007, Korc >>2007<<, Schneider and Schmid 2003).
n2:mentions: n3:17903452

Subject Item: _:vb12915075
rdf:type: n2:Context
rdf:value: of these molecular alterations, there is a high incidence of treatment failure in PDAC, due, in part, to the resistance of pancreatic cancer cells to chemotherapy and radiotherapy (Kleeff et al 2007, Korc 2007, Schneider and Schmid >>2003<<).
n2:mentions: n3:12605716

Subject Item: _:vb12915076
rdf:type: n2:Context
rdf:value: factor-2 (FGF-2), vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF), and hepatocyte growth factor (HGF) require the presence of the co-receptor glypican-1 (GPC1) for efficient signaling (Berman et al >>1999<<, Chen and Lander 2001, Gengrinovitch et al 1999). GPC1 is a heparin sulfate proteoglycan (HSPG) that is attached to the plasma membrane of epithelial and stromal cells via a glycosylphophatidylinositol (GPI) anchor.
n2:mentions: n3:10593896

Subject Item: _:vb12915077
rdf:type: n2:Context
rdf:value: vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF), and hepatocyte growth factor (HGF) require the presence of the co-receptor glypican-1 (GPC1) for efficient signaling (Berman et al 1999, Chen and Lander >>2001<<, Gengrinovitch et al 1999). GPC1 is a heparin sulfate proteoglycan (HSPG) that is attached to the plasma membrane of epithelial and stromal cells via a glycosylphophatidylinositol (GPI) anchor.
n2:mentions: n3:11106655

Subject Item: _:vb12915078
rdf:type: n2:Context
rdf:value: factor (VEGF), platelet derived growth factor (PDGF), and hepatocyte growth factor (HGF) require the presence of the co-receptor glypican-1 (GPC1) for efficient signaling (Berman et al 1999, Chen and Lander 2001, Gengrinovitch et al >>1999<<). GPC1 is a heparin sulfate proteoglycan (HSPG) that is attached to the plasma membrane of epithelial and stromal cells via a glycosylphophatidylinositol (GPI) anchor.
n2:mentions: n3:10196157

Subject Item: _:vb12915079
rdf:type: n2:Context
rdf:value: GPC1, in conjunction with HBGFs, plays a critical role in cell growth, differentiation, adhesion, and, possibly, malignant transformation (Aikawa et al >>2008<<, Blackhall et al 2001, Chen and Lander 2001, Kleeff et al 1998).
n2:mentions: n3:18064304

Subject Item: _:vb12915080
rdf:type: n2:Context
rdf:value: GPC1, in conjunction with HBGFs, plays a critical role in cell growth, differentiation, adhesion, and, possibly, malignant transformation (Aikawa et al 2008, Blackhall et al >>2001<<, Chen and Lander 2001, Kleeff et al 1998).
n2:mentions: n3:11710818

Subject Item: _:vb12915081
rdf:type: n2:Context
rdf:value: GPC1, in conjunction with HBGFs, plays a critical role in cell growth, differentiation, adhesion, and, possibly, malignant transformation (Aikawa et al 2008, Blackhall et al 2001, Chen and Lander >>2001<<, Kleeff et al 1998).
n2:mentions: n3:11106655

Subject Item: _:vb12915082
rdf:type: n2:Context
rdf:value: GPC1, in conjunction with HBGFs, plays a critical role in cell growth, differentiation, adhesion, and, possibly, malignant transformation (Aikawa et al 2008, Blackhall et al 2001, Chen and Lander 2001, Kleeff et al >>1998<<). GPC1 is overexpressed in PDAC and is required for efficient heparin binding growth factor signaling (Aikawa et al 2008, Kleeff et al 1998, Kleeff et al 1999).
n2:mentions: n3:9802880

Subject Item: _:vb12915083
rdf:type: n2:Context
rdf:value: GPC1 is overexpressed in PDAC and is required for efficient heparin binding growth factor signaling (Aikawa et al >>2008<<, Kleeff et al 1998, Kleeff et al 1999).
n2:mentions: n3:18064304

Subject Item: _:vb12915084
rdf:type: n2:Context
rdf:value: GPC1 is overexpressed in PDAC and is required for efficient heparin binding growth factor signaling (Aikawa et al 2008, Kleeff et al >>1998<<, Kleeff et al 1999).
n2:mentions: n3:9802880

