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Small Cell Ovarian Carcinoma: Genomic Stability and Responsiveness to Therapeutics
Gamwell et al. Orphanet Journal of Rare Diseases 2013, 8:33 http://www.ojrd.com/content/8/1/33 RESEARCH Open Access Small cell ovarian carcinoma: genomic stability and responsiveness to therapeutics Lisa F Gamwell1,2, Karen Gambaro3, Maria Merziotis2, Colleen Crane2, Suzanna L Arcand4, Valerie Bourada1,2, Christopher Davis2, Jeremy A Squire6, David G Huntsman7,8, Patricia N Tonin3,4,5 and Barbara C Vanderhyden1,2* Abstract Background: The biology of small cell ovarian carcinoma of the hypercalcemic type (SCCOHT), which is a rare and aggressive form of ovarian cancer, is poorly understood. Tumourigenicity, in vitro growth characteristics, genetic and genomic anomalies, and sensitivity to standard and novel chemotherapeutic treatments were investigated in the unique SCCOHT cell line, BIN-67, to provide further insight in the biology of this rare type of ovarian cancer. Method: The tumourigenic potential of BIN-67 cells was determined and the tumours formed in a xenograft model was compared to human SCCOHT. DNA sequencing, spectral karyotyping and high density SNP array analysis was performed. The sensitivity of the BIN-67 cells to standard chemotherapeutic agents and to vesicular stomatitis virus (VSV) and the JX-594 vaccinia virus was tested. Results: BIN-67 cells were capable of forming spheroids in hanging drop cultures. When xenografted into immunodeficient mice, BIN-67 cells developed into tumours that reflected the hypercalcemia and histology of human SCCOHT, notably intense expression of WT-1 and vimentin, and lack of expression of inhibin. Somatic mutations in TP53 and the most common activating mutations in KRAS and BRAF were not found in BIN-67 cells by DNA sequencing. -
Plakins, a Versatile Family of Cytolinkers: Roles in Skin Integrity and in Human Diseases Jamal-Eddine Bouameur1,2, Bertrand Favre1 and Luca Borradori1
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector REVIEW Plakins, a Versatile Family of Cytolinkers: Roles in Skin Integrity and in Human Diseases Jamal-Eddine Bouameur1,2, Bertrand Favre1 and Luca Borradori1 The plakin family consists of giant proteins involved in in (Roper et al., 2002; Jefferson et al., 2004; Sonnenberg and the cross-linking and organization of the cytoskeleton Liem, 2007; Boyer et al., 2010; Suozzi et al., 2012). and adhesion complexes. They further modulate sev- Mammalian plakins share a similar structural organization eral fundamental biological processes, such as cell and comprise seven members: bullous pemphigoid antigen 1 adhesion, migration, and polarization or signaling (BPAG1), desmoplakin, envoplakin, epiplakin, microtubule- pathways. Inherited and acquired defects of plakins actin cross-linking factor 1 (MACF1), periplakin, and plectin in humans and in animal models potentially lead to (Figure 1) (Choi et al., 2002; Jefferson et al., 2007; Choi and dramatic manifestations in the skin, striated muscles, Weis, 2011; Ortega et al., 2011). The existence of develop- and/or nervous system. These observations unequivo- mentally regulated and tissue-specific splice variants of some cally demonstrate the key role of plakins in the plakins further increases the diversity and versatility of these proteins (Table 1; Figure 1; Leung et al., 2001; Rezniczek et al., maintenance of tissue integrity. Here we review the 2003; Lin et al., 2005; Jefferson et al., 2006; Cabral et al., 2010). characteristics of the mammalian plakin members BPAG1 (bullous pemphigoid antigen 1), desmoplakin, PLAKINS IN THE EPIDERMIS plectin, envoplakin, epiplakin, MACF1 (microtubule- Epithelial BPAG1 (BPAG1e, also called BP230) constitutes the actin cross-linking factor 1), and periplakin, highlight- epithelium-specific isoform of BPAG1 and is localized in basal ing their role in skin homeostasis and diseases. -
