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Article: Rilotumumab Resistance Acquired by Intracrine Hepatocyte Growth Factor Signaling.

Cecchi, Fabiola / Rex, Karen / Schmidt, Joanna / Vocke, Cathy D / Lee, Young H / Burkett, Sandra / Baker, Daniel / Damore, Michael A / Coxon, Angela / Burgess, Teresa L / Bottaro, Donald P

Cancers

2023 Volume 15, Issue 2

Abstract: Drug resistance is a long-standing impediment to effective systemic cancer therapy and acquired drug resistance is a growing problem for molecularly-targeted therapeutics that otherwise have shown unprecedented successes in disease control. The ... ...

Abstract	Drug resistance is a long-standing impediment to effective systemic cancer therapy and acquired drug resistance is a growing problem for molecularly-targeted therapeutics that otherwise have shown unprecedented successes in disease control. The hepatocyte growth factor (HGF)/Met receptor pathway signaling is frequently involved in cancer and has been a subject of targeted drug development for nearly 30 years. To anticipate and study specific resistance mechanisms associated with targeting this pathway, we engineered resistance to the HGF-neutralizing antibody rilotumumab in glioblastoma cells harboring autocrine HGF/Met signaling, a frequent abnormality of this brain cancer in humans. We found that rilotumumab resistance was acquired through an unusual mechanism comprising dramatic HGF overproduction and misfolding, endoplasmic reticulum (ER) stress-response signaling and redirected vesicular trafficking that effectively sequestered rilotumumab and misfolded HGF from native HGF and activated Met. Amplification of
Language	English
Publishing date	2023-01-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15020460
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Article ; Online: Novel antagonists of heparin binding growth factors.

Cecchi, Fabiola / Bottaro, Donald P

Oncotarget

2012 Volume 3, Issue 9, Page(s) 911–912

Abstract: Structural and functional studies of ligand-RTK interactions over the last decade highlight the importance of multiple binding events and associated conformational changes in RTK ectodomains that are required for kinase activation. These events vary in ... ...

Abstract	Structural and functional studies of ligand-RTK interactions over the last decade highlight the importance of multiple binding events and associated conformational changes in RTK ectodomains that are required for kinase activation. These events vary in strength, and even weak interactions appear to provide necessary increments of increased stability to a signal transduction process whose complexity we are only beginning to appreciate.
MeSH term(s)	Heparan Sulfate Proteoglycans/chemistry ; Heparan Sulfate Proteoglycans/metabolism ; Heparin/chemistry ; Heparin/metabolism ; Hepatocyte Growth Factor/antagonists & inhibitors ; Hepatocyte Growth Factor/chemistry ; Hepatocyte Growth Factor/metabolism ; Humans ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Vascular Endothelial Growth Factor A/chemistry ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Heparan Sulfate Proteoglycans ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Hepatocyte Growth Factor (67256-21-7) ; Heparin (9005-49-6)
Language	English
Publishing date	2012-09-17
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.645
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Article: Regression of Human Breast Carcinoma in Nude Mice after Ad

Felici, Angelina / Bottaro, Donald P / Mangoni, Antonella / Reusch, Petra / Marmé, Dieter / Kovesdi, Imre / De Silva, Dinuka M / Lee, Young H / Capogrossi, Maurizio C / Mühlhauser, Judith

Cancers

2022 Volume 14, Issue 24

Abstract: Two vascular endothelial growth factor (VEGF) receptors, FLT-1 and KDR, are expressed preferentially in proliferating endothelium. There is increasing evidence that recombinant, soluble VEGF receptor domains interfering with VEGF signaling may inhibit in ...