Subject Item: _:vb12915085
rdf:type: n2:Context
rdf:value: GPC1 is overexpressed in PDAC and is required for efficient heparin binding growth factor signaling (Aikawa et al 2008, Kleeff et al 1998, Kleeff et al >>1999<<).
n2:mentions: n3:10505759

Subject Item: _:vb12915086
rdf:type: n2:Context
rdf:value: and human pancreatic cancer cells in an orthotopic pancreatic cancer model, we have demonstrated that both host-derived and cancer cell-derived GPC1 contribute to enhanced tumor growth and metastasis in pancreatic cancer (Aikawa et al >>2008<<, Kleeff et al 1998). It is not known, however, if GPC1 is important for both tumor initiation and progression in PDAC.
n2:mentions: n3:18064304

Subject Item: _:vb12915087
rdf:type: n2:Context
rdf:value: cancer cells in an orthotopic pancreatic cancer model, we have demonstrated that both host-derived and cancer cell-derived GPC1 contribute to enhanced tumor growth and metastasis in pancreatic cancer (Aikawa et al 2008, Kleeff et al >>1998<<). It is not known, however, if GPC1 is important for both tumor initiation and progression in PDAC.
n2:mentions: n3:9802880

Subject Item: _:vb12915088
rdf:type: n10:Section
dc:title: materials and methods
n10:contains: _:vb12915104 _:vb12915092 _:vb12915093 _:vb12915094 _:vb12915095 _:vb12915089 _:vb12915090 _:vb12915091 _:vb12915100 _:vb12915101 _:vb12915102 _:vb12915103 _:vb12915096 _:vb12915097 _:vb12915098 _:vb12915099

Subject Item: _:vb12915089
rdf:type: n2:Context
rdf:value: LSL-KrasG12D;INK4A/ArfLox/Lox;SMAD4lox/lox and Pdx1-Cre mice strains were kindly provided by Nabeel Bardeesy at Harvard University (Bardeesy et al >>2006<<) and Guo Gu at Vanderbilt University (Gu et al 2003), respectively. The SMAD4lox/lox mutation was bred out of this line prior to introducing the Pdx1-Cre and GPC1 mutations (Fig.
n2:mentions: n3:16585505

Subject Item: _:vb12915090
rdf:type: n2:Context
rdf:value: LSL-KrasG12D;INK4A/ArfLox/Lox;SMAD4lox/lox and Pdx1-Cre mice strains were kindly provided by Nabeel Bardeesy at Harvard University (Bardeesy et al 2006) and Guo Gu at Vanderbilt University (Gu et al >>2003<<), respectively. The SMAD4lox/lox mutation was bred out of this line prior to introducing the Pdx1-Cre and GPC1 mutations (Fig.
n2:mentions: n3:12490294

Subject Item: _:vb12915091
rdf:type: n2:Context
rdf:value: The GPC1-/- mice were produced by targeted mutagenesis as described previously (Aikawa et al >>2008<<, Jen et al 2009).
n2:mentions: n3:18064304

Subject Item: _:vb12915092
rdf:type: n2:Context
rdf:value: The GPC1-/- mice were produced by targeted mutagenesis as described previously (Aikawa et al 2008, Jen et al >>2009<<). All mice were genotyped twice by PCR to verify the presence of each transgene.
n2:mentions: n3:19732411

Subject Item: _:vb12915093
rdf:type: n2:Context
rdf:value: endogenous peroxidase activity, washed in PBS with 0.025% Triton-X, incubated for one hour in blocking buffer (1% BSA and 5% normal goat or horse serum), and overnight at 4°C with the appropriate monoclonal antibody (Aguirre et al >>2003<<, Aikawa et al 2008). Bound antibody was detected with the suitable biotinylated secondary antibody (1:
n2:mentions: n3:14681207

Subject Item: _:vb12915094
rdf:type: n2:Context
rdf:value: activity, washed in PBS with 0.025% Triton-X, incubated for one hour in blocking buffer (1% BSA and 5% normal goat or horse serum), and overnight at 4°C with the appropriate monoclonal antibody (Aguirre et al 2003, Aikawa et al >>2008<<). Bound antibody was detected with the suitable biotinylated secondary antibody (1:
n2:mentions: n3:18064304