Mutational Analysis of Candidate Genes in 24 Amelogenesis
Eur J Oral Sci 2006; 114 (Suppl. 1): 3–12 Copyright Ó Eur J Oral Sci 2006 Printed in Singapore. All rights reserved European Journal of Oral Sciences Jung-Wook Kim1,2, James P. Mutational analysis of candidate genes Simmer1, Brent P.-L. Lin3, Figen Seymen4, John D. Bartlett5, Jan C.-C. in 24 amelogenesis imperfecta families Hu1 1University of Michigan School of Dentistry, University of Michigan Dental Research 2 Kim J-W, Simmer JP, Lin BP-L, Seymen F, Bartlett JD, Hu JC-C. Mutational analysis Laboratory, Ann Arbor, MI, USA; Seoul National University, College of Dentistry, of candidate genes in 24 amelogenesis imperfecta families. Eur J Oral Sci 2006; 114 Department of Pediatric Dentistry & Dental (Suppl. 1): 3–12 Ó Eur J Oral Sci, 2006 Research Institute, Seoul, Korea; 3UCSF School of Dentistry, Department of Growth and Amelogenesis imperfecta (AI) is a heterogeneous group of inherited defects in dental Development, San Francisco, CA, USA; 4 enamel formation. The malformed enamel can be unusually thin, soft, rough and University of Istanbul, Faculty of Dentistry, stained. The strict definition of AI includes only those cases where enamel defects Department of Pedodontics, apa, Istanbul, Turkey; 5The Forsyth Institute, Harvard-Forsyth occur in the absence of other symptoms. Currently, there are seven candidate genes for Department of Oral Biology, Boston, MA, USA AI: amelogenin, enamelin, ameloblastin, tuftelin, distal-less homeobox 3, enamelysin, and kallikrein 4. To identify sequence variations in AI candidate genes in patients with isolated enamel defects, and to deduce the likely effect of each sequence variation on Jan C.-C. -
Transcriptional Mechanisms of Resistance to Anti-PD-1 Therapy
Author Manuscript Published OnlineFirst on February 13, 2017; DOI: 10.1158/1078-0432.CCR-17-0270 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Transcriptional mechanisms of resistance to anti-PD-1 therapy Maria L. Ascierto1, Alvin Makohon-Moore2, 11, Evan J. Lipson1, Janis M. Taube3,4, Tracee L. McMiller5, Alan E. Berger6, Jinshui Fan6, Genevieve J. Kaunitz3, Tricia R. Cottrell4, Zachary A. Kohutek7, Alexander Favorov8,10, Vladimir Makarov7,11, Nadeem Riaz7,11, Timothy A. Chan7,11, Leslie Cope8, Ralph H. Hruban4,9, Drew M. Pardoll1, Barry S. Taylor11,12,13, David B. Solit13, Christine A Iacobuzio-Donahue2,11, and Suzanne L. Topalian5 From the 1Departments of Oncology, 3Dermatology, 4Pathology, 5Surgery, 6The Lowe Family Genomics Core, 8Oncology Bioinformatics Core, and the 9 Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287; the 10Laboratory of System Biology and Computational Genetics, Vavilov Institute of General Genetics, Russian Academy of Sciences, 119991, Moscow, Russia; and 2Pathology, 7Radiation Oncology, 11Human Oncology and Pathogenesis Program, 12Department of Epidemiology and Biostatistics, and the 13Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York NY 10065. MLA, AM-M, EJL, and JMT contributed equally to this work Running title: Transcriptional mechanisms of resistance to anti-PD-1 Key Words: melanoma, cancer genetics, immunotherapy, anti-PD-1 Financial Support: This study was supported by the Melanoma Research Alliance (to SLT and CI-D), the Bloomberg~Kimmel Institute for Cancer Immunotherapy (to JMT, DMP, and SLT), the Barney Family Foundation (to SLT), Moving for Melanoma of Delaware (to SLT), the 1 Downloaded from clincancerres.aacrjournals.org on October 2, 2021. -
Type of the Paper (Article
