Papers unsubmitted for cell line issues and then resubmitted, by continent in 2011–2013.

<p>Generated from <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s001" target="_blank">S1 Data</a>.</p

Percentages of papers unsubmitted for cell line issues, by continent and by year.

<p>Generated from <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s001" target="_blank">S1 Data</a> and <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s002" target="_blank">S2 Data</a>.</p

Usage of five misidentified cell lines in the scientific literature as shown by PubMed searches for cell line name and incorrect tissue identity.

<p>Usage of five misidentified cell lines in the scientific literature as shown by PubMed searches for cell line name and incorrect tissue identity.</p

Journals that include instructions or requirements for cell line authentication in their author guidelines [28].

<p>Journals that include instructions or requirements for cell line authentication in their author guidelines [<a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.ref028" target="_blank">28</a>].</p

Acceptance rate for all submissions and for papers previously unsubmitted for cell line issues for Asia, by year.

<p>Generated from <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s001" target="_blank">S1 Data</a>, <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s002" target="_blank">S2 Data</a>, and <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s003" target="_blank">S3 Data</a>.</p

Acceptance rate for all submissions and for papers previously unsubmitted for cell line issues, by continent in 2011–2013.

<p>Generated from <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s001" target="_blank">S1 Data</a>, <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s002" target="_blank">S2 Data</a>, and <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2001438#pbio.2001438.s003" target="_blank">S3 Data</a>.</p

Workflow at the <i>IJC</i>, including checking of cell line documents.

<p>Workflow at the <i>IJC</i>, including checking of cell line documents.</p

Journal articles using the misidentified cell line HBL-100.

<p>Journal articles using the misidentified cell line HBL-100.</p

Application of aPRIMES in pediatric medulloblastoma identifying groups with low and high methylation

<p><b>Copyright information:</b></p><p>Taken from "Array-based profiling of reference-independent methylation status (aPRIMES) identifies frequent promoter methylation and consecutive downregulation of ZIC2 in pediatric medulloblastoma"</p><p></p><p>Nucleic Acids Research 2007;35(7):e51-e51.</p><p>Published online 7 Mar 2007</p><p>PMCID:PMC1874664.</p><p>© 2007 The Author(s)</p> () Scatter plots representing the correlation of methylation patterns of monozygotic twins (patients M1 and M10) with simultaneous desmoplastic medulloblastoma, a case of sporadic classic medulloblastoma (M5), and normal cerebellum. () twin one (patient M1) in comparison with normal cerebellum (pool of five unaffected donors), () twin 1 versus twin 2 (patient M10) and () twin one compared with a sporadic classic medulloblastoma (patient M5). Spearman-correlation coefficients () are given for each plot. Representative microarray sections of () patient M1 (low methylator group) and () patient M5 (high methylator group). Examples for differentially methylated clones are highlighted with white circles. () Kaplan–Meier plot of estimated survival time distribution with corresponding log-rank test. For survival analysis, patients were grouped into low and high methylator groups according to the percentage of highly methylated clones

Proliferation and accumulation of GCPs in postnatal cerebellum.

<p>(A) Immunofluorescent co-staining of NeuN (green) and Ki-67 (red) on FFPE sections from P9 cerebella showed an increased accumulation of proliferating GCP in the EGL of <i>Ptch1^+/− Nos2^−/−</i> mice. Overview sections were acquired by wide-field microscopy and detail images by confocal laser scanning microscopy. Blue: DAPI-stained nuclei. White arrows denote proliferating granule cells in the IGL. (B) High magnification images of the EGL and ML displayed altered morphologies especially in <i>Ptch1^+/− Nos2^−/−</i> and <i>Ptch1^+/+ Nos2^−/−</i> mice. (C) Cell counts from immunofluorescence images. Numbers of proliferating (Ki-67+) and non-proliferating (Ki67−) cells normalized to the length of the EGL edge show significant enrichment of dividing cells in <i>Ptch1^+/− Nos2^−/−</i> mice and correspondingly low numbers for <i>Ptch1^+/+ Nos2^−/−</i> mice. Ratios of dividing to non-dividing cells (Ki-67+, Ki-67− NeuN+) are indicated for each genotype. Significant differences are indicated by asterisks (*p<0.05). Scale bars = 50 µM. EGL: external granule layer, ML: molecular layer, IGL: internal granule layer.</p