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No Cell Line Source 1 NCI-H28 ATCC 2 NCI-H2452 ATCC 3 NCI-H2052

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SUPPLEMENTARY TABLE S1. List of 19 MM cell lines used in this study. No Cell line Source 1 NCI-H28 ATCC 2 NCI-H2452 ATCC 3 NCI-H2052 ATCC 4 MSTO-211H ATCC 5 ACC-MESO-1 RBCCB 6 ACC-MESO-4 RBCCB 7 HMMME RBCCB 8 ONE58 ECACC 9 NO36 ECACC 10 LO68 ECACC 11 Mero-14 ECACC 12 Mero-25 ECACC 13 Mero-41 ECACC 14 Mero-48a ECACC 15 Mero-82 ECACC 16 Mero-83 ECACC 17 Mero-84 ECACC 18 Mero-95 ECACC 19 NCI-H226 ATCC Abbreviations: ATCC, American Type Culture Collection (Manassas,VA); RBCCB, RIKEN BioResource Center Cell Bank (Tsukuba, Japan); ECACC, European Collection of Cell Cultures (Salisbury, UK). SUPPLEMENTARY TABLE S2. Clinicopathological characteristics of 23 MM cases subjected to targeted exon sequ Asbestos Pathological Sample Tumor / normal Gender Age Smoking Surgery exposure type CT-1T Tumor and normal F 40 no yes B panpleuropneumonectomy CT-2T Tumor and normal M 51 yes no E panpleuropneumonectomy CT-3T Tumor and normal M 50 yes no B panpleuropneumonectomy CT-4T Tumor and normal M 56 yes no E panpleuropneumonectomy CT-5T Tumor and normal M 67 yes no E panpleuropneumonectomy CT-6T Tumor and normal M 60 yes yes B panpleuropneumonectomy CT-7T Tumor and normal M 48 yes no E panpleuropneumonectomy CT-9T Tumor and normal M 46 no no B panpleuropneumonectomy CT-10T Tumor and normal M 54 yes yes E panpleuropneumonectomy CT-11T Tumor and normal M 61 yes yes B panpleuropneumonectomy CT-12T Tumor and normal M 50 yes no E panpleuropneumonectomy CT-13T Tumor and normal F 56 no no E panpleuropneumonectomy CT-14T Tumor and normal M 62 yes yes E panpleuropneumonectomy CT-15T Tumor and normal M 66 no yes B panpleuropneumonectomy CT-18T Tumor and normal M 61 yes unknown S panpleuropneumonectomy CT-19T Tumor and normal M 68 yes yes B panpleuropneumonectomy CT-20T Tumor and normal M 60 yes unknown E panpleuropneumonectomy CT-21T Tumor and normal M 71 yes yes S panpleuropneumonectomy CT-22T Tumor and normal M 58 yes no E panpleuropneumonectomy CT-23T Tumor and normal F 52 yes unknown E panpleuropneumonectomy CT-24T Tumor and normal M 65 yes yes B panpleuropneumonectomy CT-33T Tumor and normal M 55 yes yes B panpleuropneumonectomy CT-46T Tumor and normal M 41 yes unknown B panpleuropneumonectomy Abbreviations: B, Biphasic; E, Epithelial; S, Sarcomatous; F, Female; M, Male. SUPPLEMENTARY TABLE S3. Hippo pathway genes sequenced in this study. Gene symbol Target HGNC ID Function Location LATS1 exon + intron HGNC:6514 LATS, large tumor suppressor, homolog 1 (Drosophila) 6q25.1 LATS2 exon + intron HGNC:6515 LATS, large tumor suppressor, homolog 2 (Drosophila) 13q11-q12 FAT4 exon HGNC:23109 FAT tumor suppressor homolog 4 (Drosophila) 4q28.1 CRB1 exon HGNC:2343 crumbs homolog 1 (Drosophila) 1q31-q32.1 CRB2 exon HGNC:18688 crumbs homolog 2 (Drosophila) 9q33.2 CRB3 exon HGNC:20237 crumbs homolog 3 (Drosophila) 19p13.3 NF2 exon HGNC:7773 neurofibromin 2 (merlin) 22q12.2 FRMD1 exon HGNC:21240 FERM domain containing 1 6q27 RASSF2 exon HGNC:9883 Ras association (RalGDS/AF-6) domain family member 2 20p13 RASSF3 exon HGNC:14271 Ras association (RalGDS/AF-6) domain family member 3 12q14.2 RASSF4 exon HGNC:20793 Ras association (RalGDS/AF-6) domain family member 4 10q11.1 RASSF5 exon HGNC:17609 Ras association (RalGDS/AF-6) domain family member 5 1q31 RASSF6 exon HGNC:20796 Ras association (RalGDS/AF-6) domain family member 6 4q21.1 KIBRA exon HGNC:29435 WW and C2 domain containing 1 5q34 MST2 exon HGNC:11406 serine/threonine kinase 3 8q22.2 MST3 exon HGNC:11403 serine/threonine kinase 24 13q31.2-q32.3 MST4 exon Gene