Cancers 2020, 12, S1 of S11 Supplementary Materials: Inflammatory Proteins HMGA2 and PRTN3 as Drivers of Vulvar Squamous Cell Carcinoma Pro- gression Agnieszka Fatalska, Natalia Rusetska, Elwira Bakuła-Zalewska, Artur Kowalik, Sebastian Zięba, Agnieszka Wroblewska, Kamil Zalewski, Krzysztof Goryca, Dominik Domański and Magdalena Kowalewska Text S1: Supplementary Methods iTRAQ (Isobaric Tags for Relative and Absolute Quantitation) Cell Lysis The samples were snap-frozen in liquid nitrogen immediately after collection and stored at −70°C before pulverization (with the Microdismembrator II, B Braun Biotech In- ternational, Melsungen, Germany). Forty-two (14 control, 16 d-fVSCC and 12 progVSCC) samples were subjected to deep proteomic analysis. Total cell lysates were obtained from approximately 100 mg of pulverized patient tissue samples. The frozen pulverized tissue samples were resuspended in 300 µl of cold Lysis Buffer (1% sodium deoxycholate (NaDOC) in 25 mM HEPES (4-(2-hydroxyethyl)-1-pipera- zineethanesulfonic acid), boiled for 5 min at 100 °C, and cooled to room temperature (RT) on ice. Next, nucleic acids were degraded with 30 µL of benzonase nuclease (2.5 U/µL in 25 mM HEPES) at 4 °C for 30 min. Samples were then centrifuged twice at 12,000 × g for 10 min at 4 °C and the supernatants were stored at −80 °C. Protein concentrations were determined using the Pierce (Appleton, WI, USA) Bicinchoninic Acid (BCA) Assay Kit according to the manufacturer’s instructions, for the 96-well plate format, in duplicate, at two different sample dilutions (ThermoFisher Scientific, Waltham, MA, USA). Sample Protein Extract Digestion and iTRAQ Labeling Protein extract digestion and iTRAQ tag labeling was conducted using the 8-plex iTRAQ assay and iTRAQ Reagent and Buffer Kits (AB SCIEX, Framingham, MA, USA). -
Amelogenesis Imperfecta - Literature Review
IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-ISSN: 2279-0853, p-ISSN: 2279-0861. Volume 13, Issue 1 Ver. IX. (Feb. 2014), PP 48-51 www.iosrjournals.org Amelogenesis Imperfecta - Literature Review GemimaaHemagaran1 ,Arvind. M2 1B.D.S.,Saveetha Dental College, Chennai, India 2B.D.S., M.D.S., Dip Oral medicine, Prof. of Oral Medicine, Saveetha Dental College, Chennai, India. Abstract: Amelogenesis Imperfecta (AI) is a group of inherited disorder of dental enamel formation in the absence of systemic manifestations. AI is also known as Hereditary enamel dysplasia, Hereditary brown enamel, Hereditary brown opalescent teeth. Since the mesodermal components of the teeth is normal, this defect is entirely ectodermal in origin. Variants of AI generally are classified as hypoplastic, hypocalcified, or hypomineralised types based on the primary enamel defect. The affected teeth may be discoloured, sensitive or prone to disintegration, leading to loss of occlusal vertical dimensions and very poor aesthetics. They exists in isolation or associated with other abnormalities in syndromes. It may show autosomal dominant, autosomal recessive, sex-linked and sporadic inheritance patterns. Mutations in the amelogenin, enamelin, and kallikrein-4 genes have been demonstrated to different types of AI. Keywords: AmelogenesisImperfecta, Hypoplastic, Hypocalcific, Hypomineralised. I. Introduction: Amelogenesis imperfecta (AI) is a term for a clinically and genetically heterogeneous group of conditions that affect the dental enamel, occasionally in conjunction with other dental, oral and extraoral tissues.[1] Dental enamel formation is divided into secretory, transition, and maturation stages. During the secretory stage, enamel crystals grow primarily in length. During the maturation stage, mineral is deposited exclusively on the sides of the crystallites, which grow in width and thickness to coalesce with adjacent crystals.[2]The main structural proteins in forming enamel are amelogenin, ameloblastin, and enamelin. -