Abstract	Two vascular endothelial growth factor (VEGF) receptors, FLT-1 and KDR, are expressed preferentially in proliferating endothelium. There is increasing evidence that recombinant, soluble VEGF receptor domains interfering with VEGF signaling may inhibit in vivo neoangiogenesis, tumor growth and metastatic spread. We hypothesized that a soluble form of FLT-1 receptor (sFLT-1) could inhibit the growth of pre-established tumors via an anti-angiogenic mechanism. A replication-deficient adenovirus (Ad) vector carrying the sflt-1 cDNA (Adsflt) was used to overexpress the sFLT-1 receptor in a breast cancer animal model. MCF-7 cells, which produce VEGF, were used to establish solid tumors in the mammary fat pads of female nude mice. After six weeks, tumors were injected either with Adsflt or a negative control virus (AdCMV.βgal). After six months, average tumor volume in the Adsflt-infected group (33 ± 22 mm3) decreased by 91% relative to that of the negative control group (388 ± 94 mm3; p < 0.05). Moreover, 10 of 15 Adsflt-infected tumors exhibited complete regression. The vascular density of Adsflt-infected tumors was reduced by 50% relative to that of negative controls (p < 0.05), which is consistent with sFLT-1-mediated tumor regression through an anti-angiogenic mechanism. Moreover, cell necrosis and fibrosis associated with long-term regression of Adsflt−infected tumors were preceded by apoptosis of tumor vascular endothelial cells. Mice treated with Adsflt intratumorally showed no delay in the healing of cutaneous wounds, providing preliminary evidence that Ad-mediated sFLT-1 overexpression may be an effective anti-angiogenic therapy for cancer without the risk of systemic anti-angiogenic effects.
Language	English
Publishing date	2022-12-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14246175
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Article ; Online: Stable Ectopic Expression of ST6GALNAC5 Induces Autocrine MET Activation and Anchorage-Independence in MDCK Cells.

Chu, Chia / Bottaro, Donald P / Betenbaugh, Michael J / Shiloach, Joseph

PloS one

2016 Volume 11, Issue 2, Page(s) e0148075

Abstract: The epithelial-mesenchymal transition (EMT) is a complex cancer progression that can boost the metastatic potential of transformed cells by inducing migration, loss of cell adhesion, and promoting proliferation under anchorage-independent conditions. A ... ...

Abstract	The epithelial-mesenchymal transition (EMT) is a complex cancer progression that can boost the metastatic potential of transformed cells by inducing migration, loss of cell adhesion, and promoting proliferation under anchorage-independent conditions. A DNA microarray analysis was performed comparing parental anchorage-dependent MDCK cells and anchorage-independent MDCK cells that were engineered to express human siat7e (ST6GALNAC5). The comparison identified several genes involved in the EMT process that were differentially expressed between the anchorage-dependent and the anchorage-independent MDCK cell lines. The hepatocyte growth factor gene (hgf) was found to be over-expressed in the engineered MDCK-siat7e cells at both transcription and protein expression levels. Phosphorylation analysis of the MET receptor tyrosine kinase confirmed the activation of an autocrine loop of the HGF/ MET signaling pathway in the MDCK-siat7e cells. When MET activities were suppressed by using the small-molecular inhibitor drug PF-02341066 (Crizotinib), the anchorage-independent MDCK-siat7e cells reverted to the cellular morphology of the parental anchorage-dependent MDCK cells. These observations indicate that the MET receptor plays a central role in the growth properties of the MDCK cells and its phosphorylation status is likely dependent on sialylation. Further investigation of the downstream signaling targets in the MET network showed that the degree of MDCK cell adhesion correlated with secretion levels of a matrix metalloproteinase, MMP1, suggesting a role of metalloproteinases in the EMT process. These results demonstrate that in addition to its application in biotechnology processes, MDCK-siat7e may serve as a model cell for metastasis studies to decipher the sequence of events leading up to the activation of EMT.
MeSH term(s)	Animals ; Autocrine Communication/genetics ; Cell Adhesion/genetics ; Dogs ; Ectopic Gene Expression ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression ; Hepatocyte Growth Factor/genetics ; Madin Darby Canine Kidney Cells ; Matrix Metalloproteinase 1/genetics ; Matrix Metalloproteinase 1/metabolism ; Models, Biological ; Phenotype ; Phosphorylation ; Proto-Oncogene Proteins c-met/metabolism ; Sialyltransferases/genetics ; Signal Transduction
Chemical Substances	Hepatocyte Growth Factor (67256-21-7) ; Sialyltransferases (EC 2.4.99.-) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Matrix Metalloproteinase 1 (EC 3.4.24.7)
Language	English
Publishing date	2016-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0148075
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Article ; Online: The hepatocyte growth factor isoform NK2 activates motogenesis and survival but not proliferation due to lack of Akt activation.