ID: 51765 Serine/threonine protein kinase MST4 Xq26.2 MOB3C exon HGNC:29800 MOB kinase activator 3C 1p34.1 MOB4 exon HGNC:17261 MOB family member 4, phocein 2q33.1 MOB1B exon HGNC:29801 MOB kinase activator 1B 4q13.3 MOB2 exon HGNC:24904 MOB kinase activator 2 11p15.5 MOB3A exon HGNC:29802 MOB kinase activator 3A 19p13.3 MOB3B exon HGNC:23825 MOB kinase activator 3B 9p21.1 FRMD6 exon HGNC:19839 FERM domain containing 6 14q22.1 RASSF1A exon HGNC:9882 Ras association (RalGDS/AF-6) domain family member 1 3p21.3 SAV1 exon HGNC:17795 salvador homolog 1 (Drosophila) 14q13-q23 MST1 exon HGNC:7380 macrophage stimulating 1 (hepatocyte growth factor-like) 3p21 MOB1A exon HGNC:16015 MOB kinase activator 1A 2p13.1 TAZ exon HGNC:11577 tafazzin Xq28 YWHAB exon HGNC:12849 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, beta polypeptide 20q13.1 YWHAE exon HGNC:12851 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, epsilon polypeptide 17p13.3 YWHAG exon HGNC:12852 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide 7q11.23 YWHAH exon HGNC:12853 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, eta polypeptide 22q12.1-q13.1 YWHAQ exon HGNC:12854 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, theta polypeptide 2p25.2-p25.1 YWHAZ exon HGNC:12855 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide 8q22.3 YWHAS exon HGNC:10773 stratifin 1p36.11 TEAD1 exon HGNC:11714 TEA domain family member 1 (SV40 transcriptional enhancer factor) 11p15.4 TEAD2 exon HGNC:11715 TEA domain family member 2 19q13.3 TEAD3 exon HGNC:11716 TEA domain family member 3 6p21.2 TEAD4 exon HGNC:11717 TEA domain family member 4 12p13.3-p13.2 SUPPLEMENTARY TABLE S4. Whole-exon sequencing of 6 MM cell lines. No. Gene symbol Chr RefSeqb cDNA Amino acid Type 211H H2452 H28 MESO4 H2052 MESO1 1 EI24 11 NM_001007277 c.732_733insC p.R244fs frameshift insertion ○ ○ ○ ○ ○ ○ 2 KRTAP4-8 17 NM_031960 c.C204A p.S68R nonsynonymous SNV - - ○ - - ○ KRTAP4-8 17 NM_031960 c.2_3insA p.M1fs frameshift insertion ○ ○ ○ ○ ○ ○ 3 PRIM2 6 NM_000947 c.889_890insA p.E297fs frameshift insertion ○ ○ ○ ○ ○ ○ PRIM2 6 NM_000947 c.C916T p.R306X stopgain SNV - ○ - - - - 4 PRSS1 7 NM_002769 c.A508G p.K170E nonsynonymous SNV ○ ○ - - ○ ○ PRSS1 7 NM_002769 c.G512A p.C171Y nonsynonymous SNV ○ - - ○ - - PRSS1 7 NM_002769 c.G542A p.S181N nonsynonymous SNV ○ ○ ○ ○ ○ ○ 5 PRSS2 7 NM_002770 c.C10T p.P4S nonsynonymous SNV - - ○ ○ - - PRSS2 7 NM_002770 c.C47T p.T16I nonsynonymous SNV ○ ○ ○ ○ ○ ○ PRSS2 7 NM_002770 c.C95A p.S32Y nonsynonymous SNV ○ ○ ○ ○ ○ ○ 6 PRSS3 9 NM_001197098 c.284_285del p.95_95del frameshift deletion ○ - ○ - - - PRSS3 9 NM_001197098 c.A493G p.K165E nonsynonymous SNV - ○ - - - - PRSS3 9 NM_001197098 c.G524A p.S175N nonsynonymous SNV ○ ○ ○ ○ ○ ○ PRSS3 9 NM_001197098 c.639delT p.C213fs frameshift deletion - - ○ - - - 7 ZNF595 4 NM_182524 c.600_601insA p.Y200fs frameshift insertion ○ ○ ○ ○ ○ ○ 8 DDHD1 14 NM_001160148 c.337_338insGGCGGC p.S113delinsGGS nonframeshift insertion ○ ○ - ○ ○ ○ 9 KRT10 17 NM_000421 c.1637_1638del p.546_546del frameshift deletion - - ○ - - - KRT10 17 NM_000421 c.1468_1479del p.490_493del nonframeshift deletion ○ - - ○ ○ ○ KRT10 17 NM_000421 c.1473_1477del p.491_493del frameshift deletion - - ○ - - - 10 MLL3 7 NM_170606 c.A11405G p.D3802G nonsynonymous SNV - - - - ○ - MLL3 7 NM_170606 c.2448_2449insA p.Y816_I817delinsX stopgain SNV ○ ○ ○ - - ○ 11 OR1B1 9 NM_001004450 c.45_46insT p.L15fs frameshift insertion ○ ○ ○ ○ ○ - 12 ZAN 7 NM_173059 c.3290_3292del p.1097_1098del nonframeshift deletion - ○ - - ○ - ZAN 7 NM_003386 c.5767_5768insG p.F1923fs frameshift insertion ○ ○ - ○ - ○ 13 ALMS1 2 NM_015120 c.1570_1571insCTC p.S524delinsSP nonframeshift insertion ○ ○ - - ○ ○ 14 FZD1 7 NM_003505 c.264_265insCCG p.Q88delinsQP nonframeshift insertion ○ - ○ - ○ ○ 15 HOXD9 2 NM_014213 c.794_795insGCA p.P265delinsPQ nonframeshift insertion ○ ○ ○ ○ - - 16 KDM6B 17 NM_001080424 c.752_753insACCACC p.L251delinsLPP nonframeshift insertion - ○ - - ○ - KDM6B 17 NM_001080424 c.753_755del p.251_252del nonframeshift deletion - - - ○ - - KDM6B 17 NM_001080424 c.C1881G p.S627R nonsynonymous SNV - - ○ - - - 17 SLC9B1 4 NM_139173 c.1338_1339del p.446_447del frameshift deletion - - ○ ○ ○ ○ 18 AHNAK 11 NM_001620 c.C8897T p.P2966L nonsynonymous SNV ○ - - - - - AHNAK 11 NM_001620 c.C7225T p.P2409S nonsynonymous SNV - - - - ○ - AHNAK 11 NM_001620 c.C5565G p.I1855M nonsynonymous SNV - - - - - ○ 19 C15orf40 15 NM_001160113 c.396_397insT p.L132fs frameshift insertion ○ ○ - - - - C15orf40 15 NM_001160113 c.395delT p.L132X stopgain SNV - - - - - ○ 20 CDC27 17 NM_001114091 c.C818G p.A273G nonsynonymous SNV ○ - - ○ ○ - 21 COL6A6 3 NM_001102608 c.T3410C p.I1137T nonsynonymous SNV ○ - - - - - COL6A6 3 NM_001102608 c.C3883T p.R1295X stopgain SNV - - - - ○ - COL6A6 3 NM_001102608 c.T5542C p.F1848L nonsynonymous SNV - - ○ - - - 22 LOC388946 2 NM_001145051 c.462delG p.E154fs frameshift deletion ○ - - - ○ ○ 23 MAGEF1 3 NM_022149 c.477_478insGGA p.D159delinsED nonframeshift insertion ○ ○ ○ - - - 24 MCC 5 NM_001085377 c.64_65insGGC p.S22delinsGS nonframeshift insertion - ○ - ○ - ○ 25 MEGF9 9 NM_001080497 c.89_94del p.30_32del nonframeshift deletion - ○ ○ ○ - - 26 NBPF9 1 NM_001037675 c.116_117insAG p.K39fs frameshift insertion ○ ○ - ○ - - 27 NUDT11 X NM_018159 frameshift deletion ○ - - ○ - ○ 28 OVGP1 1 NM_002557 c.1560_1561insA p.G520fs frameshift insertion ○ - - - ○ ○ 29 RBMX X NM_002139 c.906_907insCC p.P302fs frameshift insertion ○ - - - ○ - RBMX X NM_002139 c.316_317insTT p.P106fs frameshift insertion ○ - ○ - ○ - 30 TDG 12 NM_003211 c.286_287insA p.E96fs frameshift insertion - ○ ○ ○ - - 31 ZFHX3 16 NM_001164766 c.2482_2483insCAA p.A828delinsQA nonframeshift insertion - - ○ - - - ZFHX3 16 NM_001164766 c.2476_2481del p.826_827del nonframeshift deletion - - - - - ○ ZFHX3 16 NM_006885 c.C1114G p.R372G nonsynonymous SNV - - - ○ - - 32 ABCA7 19 NM_019112 c.1180_1190del p.394_397del frameshift deletion
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    Inferring the progression of multifocal liver cancer from spatial and temporal genomic heterogeneity The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Shi, J., Q. Xing, M. Duan, Z. Wang, L. Yang, Y. Zhao, X. Wang, et al. 2016. “Inferring the progression of multifocal liver cancer from spatial and temporal genomic heterogeneity.” Oncotarget 7 (3): 2867-2877. doi:10.18632/oncotarget.6558. http:// dx.doi.org/10.18632/oncotarget.6558. Published Version doi:10.18632/oncotarget.6558 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:27320297 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA www.impactjournals.com/oncotarget/ Oncotarget, Vol. 7, No. 3 Inferring the progression of multifocal liver cancer from spatial and temporal genomic heterogeneity Jie-Yi Shi1,†, Qingfeng Xing2,†, Meng Duan1,†, Zhi-Chao Wang1,†, Liu-Xiao Yang1, Ying-Jun Zhao3, Xiao-Ying Wang1, Yun Liu2, Minghua Deng2, Zhen-Bin Ding1, Ai-Wu Ke1, Jian Zhou1,4, Jia Fan1,4, Ya Cao5, Jiping Wang6, Ruibin Xi2, Qiang Gao1 1 Liver Cancer Institute, Zhongshan Hospital, and Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, P. R. China 2School of Mathematical Sciences and Center for Statistical Science, Peking University, Beijing, P. R. China 3 Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shangai, P.
  • Essential Oil from Pinus Koraiensis Pinecones Inhibits Gastric Cancer Cells Via the HIPPO/YAP Signaling Pathway