Subject Item: _:vb12915095
rdf:type: n2:Context
rdf:value: was detected with the suitable biotinylated secondary antibody (1:500) and VECTASTAIN ABC Reagent (Vector Laboratories, Burlingame, CA) complex, using diaminobenzidine tetrahydrochloride (DAB) as the substrate (Rowland-Goldsmith et al >>2002<<).
n2:mentions: n3:12467210

Subject Item: _:vb12915096
rdf:type: n2:Context
rdf:value: To isolate and establish primary cancer cell lines, pancreatic tumors were rapidly harvested from Pdx1-Cre;LSL-KrasG12D;INK4ALox/Lox;GPC1+/+ or GPC1-/- transgenic mice that were 60 to 65 days old (Seeley et al >>2009<<). The tumors were minced with sterile scissors, digested with collagenase IV (2.5 mg/ml) for 1 h at 37°C, and resuspended in cancer cell growth media (RPMI 1640 with 20% FBS, 100 units/ml penicillin/streptomycin).
n2:mentions: n3:19147554

Subject Item: _:vb12915097
rdf:type: n2:Context
rdf:value: Primary endothelial cells were isolated from adult livers as described previously (13), using Dynalbeads (Invitrogen) labeled with anti-CD31 antibodies (Aikawa et al >>2008<<). Endothelial cells were similarly isolated from tumors arising in Pdx1-Cre;LSL-KrasG12D;INK4ALox/Lox;GPC1+/+ or GPC1-/- transgenic mice that were 60 to 65 days old.
n2:mentions: n3:18064304

Subject Item: _:vb12915098
rdf:type: n2:Context
rdf:value: 48 hours in serum free media (DMEM, 5 μg/ml apotransferrin, 5 ng/ml selenium, 0.01% BSA, and 100 U/ml penicillin/streptomycin) and then utilizing the 3-(4,5-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay (Kleeff et al >>1998<<). Doubling times were determined by plating 2×104 cells/well in 6-well plates and counting cells with a hemocytometer every 24 hours for five days.
n2:mentions: n3:9802880

Subject Item: _:vb12915099
rdf:type: n2:Context
rdf:value: Wounding assays were performed to assess the ability of immortalized MEFs to migrate in response to growth factors (Arnold et al >>2004<<, Rowland-Goldsmith et al 2001). Briefly, 75×103 MEFs originally isolated from GPC1+/+ or GPC1-/- mice were plated in each well of a 6-well plate and serum starved overnight.
n2:mentions: n3:15150118

Subject Item: _:vb12915100
rdf:type: n2:Context
rdf:value: Wounding assays were performed to assess the ability of immortalized MEFs to migrate in response to growth factors (Arnold et al 2004, Rowland-Goldsmith et al >>2001<<). Briefly, 75×103 MEFs originally isolated from GPC1+/+ or GPC1-/- mice were plated in each well of a 6-well plate and serum starved overnight.
n2:mentions: n3:11555612

Subject Item: _:vb12915101
rdf:type: n2:Context
rdf:value: Photos taken at 0 and 8 hours allowed for analysis of the migration distance (Suyama et al >>2003<<).
n2:mentions: n3:12719525

Subject Item: _:vb12915102
rdf:type: n2:Context
rdf:value: The cells were then fixed with 4% paraformaldehyde, stained with 1% toluidine blue and 2% sodium borate, and counted on an inverted microscope with the 20X objective (Neupane and Korc >>2008<<).
n2:mentions: n3:19047086

Subject Item: _:vb12915103
rdf:type: n2:Context
rdf:value: To assess the impact of GPC1 on the expression levels of VEGF-A and GPC2-6, total RNA was isolated from tumors arising in 60 day old GPC1+/+ and 5 GPC1-/- mice, using the low temperature guanidine isothiocyanate method (Chang et al >>1990<<, Han et al 1987). The concentration of RNA was determined spectrophometrically and RNA integrity was verified on a 1% agarose gel.
n2:mentions: n3:1698952