Mungunsukh, Ognoon / Lee, Young H / Bottaro, Donald P / Day, Regina M

Cellular signalling

2016 Volume 28, Issue 8, Page(s) 1114–1123

Abstract: Hepatocyte growth factor (HGF) is a pleiotrophic factor involved in cellular proliferation, migration and morphogenesis. HGF is required for normal tissue and organ development during embryogenesis, but in the adult HGF has been demonstrated to drive ... ...

Abstract	Hepatocyte growth factor (HGF) is a pleiotrophic factor involved in cellular proliferation, migration and morphogenesis. HGF is required for normal tissue and organ development during embryogenesis, but in the adult HGF has been demonstrated to drive normal tissue repair and inhibit fibrotic remodeling. HGF has two naturally occurring human isoforms as a result of alternative splicing, NK1 and NK2. While NK1 has been defined as an agonist for HGF receptor, Met, NK2 is defined as a partial Met antagonist. Furthermore, under conditions of fibrotic remodeling, NK2 is still expressed while full length HGF is suppressed. Furthermore, the mechanism by which NK2 partially signals through Met is not completely understood. Here, we investigated the mitogenic, motogenic, and anti-apoptotic activities of NK2 compared with full length HGF in primary human bronchial epithelial cells (BEpC) and bovine pulmonary artery endothelial cells (PAEC). In human BEpC, NK2 partial activated Met, inducing Met phosphorylation at Y1234/1235 in the tyrosine-kinase domain but not at Y1349 site in the multifunctional docking domain. Partial phosphorylation of Met by NK2 resulted in activation of MAPK and STAT3, but not AKT. This correlated with motogenesis and survival in a MAPK-dependent manner, but not cell proliferation. Overexpression of a constitutively active AKT complemented NK2 signaling, allowing NK2 to induce cell proliferation. These data indicate that NK2 and HGF drive motogenic and anti-apoptotic signaling but only HGF drives cell proliferation by activating AKT-pathway signaling. These results have implications for the biological consequences of differential regulation of the two isoforms under pro-fibrotic conditions.
MeSH term(s)	Angiotensin II/pharmacology ; Animals ; Apoptosis/drug effects ; Cattle ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Enzyme Activation/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hepatocyte Growth Factor/pharmacology ; Humans ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation/drug effects ; Protein Binding/drug effects ; Protein Isoforms/pharmacology ; Proteolysis/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-met/metabolism ; Signal Transduction/drug effects ; bcl-X Protein/metabolism
Chemical Substances	Protein Isoforms ; bcl-X Protein ; Angiotensin II (11128-99-7) ; Hepatocyte Growth Factor (67256-21-7) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2016-05-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2016.05.012
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Article: The Hepatocyte Growth Factor Receptor: Structure, Function and Pharmacological Targeting in Cancer.

Cecchi, Fabiola / Rabe, Daniel C / Bottaro, Donald P

Current signal transduction therapy

2014 Volume 6, Issue 2, Page(s) 146–151

Abstract: Under normal conditions, hepatocyte growth factor (HGF)-induced activation of its cell surface receptor, the Met tyrosine kinase (TK), is tightly regulated by paracrine ligand delivery, ligand activation at the target cell surface, and ligand activated ... ...

Abstract	Under normal conditions, hepatocyte growth factor (HGF)-induced activation of its cell surface receptor, the Met tyrosine kinase (TK), is tightly regulated by paracrine ligand delivery, ligand activation at the target cell surface, and ligand activated receptor internalization and degradation. Despite these controls, HGF/Met signaling contributes to oncogenesis and tumor progression in several cancers and promotes aggressive cellular invasiveness that is strongly linked to tumor metastasis. The prevalence of HGF/Met pathway activation in human malignancies has driven rapid growth in cancer drug development programs. Pathway inhibitors can be divided broadly into biologicals and low molecular weight synthetic TK inhibitors; of these, the latter now outnumber all other inhibitor types. We review here Met structure and function, the basic properties of HGF/Met pathway antagonists now in preclinical and clinical development, as well as the latest clinical trial results. The main challenges facing the effective use of HGF/Met-targeted antagonists for cancer treatment include optimal patient selection, diagnostic and pharmacodynamic biomarker development, and the identification and testing of optimal therapy combinations. The wealth of basic information, analytical reagents and model systems available concerning HGF/Met oncogenic signaling will continue to be invaluable in meeting these challenges and moving expeditiously toward more effective disease control.
Language	English
Publishing date	2014-08-14
Publishing country	United Arab Emirates
Document type	Journal Article
ISSN	1574-3624
ISSN	1574-3624
DOI	10.2174/157436211795659955
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Article ; Online: Synergistic signaling of tumor cell invasiveness by hepatocyte growth factor and hypoxia.