    Essential Oil from Pinus Koraiensis Pinecones Inhibits Gastric Cancer Cells Via the HIPPO/YAP Signaling Pathway

    molecules Article Essential Oil from Pinus Koraiensis Pinecones Inhibits Gastric Cancer Cells via the HIPPO/YAP Signaling Pathway Yandong Zhang 1, Chao Xin 1, Junqiang Qiu 2 and Zhenyu Wang 1,* 1 Department of Food Science and Engineering, School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin 150090, China; [email protected] (Y.Z.); [email protected] (C.X.) 2 Department of Inorganic Chemistry and Analytical Chemistry, School of Pharmacy, Hainan Medical University, Haikou 570100, China; [email protected] * Correspondence: [email protected] Received: 17 September 2019; Accepted: 22 October 2019; Published: 25 October 2019 Abstract: Pinecone is a traditional folk herb, which has been used in China for many years. In this paper, the essential oil from Pinus koraiensis pinecones (PEO) was obtained by hydrodistillation and 41 compounds were identified by gas chromatography–mass spectrometry (GC-MS), mainly including α-Pinene (40.91%), Limonene (24.82%), and β-Pinene (7.04%). The purpose of this study was to investigate the anti-tumor activity of PEO on MGC-803 cells and its mechanism. Anti-tumor experiments in vitro showed PEO could significantly inhibit the proliferation and migration of MGC-803 cells, and it also could arrest the cell cycle in the G2/M phase, decrease the mitochondrial membrane potential, and induce apoptosis. Finally, the effects of PEO on genes expression on MGC-803 cells were analyzed by RNA sequencing, and results showed that after treatment with PEO, 100 genes were up-regulated, and 57 genes were down-regulated. According to the KEGG pathway and GSEA, FAT4, STK3, LATS2, YAP1, and AJUBA were down-regulated, which were related to HIPPO signaling pathway.
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD

    Supplementary Table S4. FGA Co-Expressed Gene List in LUAD

    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
  • Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene

    Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene

    Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A.
  • This Thesis Has Been Submitted in Fulfilment of the Requirements for a Postgraduate Degree (E.G

    This Thesis Has Been Submitted in Fulfilment of the Requirements for a Postgraduate Degree (E.G

    This thesis has been submitted in fulfilment of the requirements for a postgraduate degree (e.g. PhD, MPhil, DClinPsychol) at the University of Edinburgh. Please note the following terms and conditions of use: This work is protected by copyright and other intellectual property rights, which are retained by the thesis author, unless otherwise stated. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author. The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author. When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given. The CX3CR1/CX3CL1 Axis Drives the Migration and Maturation of Oligodendroglia in the Central Nervous System Catriona Ford Thesis Submitted for the Degree of Doctor of Philosophy The University of Edinburgh 2017 Abstract In the central nervous system, the axons of neurons are protected from damage and aided in electrical conductivity by the myelin sheath, a complex of proteins and lipids formed by oligodendrocytes. Loss or damage to the myelin sheath may result in impairment of electrical axonal conduction and eventually to neuronal death. Such demyelination is responsible, at least in part, for the disabling neurodegeneration observed in pathologies such as Multiple Sclerosis (MS) and Spinal Cord Injury. In the regenerative process of remyelination, oligodendrocyte precursor cells (OPCs), the resident glial stem cell population of the adult CNS, migrate toward the injury site, proliferate and differentiate into adult oligodendrocytes which subsequently reform the myelin sheath.