Subject Item: _:vb12915104
rdf:type: n2:Context
rdf:value: impact of GPC1 on the expression levels of VEGF-A and GPC2-6, total RNA was isolated from tumors arising in 60 day old GPC1+/+ and 5 GPC1-/- mice, using the low temperature guanidine isothiocyanate method (Chang et al 1990, Han et al >>1987<<). The concentration of RNA was determined spectrophometrically and RNA integrity was verified on a 1% agarose gel.
n2:mentions: n3:3593682

Subject Item: _:vb12915105
rdf:type: n10:Section
dc:title: results
n10:contains: _:vb12915106 _:vb12915107 _:vb12915108

Subject Item: _:vb12915106
rdf:type: n2:Context
rdf:value: maintain a similar genetic background for both the GPC1 wild type (GPC1+/+) and knockout (GPC1-/-) transgenic mouse lines and to avoid lethality caused by homozygosity of either the mutant Kras or the Pdx1-Cre alleles (Johnson et al >>1997<<), generation of the mouse model was carried out in a step-wise manner (Fig. S1).
n2:mentions: n3:9334313

Subject Item: _:vb12915107
rdf:type: n2:Context
rdf:value: By contrast, Ki67 and CD34, which are markers for proliferation and angiogenesis, respectively (Le Mercier et al >>2009<<, Vilar et al 2007), were markedly decreased in tumors from GPC1-/- by comparison with GPC+/+ mice (Fig.
n2:mentions: n3:19412433

Subject Item: _:vb12915108
rdf:type: n2:Context
rdf:value: By contrast, Ki67 and CD34, which are markers for proliferation and angiogenesis, respectively (Le Mercier et al 2009, Vilar et al >>2007<<), were markedly decreased in tumors from GPC1-/- by comparison with GPC+/+ mice (Fig.
n2:mentions: n3:17639039

Subject Item: _:vb12915109
rdf:type: n10:Section
dc:title: discussion
n10:contains: _:vb12915136 _:vb12915137 _:vb12915138 _:vb12915120 _:vb12915121 _:vb12915122 _:vb12915123 _:vb12915124 _:vb12915125 _:vb12915126 _:vb12915127 _:vb12915128 _:vb12915129 _:vb12915130 _:vb12915131 _:vb12915132 _:vb12915133 _:vb12915134 _:vb12915135 _:vb12915110 _:vb12915111 _:vb12915112 _:vb12915113 _:vb12915114 _:vb12915115 _:vb12915116 _:vb12915117 _:vb12915118 _:vb12915119

Subject Item: _:vb12915110
rdf:type: n2:Context
rdf:value: First, studies with human pancreatic cancer cell lines injected subcutaneously in athymic mice have demonstrated that GPC1 expression is required for efficient pancreatic tumor growth and angiogenesis (Kleeff et al >>1998<<, Kleeff et al 1999).
n2:mentions: n3:9802880

Subject Item: _:vb12915111
rdf:type: n2:Context
rdf:value: First, studies with human pancreatic cancer cell lines injected subcutaneously in athymic mice have demonstrated that GPC1 expression is required for efficient pancreatic tumor growth and angiogenesis (Kleeff et al 1998, Kleeff et al >>1999<<). Second, GPC1 is overexpressed in resected PDAC samples, and both the cancer cells and the cancer-associated fibroblasts express GPC1 at the mRNA and protein level (Kleeff et al 1998), indicating that both cell types synthesize GPC1.
n2:mentions: n3:10505759

Subject Item: _:vb12915112
rdf:type: n2:Context
rdf:value: Second, GPC1 is overexpressed in resected PDAC samples, and both the cancer cells and the cancer-associated fibroblasts express GPC1 at the mRNA and protein level (Kleeff et al >>1998<<), indicating that both cell types synthesize GPC1.
n2:mentions: n3:9802880

Subject Item: _:vb12915113
rdf:type: n2:Context
rdf:value: Third, GPC1 is abundant in the stroma adjacent to the cancer cells in PDAC, and in vitro studies with human pancreatic cancer cell lines have shown that GPC1 is readily released by these cells (Matsuda et al >>2001<<), pointing to a possible role for GPC1 within the tumor microenvironment.
n2:mentions: n3:11454708