Lee, Young H / Morrison, Bethanie L / Bottaro, Donald P

The Journal of biological chemistry

2014 Volume 289, Issue 30, Page(s) 20448–20461

Abstract: Hepatocyte growth factor (HGF) signaling promotes tumor invasiveness in renal cell carcinoma (RCC) and other cancers. In clear cell RCC, VHL loss generates pseudohypoxia that exacerbates HGF-driven invasion through β-catenin deregulation. Hypoxia also ... ...

Abstract	Hepatocyte growth factor (HGF) signaling promotes tumor invasiveness in renal cell carcinoma (RCC) and other cancers. In clear cell RCC, VHL loss generates pseudohypoxia that exacerbates HGF-driven invasion through β-catenin deregulation. Hypoxia also enhances HGF-driven invasiveness by papillary RCC cells, but in the absence of VHL, loss signaling integration involves three parallel routes: 1) hypoxia-induced reactive oxygen species production and decreased DUSP2 expression, leading to enhanced mitogen-activated protein kinase (MAPK) cascade activation; 2) reactive oxygen species-induced diacylglycerol production by phospholipase Cγ, leading to protein kinase C activation and increased protein phosphatase- 2A activity, thereby suppressing HGF-induced Akt activation; and 3) a profound shift from HGF-enhanced, proliferation- oriented metabolism to autophagy-dependent invasion and suppression of proliferation. This tripartite signaling integration was not unique to RCC or HGF; in RCC cells, invasive synergy induced by the combination of hypoxia and epidermal growth factor occurred through the same mechanism, and in estrogen receptor-positive breast cancer cells, this mechanism was suppressed in the absence of estrogen. These results define the molecular basis of growth factor and hypoxia invasive synergy in VHL-competent papillary RCC cells, illustrate the plasticity of invasive and proliferative tumor cell states, and provide signaling profiles by which they may be predicted.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Cell Hypoxia/genetics ; Cell Line, Tumor ; Dual Specificity Phosphatase 2/genetics ; Dual Specificity Phosphatase 2/metabolism ; Female ; Gene Expression Regulation, Enzymologic/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Hepatocyte Growth Factor/genetics ; Hepatocyte Growth Factor/metabolism ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; MAP Kinase Signaling System ; Neoplasm Invasiveness ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Protein Phosphatase 2/genetics ; Protein Phosphatase 2/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism
Chemical Substances	HGF protein, human ; Reactive Oxygen Species ; Hepatocyte Growth Factor (67256-21-7) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13) ; Protein Phosphatase 2 (EC 3.1.3.16) ; DUSP2 protein, human (EC 3.1.3.48) ; Dual Specificity Phosphatase 2 (EC 3.1.3.48) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2014-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M114.580597
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Article: The role of extracellular matrix heparan sulfate glycosaminoglycan in the activation of growth factor signaling pathways.

Bottaro, Donald P

Annals of the New York Academy of Sciences

2002 Volume 961, Page(s) 158

MeSH term(s)	Animals ; Extracellular Matrix/metabolism ; Glycosaminoglycans/physiology ; Growth Substances/metabolism ; Heparitin Sulfate/physiology ; Humans ; Regeneration ; Signal Transduction ; Tissue Engineering ; Wound Healing
Chemical Substances	Glycosaminoglycans ; Growth Substances ; Heparitin Sulfate (9050-30-0)
Language	English
Publishing date	2002-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2002.tb03071.x
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Article ; Online: Inhibition of HSP 90 is associated with potent anti-tumor activity in Papillary Renal Cell Carcinoma.