Protein Nanoribbons Template Enamel Mineralization
Protein nanoribbons template enamel mineralization Yushi Baia, Zanlin Yub, Larry Ackermana, Yan Zhangc, Johan Bonded,WuLic, Yifan Chengb, and Stefan Habelitza,1 aDepartment of Preventative and Restorative Dental Sciences, School of Dentistry, University of California, San Francisco, CA 94143; bDepartment of Biochemistry and Biophysics, School of Medicine, University of California, San Francisco, CA 94158; cDepartment of Oral and Craniofacial Sciences, School of Dentistry, University of California, San Francisco, CA 94143; and dDivision of Pure and Applied Biochemistry, Center for Applied Life Sciences, Lund University, Lund, SE-221 00, Sweden Edited by Patricia M. Dove, Virginia Tech, Blacksburg, VA, and approved July 2, 2020 (received for review April 22, 2020) As the hardest tissue formed by vertebrates, enamel represents early tissue-based transmission electron microscopy (TEM) nature’s engineering masterpiece with complex organizations of studies also show the presence of filamentous protein assemblies fibrous apatite crystals at the nanometer scale. Supramolecular (18–20) that share great structural similarity with the recombi- assemblies of enamel matrix proteins (EMPs) play a key role as nant amelogenin nanoribbons (7, 12). Even though previous the structural scaffolds for regulating mineral morphology during XRD and TEM characterizations suggest that nanoribbons may enamel development. However, to achieve maximum tissue hard- represent the structural nature of the in vivo observed filamen- ness, most organic content in enamel is digested and removed at tous proteins, they do not provide sufficient resolution to make the maturation stage, and thus knowledge of a structural protein detailed comparison. In addition, the filamentous proteins in the template that could guide enamel mineralization is limited at this DEM match the size and alignment of apatite crystal ribbons date. -
(P -Value<0.05, Fold Change≥1.4), 4 Vs. 0 Gy Irradiation
Table S1: Significant differentially expressed genes (P -Value<0.05, Fold Change≥1.4), 4 vs. 0 Gy irradiation Genbank Fold Change P -Value Gene Symbol Description Accession Q9F8M7_CARHY (Q9F8M7) DTDP-glucose 4,6-dehydratase (Fragment), partial (9%) 6.70 0.017399678 THC2699065 [THC2719287] 5.53 0.003379195 BC013657 BC013657 Homo sapiens cDNA clone IMAGE:4152983, partial cds. [BC013657] 5.10 0.024641735 THC2750781 Ciliary dynein heavy chain 5 (Axonemal beta dynein heavy chain 5) (HL1). 4.07 0.04353262 DNAH5 [Source:Uniprot/SWISSPROT;Acc:Q8TE73] [ENST00000382416] 3.81 0.002855909 NM_145263 SPATA18 Homo sapiens spermatogenesis associated 18 homolog (rat) (SPATA18), mRNA [NM_145263] AA418814 zw01a02.s1 Soares_NhHMPu_S1 Homo sapiens cDNA clone IMAGE:767978 3', 3.69 0.03203913 AA418814 AA418814 mRNA sequence [AA418814] AL356953 leucine-rich repeat-containing G protein-coupled receptor 6 {Homo sapiens} (exp=0; 3.63 0.0277936 THC2705989 wgp=1; cg=0), partial (4%) [THC2752981] AA484677 ne64a07.s1 NCI_CGAP_Alv1 Homo sapiens cDNA clone IMAGE:909012, mRNA 3.63 0.027098073 AA484677 AA484677 sequence [AA484677] oe06h09.s1 NCI_CGAP_Ov2 Homo sapiens cDNA clone IMAGE:1385153, mRNA sequence 3.48 0.04468495 AA837799 AA837799 [AA837799] Homo sapiens hypothetical protein LOC340109, mRNA (cDNA clone IMAGE:5578073), partial 3.27 0.031178378 BC039509 LOC643401 cds. [BC039509] Homo sapiens Fas (TNF receptor superfamily, member 6) (FAS), transcript variant 1, mRNA 3.24 0.022156298 NM_000043 FAS [NM_000043] 3.20 0.021043295 A_32_P125056 BF803942 CM2-CI0135-021100-477-g08 CI0135 Homo sapiens cDNA, mRNA sequence 3.04 0.043389246 BF803942 BF803942 [BF803942] 3.03 0.002430239 NM_015920 RPS27L Homo sapiens ribosomal protein S27-like (RPS27L), mRNA [NM_015920] Homo sapiens tumor necrosis factor receptor superfamily, member 10c, decoy without an 2.98 0.021202829 NM_003841 TNFRSF10C intracellular domain (TNFRSF10C), mRNA [NM_003841] 2.97 0.03243901 AB002384 C6orf32 Homo sapiens mRNA for KIAA0386 gene, partial cds. -