Subject Item: _:vb12915114
rdf:type: n2:Context
rdf:value: Fourth, studies with athymic GPC1-/- mice have demonstrated that host-derived GPC1, produced by stromal and endothelial cells, contributes to pancreatic tumor growth, metastasis, and angiogenesis (Aikawa et al >>2008<<). Fifth, gene expression profiling in pancreatic intraductal papillary-mucinous tumors (IPMTs) revealed that GPC1 is upregulated in these lesions, but nearly exclusively in invasive IPMTs, suggesting a potential role in tumor invasion
n2:mentions: n3:18064304

Subject Item: _:vb12915115
rdf:type: n2:Context
rdf:value: expression profiling in pancreatic intraductal papillary-mucinous tumors (IPMTs) revealed that GPC1 is upregulated in these lesions, but nearly exclusively in invasive IPMTs, suggesting a potential role in tumor invasion (Terris et al >>2002<<).
n2:mentions: n3:12000726

Subject Item: _:vb12915116
rdf:type: n2:Context
rdf:value: Kras (KrasG12D) allele that has been knocked-in within its own locus but which is transcriptionally silenced by the insertion of a LoxP-Stop-LoxP element (LSL) located upstream of the transcriptional start site (Aguirre et al >>2003<<, Hingorani et al 2003).
n2:mentions: n3:14681207

Subject Item: _:vb12915117
rdf:type: n2:Context
rdf:value: allele that has been knocked-in within its own locus but which is transcriptionally silenced by the insertion of a LoxP-Stop-LoxP element (LSL) located upstream of the transcriptional start site (Aguirre et al 2003, Hingorani et al >>2003<<). Oncogenic Kras expression remains under the control of its own endogenous promoter, and the transcript is produced only in early pancreatic progenitor cells after excision of the LSL sequence via the Pdx-1 driven Cre recombinase.
n2:mentions: n3:14706336

Subject Item: _:vb12915118
rdf:type: n2:Context
rdf:value: The Pdx1-Cre;LSL-KrasG12D mice develop low grade PanIN and exhibit areas of acinar to ductal metaplasia by 2 months of age (Aguirre et al >>2003<<). When the mice are 8 to 12 months old, they develop PDAC at low penetrance (Aguirre et al 2003, Habbe et al 2008). PanIN progression to pancreatic cancer is an important feature of PDAC initiation in both human and mouse models and is
n2:mentions: n3:14681207

Subject Item: _:vb12915119
rdf:type: n2:Context
rdf:value: When the mice are 8 to 12 months old, they develop PDAC at low penetrance (Aguirre et al >>2003<<, Habbe et al 2008).
n2:mentions: n3:14681207

Subject Item: _:vb12915120
rdf:type: n2:Context
rdf:value: When the mice are 8 to 12 months old, they develop PDAC at low penetrance (Aguirre et al 2003, Habbe et al >>2008<<). PanIN progression to pancreatic cancer is an important feature of PDAC initiation in both human and mouse models and is dramatically accelerated in Pdx1-Cre;LSL-KrasG12D;INK4Alox/lox mice. In addition to harboring oncogenic KrasG12D,
n2:mentions: n3:19028870

Subject Item: _:vb12915121
rdf:type: n2:Context
rdf:value: In addition to harboring oncogenic KrasG12D, the pancreata of these mice have sustained a homozygous deletion of the INK4A locus, resulting in large, highly invasive tumors by 7-11 weeks of age (Aguirre et al >>2003<<, Jackson et al 2001).
n2:mentions: n3:14681207

Subject Item: _:vb12915122
rdf:type: n2:Context
rdf:value: In addition to harboring oncogenic KrasG12D, the pancreata of these mice have sustained a homozygous deletion of the INK4A locus, resulting in large, highly invasive tumors by 7-11 weeks of age (Aguirre et al 2003, Jackson et al >>2001<<).
n2:mentions: n3:11751630

Subject Item: _:vb12915123
rdf:type: n2:Context
rdf:value: Recent studies underscore the importance of the cancer-associated stroma in facilitating tumor spread, invasion, and metastasis, enhancing chemoresistance and promoting apoptosis resistance (Hwang et al >>2008<<, Vonlaufen et al 2008).
n2:mentions: n3:18245495

