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Tumor-Specific Chromosome Mis-Segregation Controls Cancer Plasticity by Maintaining Tumor Heterogeneity

Figure 1

Proportion of cells with Chr7 number variation in high- and low-grade gliomas and glioma primary cultures.

A, ternary plot of population proportions with 1 copy (deletion), 2 copies (normal), and 3 or more (amplification) copies of Chr7, based on CEP7 signals in Ffuorescent in situ hybridization (FISH) of 14 glioblastoma multiformes (GBMs, Red triangle) and 12 oligodendroglial tumor (OGs, black square), P = 0.0012 from MANOVA analysis. B, comparison of tumor heterogeneity with regard to chromosome 7 (Chr7) aneuploidy in the original tumor (T) and corresponding 3ā€“4 week-old primary cultures under serum adherent (SA) or neural sphere (NS) culture conditions. Cā€“D, patterns of cells with Chr7-CNV in sequential and high-EGFR amplified GBMs. Representative FISH pictures of cells carrying 1ā€“4 copies of Chr7 with focal EGFR amplification.

Figure 1