Appendix 2. Significantly Differentially Regulated Genes in Term Compared with Second Trimester Amniotic Fluid Supernatant
Appendix 2. Significantly Differentially Regulated Genes in Term Compared With Second Trimester Amniotic Fluid Supernatant Fold Change in term vs second trimester Amniotic Affymetrix Duplicate Fluid Probe ID probes Symbol Entrez Gene Name 1019.9 217059_at D MUC7 mucin 7, secreted 424.5 211735_x_at D SFTPC surfactant protein C 416.2 206835_at STATH statherin 363.4 214387_x_at D SFTPC surfactant protein C 295.5 205982_x_at D SFTPC surfactant protein C 288.7 1553454_at RPTN repetin solute carrier family 34 (sodium 251.3 204124_at SLC34A2 phosphate), member 2 238.9 206786_at HTN3 histatin 3 161.5 220191_at GKN1 gastrokine 1 152.7 223678_s_at D SFTPA2 surfactant protein A2 130.9 207430_s_at D MSMB microseminoprotein, beta- 99.0 214199_at SFTPD surfactant protein D major histocompatibility complex, class II, 96.5 210982_s_at D HLA-DRA DR alpha 96.5 221133_s_at D CLDN18 claudin 18 94.4 238222_at GKN2 gastrokine 2 93.7 1557961_s_at D LOC100127983 uncharacterized LOC100127983 93.1 229584_at LRRK2 leucine-rich repeat kinase 2 HOXD cluster antisense RNA 1 (non- 88.6 242042_s_at D HOXD-AS1 protein coding) 86.0 205569_at LAMP3 lysosomal-associated membrane protein 3 85.4 232698_at BPIFB2 BPI fold containing family B, member 2 84.4 205979_at SCGB2A1 secretoglobin, family 2A, member 1 84.3 230469_at RTKN2 rhotekin 2 82.2 204130_at HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2 81.9 222242_s_at KLK5 kallikrein-related peptidase 5 77.0 237281_at AKAP14 A kinase (PRKA) anchor protein 14 76.7 1553602_at MUCL1 mucin-like 1 76.3 216359_at D MUC7 mucin 7, -
Microarray Analysis of Novel Genes Involved in HSV- 2 Infection
Microarray analysis of novel genes involved in HSV- 2 infection Hao Zhang Nanjing University of Chinese Medicine Tao Liu ( [email protected] ) Nanjing University of Chinese Medicine https://orcid.org/0000-0002-7654-2995 Research Article Keywords: HSV-2 infection,Microarray analysis,Histospecic gene expression Posted Date: May 12th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-517057/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/19 Abstract Background: Herpes simplex virus type 2 infects the body and becomes an incurable and recurring disease. The pathogenesis of HSV-2 infection is not completely clear. Methods: We analyze the GSE18527 dataset in the GEO database in this paper to obtain distinctively displayed genes(DDGs)in the total sequential RNA of the biopsies of normal and lesioned skin groups, healed skin and lesioned skin groups of genital herpes patients, respectively.The related data of 3 cases of normal skin group, 4 cases of lesioned group and 6 cases of healed group were analyzed.The histospecic gene analysis , functional enrichment and protein interaction network analysis of the differential genes were also performed, and the critical components were selected. Results: 40 up-regulated genes and 43 down-regulated genes were isolated by differential performance assay. Histospecic gene analysis of DDGs suggested that the most abundant system for gene expression was the skin, immune system and the nervous system.Through the construction of core gene combinations, protein interaction network analysis and selection of histospecic distribution genes, 17 associated genes were selected CXCL10,MX1,ISG15,IFIT1,IFIT3,IFIT2,OASL,ISG20,RSAD2,GBP1,IFI44L,DDX58,USP18,CXCL11,GBP5,GBP4 and CXCL9.The above genes are mainly located in the skin, immune system, nervous system and reproductive system. -