Subject Item: _:vb12915124
rdf:type: n2:Context
rdf:value: Recent studies underscore the importance of the cancer-associated stroma in facilitating tumor spread, invasion, and metastasis, enhancing chemoresistance and promoting apoptosis resistance (Hwang et al 2008, Vonlaufen et al >>2008<<). PDAC is characterized by an abundant desmoplastic reaction that is rich in collagen I, pancreatic stellate cells (PSCs), fibroblasts, and inflammatory cells, which collectively promote cancer cell growth and invasiveness and contribute
n2:mentions: n3:18829522

Subject Item: _:vb12915125
rdf:type: n2:Context
rdf:value: desmoplastic reaction that is rich in collagen I, pancreatic stellate cells (PSCs), fibroblasts, and inflammatory cells, which collectively promote cancer cell growth and invasiveness and contribute to chemoresistance (Kleeff et al >>2007<<). While orthotopic models of PDAC have generally not been associated with desmoplasia, many genetic mouse models of PDAC, including the Pdx1-Cre;LSL-KrasG12D;INK4A/Arflox/lox mice used in the current study, exhibit desmoplasia (Aguirre et
n2:mentions: n3:17534898

Subject Item: _:vb12915126
rdf:type: n2:Context
rdf:value: orthotopic models of PDAC have generally not been associated with desmoplasia, many genetic mouse models of PDAC, including the Pdx1-Cre;LSL-KrasG12D;INK4A/Arflox/lox mice used in the current study, exhibit desmoplasia (Aguirre et al >>2003<<, Tuveson and Hingorani 2005).
n2:mentions: n3:14681207

Subject Item: _:vb12915127
rdf:type: n2:Context
rdf:value: generally not been associated with desmoplasia, many genetic mouse models of PDAC, including the Pdx1-Cre;LSL-KrasG12D;INK4A/Arflox/lox mice used in the current study, exhibit desmoplasia (Aguirre et al 2003, Tuveson and Hingorani >>2005<<). By contrast, orthotopic models exhibit aberrant angiogenesis (Rowland-Goldsmith et al 2002), whereas genetic mouse models of PDAC are ostensibly not angiogenesis-dependent and consequently are more resistant to chemotherapy (Olive et al
n2:mentions: n3:16869739

Subject Item: _:vb12915128
rdf:type: n2:Context
rdf:value: By contrast, orthotopic models exhibit aberrant angiogenesis (Rowland-Goldsmith et al >>2002<<), whereas genetic mouse models of PDAC are ostensibly not angiogenesis-dependent and consequently are more resistant to chemotherapy (Olive et al 2009).
n2:mentions: n3:12467210

Subject Item: _:vb12915129
rdf:type: n2:Context
rdf:value: contrast, orthotopic models exhibit aberrant angiogenesis (Rowland-Goldsmith et al 2002), whereas genetic mouse models of PDAC are ostensibly not angiogenesis-dependent and consequently are more resistant to chemotherapy (Olive et al >>2009<<). It is noteworthy, therefore, that there was abundant angiogenesis in the tumors arising in Pdx1-Cre;LSL-KrasG12D;INK4A/Arflox/lox;GPC1+/+ mice, and that tumors in GPC1-/- pancreata displayed markedly reduced angiogenesis.
n2:mentions: n3:19460966

Subject Item: _:vb12915130
rdf:type: n2:Context
rdf:value: Inasmuch as VEGF-A is known to up-regulate the expression of ephrin-A1 (Cheng et al >>2002<<), it is possible that loss of GPC1, by leading to decreased VEGF-A expression and function, results in the down-regulation of downstream genes such as ephrin-A1, further impeding angiogenesis.
n2:mentions: n3:12496364

Subject Item: _:vb12915131
rdf:type: n2:Context
rdf:value: Sox17 is a transcriptional regulator that is expressed in fetal and neonatal hematopoietic stem cells (HSCs), but not in adult HSCs (Kim et al >>2007<<). Inasmuch as HSCs have been implicated in PDAC angiogenesis (Li et al 2011) it is possible that GPC1 is also important for PDAC's ability to recruit HSCs to promote tumor angiogenesis. Fourth, by contrast to endothelial cells isolated
n2:mentions: n3:17655922