Pahwa, Roma / Dubhashi, Janhavi / Singh, Anand / Jailwala, Parthav / Lobanov, Alexei / Thomas, Craig J / Ceribelli, Michele / Wilson, Kelli / Ricketts, Christopher J / Vocke, Cathy D / Wells, Catherine / Bottaro, Donald P / Linehan, W Marston / Neckers, Len / Srinivasan, Ramaprasad

Journal of experimental & clinical cancer research : CR

2022 Volume 41, Issue 1, Page(s) 208

Abstract: Background: There is no universally accepted treatment for patients with advanced papillary renal cell carcinoma (PRCC). The presence of activating mutations in MET, as well as gain of chromosome 7, where the MET gene is located, are the most common ... ...

Abstract	Background: There is no universally accepted treatment for patients with advanced papillary renal cell carcinoma (PRCC). The presence of activating mutations in MET, as well as gain of chromosome 7, where the MET gene is located, are the most common genetic alterations associated with PRCC, leading to the clinical evaluation of MET tyrosine kinase inhibitors (TKIs) in this cancer. However, TKIs targeting MET selectively, as well as multitargeted TKIs with activity against MET demonstrate modest efficacy in PRCC and primary and secondary treatment failure is common; other approaches are urgently needed to improve outcomes in these patients. Methods: High throughput screening with small molecule libraries identified HSP90 inhibitors as agents of interest based on antitumor activity against patient derived PRCC cell lines. We investigated the activity of the orally available HSP90 inhibitor, SNX2112 in vitro, using 2D/3D PRCC cell culture models and in vivo, in mice tumor xenograft models. The molecular pathways mediating antitumor activity of SNX2112 were assessed by Western blot analysis, Flow cytometry, RNA-seq analysis, Real Time qPCR and imaging approaches. Results: SNX2112 significantly inhibited cellular proliferation, induced G2/M cell cycle arrest and apoptosis in PRCC lines overexpressing MET. In contrast to TKIs targeting MET, SNX2112 inhibited both MET and known downstream mediators of MET activity (AKT, pAKT1/2 and pERK1/2) in PRCC cell lines. RNAi silencing of AKT1/2 or ERK1/2 expression significantly inhibited growth in PRCC cells. Furthermore, SNX2112 inhibited a unique set of E2F and MYC targets and G2M-associated genes. Interestingly, interrogation of the TCGA papillary RCC cohort revealed that these genes were overexpressed in PRCC and portend a poor prognosis. Finally, SNX-2112 demonstrated strong antitumor activity in vivo and prolonged survival of mice bearing human PRCC xenograft. Conclusions: These results demonstrate that HSP90 inhibition is associated with potent activity in PRCC, and implicate the PI3K/AKT and MEK/ERK1/2 pathways as important mediators of tumorigenesis. These data also provide the impetus for further clinical evaluation of HSP90, AKT, MEK or E2F pathway inhibitors in PRCC.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Renal Cell/drug therapy ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/pathology ; HSP90 Heat-Shock Proteins/genetics ; Humans ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Mice ; Mitogen-Activated Protein Kinase Kinases ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt
Chemical Substances	Antineoplastic Agents ; HSP90 Heat-Shock Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2022-06-27
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-022-02416-z
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Article ; Online: Correction: Phase II Study Evaluating 2 Dosing Schedules of Oral Foretinib (GSK1363089), cMET/VEGFR2 Inhibitor, in Patients with Metastatic Gastric Cancer.

Shah, Manish A / Wainberg, Zev A / Catenacci, Daniel V T / Hochster, Howard S / Ford, James / Kunz, Pamela / Lee, Fa-Chyi / Kallender, Howard / Cecchi, Fabiola / Rabe, Daniel C / Keer, Harold / Martin, Anne-Marie / Liu, Yuan / Gagnon, Robert / Bonate, Peter / Liu, Li / Gilmer, Tona / Bottaro, Donald P

PloS one

2022 Volume 17, Issue 10, Page(s) e0276211

Abstract: This corrects the article DOI: 10.1371/journal.pone.0054014.]. ...

Abstract	[This corrects the article DOI: 10.1371/journal.pone.0054014.].
Language	English
Publishing date	2022-10-10
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0276211
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