The Transition from Primary Colorectal Cancer to Isolated Peritoneal Malignancy
medRxiv preprint doi: https://doi.org/10.1101/2020.02.24.20027318; this version posted February 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . The transition from primary colorectal cancer to isolated peritoneal malignancy is associated with a hypermutant, hypermethylated state Sally Hallam1, Joanne Stockton1, Claire Bryer1, Celina Whalley1, Valerie Pestinger1, Haney Youssef1, Andrew D Beggs1 1 = Surgical Research Laboratory, Institute of Cancer & Genomic Science, University of Birmingham, B15 2TT. Correspondence to: Andrew Beggs, [email protected] KEYWORDS: Colorectal cancer, peritoneal metastasis ABBREVIATIONS: Colorectal cancer (CRC), Colorectal peritoneal metastasis (CPM), Cytoreductive surgery and heated intraperitoneal chemotherapy (CRS & HIPEC), Disease free survival (DFS), Differentially methylated regions (DMR), Overall survival (OS), TableFormalin fixed paraffin embedded (FFPE), Hepatocellular carcinoma (HCC) ARTICLE CATEGORY: Research article NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. 1 medRxiv preprint doi: https://doi.org/10.1101/2020.02.24.20027318; this version posted February 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . NOVELTY AND IMPACT: Colorectal peritoneal metastasis (CPM) are associated with limited and variable survival despite patient selection using known prognostic factors and optimal currently available treatments. -
Sequence Diversity of Pan Troglodytes Subspecies and the Impact of WFDC6 Selective Constraints in Reproductive Immunity
GBE Sequence Diversity of Pan troglodytes Subspecies and the Impact of WFDC6 Selective Constraints in Reproductive Immunity Ze´lia Ferreira1,2,3,4,*,y, Belen Hurle1,y, Aida M. Andre´s5,WarrenW.Kretzschmar6, James C. Mullikin7, Praveen F. Cherukuri7, Pedro Cruz7, Mary Katherine Gonder8,AnneC.Stone9, Sarah Tishkoff10, Willie J. Swanson11, NISC Comparative Sequencing Program1,7, Eric D. Green1, Andrew G. Clark12,and Downloaded from Susana Seixas2 1National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 2Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal 3Department of Zoology and Anthropology, Faculty of Sciences, University of Porto, Porto, Portugal http://gbe.oxfordjournals.org/ 4Department of Computational and Systems Biology, University of Pittsburgh 5Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany 6Genomic Medicine and Statistics, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom 7NIH Intramural Sequencing Center (NISC), National Human Genome Research Institute, National Institutes of Health, Rockville, MD 8Department of Biology, Drexel University 9School of Human Evolution and Social Change, Arizona State University 10Departments of Genetics and Biology, University of Pennsylvania at Max Planck Institut Fuer Evolutionaere Anthropologie on February 11, 2014 11Department of Genome Sciences, University of Washington 12Department of Biology of Molecular Biology and Genetics, Cornell University *Corresponding author: Department of Computational and Systems Biology, University of Pittsburgh. E-mail: [email protected]. yThese authors contributed equally to this work. Accepted: December 2, 2013 Abstract Recent efforts have attempted to describe the population structure of common chimpanzee, focusing on four subspecies: Pan troglodytes verus, P.