Subject Item: _:vb12915132
rdf:type: n2:Context
rdf:value: Inasmuch as HSCs have been implicated in PDAC angiogenesis (Li et al >>2011<<) it is possible that GPC1 is also important for PDAC's ability to recruit HSCs to promote tumor angiogenesis.
n2:mentions: n3:21286374

Subject Item: _:vb12915133
rdf:type: n2:Context
rdf:value: Fifth, GPC1 may also act to promote growth factor sequestration within the tumor microenvironment, enhancing their stability and ability to act as morphogens (Lander et al >>2002<<, Vlodavsky et al 1990).
n2:mentions: n3:12062090

Subject Item: _:vb12915134
rdf:type: n2:Context
rdf:value: Fifth, GPC1 may also act to promote growth factor sequestration within the tumor microenvironment, enhancing their stability and ability to act as morphogens (Lander et al 2002, Vlodavsky et al >>1990<<). Thus, the absence of GPC1 within the tumors of GPC1-/- mice may decrease the pool of heparan sulfate side chains, thereby decreasing the amount of stored HBGFs, such as VEGF-A (41, 42), that can be released by the actions of the
n2:mentions: n3:1705486

Subject Item: _:vb12915135
rdf:type: n2:Context
rdf:value: the pool of heparan sulfate side chains, thereby decreasing the amount of stored HBGFs, such as VEGF-A (41, 42), that can be released by the actions of the endoglycosidase heparanase, which is up-regulated in PDAC (Zetser et al >>2006<<). Sixth, the absence of GPC1 may also interfere with the shedding of active MMP7 (Ding et al 2005), which acts to release all stored growth factors, irrespective of their heparin-binding ability.
n2:mentions: n3:16452201

Subject Item: _:vb12915136
rdf:type: n2:Context
rdf:value: Sixth, the absence of GPC1 may also interfere with the shedding of active MMP7 (Ding et al >>2005<<), which acts to release all stored growth factors, irrespective of their heparin-binding ability.
n2:mentions: n3:16286510

Subject Item: _:vb12915137
rdf:type: n2:Context
rdf:value: Using athymic mice, both host-derived and cancer cell-derived GPC1 has been shown to contribute to enhanced pancreatic cancer growth (Aikawa et al >>2008<<, Kleeff et al 1998).
n2:mentions: n3:18064304

Subject Item: _:vb12915138
rdf:type: n2:Context
rdf:value: Using athymic mice, both host-derived and cancer cell-derived GPC1 has been shown to contribute to enhanced pancreatic cancer growth (Aikawa et al 2008, Kleeff et al >>1998<<). In the present study, pancreatic cancer cell lines established from GPC1-/- mice demonstrated a marked decrease in invasiveness in vitro, as well as attenuated growth and metastatic potential following intra-pancreatic implantation in
n2:mentions: n3:9802880

Subject Item: _:vb475014649
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 13
n2:hasRelevantPaperId: n3:18064304

Subject Item: _:vb475014650
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 10
n2:hasRelevantPaperId: n3:26106858

Subject Item: _:vb475014651
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 9
n2:hasRelevantPaperId: n3:9802880

Subject Item: _:vb475014652
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 7
n2:hasRelevantPaperId: n3:11454708

Subject Item: _:vb475014653
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 6
n2:hasRelevantPaperId: n3:16723715

Subject Item: _:vb475014654
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 5
n2:hasRelevantPaperId: n3:23270819

Subject Item: _:vb475014655
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 5
n2:hasRelevantPaperId: n3:15249209

Subject Item: _:vb475014656
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 5
n2:hasRelevantPaperId: n3:18505598

Subject Item: _:vb475014657
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 4
n2:hasRelevantPaperId: n3:14706336

Subject Item: _:vb475014658
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 4
n2:hasRelevantPaperId: n3:27310703

Subject Item: _:vb475014659
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 4
n2:hasRelevantPaperId: n3:28440066

Subject Item: _:vb475014660
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:17016645

Subject Item: _:vb475014661
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:24755488

Subject Item: _:vb475014662
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:26332121

Subject Item: _:vb475014663
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:29721179

Subject Item: _:vb475014664
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:30358133

Subject Item: _:vb475014665
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:28232049

Subject Item: _:vb475014666
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:28233416

Subject Item: _:vb475014667
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:20610624

Subject Item: _:vb475014668
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:27313791

Subject Item: _:vb475014669
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:28602885

Subject Item: _:vb475014670
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:21155971

Subject Item: _:vb475014671
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:24736782

Subject Item: _:vb475014672
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:12591930

Subject Item: _:vb475014673
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:22975374

Subject Item: _:vb475014674
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 3
n2:hasRelevantPaperId: n3:24463821

Subject Item: _:vb475014675
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15894267

Subject Item: _:vb475014676
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21625220

Subject Item: _:vb475014677
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26482785

Subject Item: _:vb475014678
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11555612

Subject Item: _:vb475014679
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22975375

Subject Item: _:vb475014680
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26021314

Subject Item: _:vb475014681
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:29672570

Subject Item: _:vb475014682
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:15297422

Subject Item: _:vb475014683
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:19574223

Subject Item: _:vb475014684
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28848451

Subject Item: _:vb475014685
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17337080

Subject Item: _:vb475014686
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20981102

Subject Item: _:vb475014687
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23471984

Subject Item: _:vb475014688
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24840647

Subject Item: _:vb475014689
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25118277

Subject Item: _:vb475014690
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:29254156

Subject Item: _:vb475014691
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23103869

Subject Item: _:vb475014692
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25270552

Subject Item: _:vb475014693
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26389634

Subject Item: _:vb475014694
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:27461391

Subject Item: _:vb475014695
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20824144

Subject Item: _:vb475014696
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23624389

Subject Item: _:vb475014697
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11846609

Subject Item: _:vb475014698
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10962434

Subject Item: _:vb475014699
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24412155

Subject Item: _:vb475014700
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28510121

Subject Item: _:vb475014701
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20840587

Subject Item: _:vb475014702
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26057990

Subject Item: _:vb475014703
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:30204432

Subject Item: _:vb475014704
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:31355137

Subject Item: _:vb475014705
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:30352677

Subject Item: _:vb475014706
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:1850375

Subject Item: _:vb475014707
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:27004211

Subject Item: _:vb475014708
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17460664

Subject Item: _:vb475014709
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23951320

Subject Item: _:vb475014710
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28739923

Subject Item: _:vb475014711
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21586612

Subject Item: _:vb475014712
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23151657

Subject Item: _:vb475014713
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23446997

Subject Item: _:vb475014714
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23726834

Subject Item: _:vb475014715
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:9371521

Subject Item: _:vb475014716
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10402475

Subject Item: _:vb475014717
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16557279

Subject Item: _:vb475014718
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23846917

Subject Item: _:vb475014719
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24185138

Subject Item: _:vb475014720
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24496449

Subject Item: _:vb475014721
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20966025

Subject Item: _:vb475014722
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23741253

Subject Item: _:vb475014723
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:8252621

Subject Item: _:vb475014724
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16024626

Subject Item: _:vb475014725
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:28575679

Subject Item: _:vb475014726
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:30730015

Subject Item: _:vb475014727
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:9712917

Subject Item: _:vb475014728
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21613822

Subject Item: _:vb475014729
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22402744

Subject Item: _:vb475014730
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23752186

Subject Item: _:vb475014731
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25727148

Subject Item: _:vb475014732
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:11518720

Subject Item: _:vb475014733
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16072037

Subject Item: _:vb475014734
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18772397

Subject Item: _:vb475014735
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:21690215

Subject Item: _:vb475014736
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:22467855

Subject Item: _:vb475014737
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:26289314

Subject Item: _:vb475014738
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16789792

Subject Item: _:vb475014739
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:18039136

Subject Item: _:vb475014740
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:20427809

Subject Item: _:vb475014741
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10872425

Subject Item: _:vb475014742
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:24101524

Subject Item: _:vb475014743
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17126425

Subject Item: _:vb475014744
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:29245923

Subject Item: _:vb475014745
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:12373287

Subject Item: _:vb475014746
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:17249709

Subject Item: _:vb475014747
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:10505759

Subject Item: _:vb475014748
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23592772

Subject Item: _:vb475014749
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:25595436

Subject Item: _:vb475014750
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:16823988

Subject Item: _:vb475014751
rdf:type: n2:RelevantBibliographicResource
n2:RelevantScore: 2
n2:hasRelevantPaperId: n3:23691363