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. 2021 May 24;12:3046. doi: 10.1038/s41467-021-23379-3

Fig. 2. NPC cancer driver pathways and networks revealed by somatic CNVs.

Fig. 2

a Global chromosomal gains (red) and deletions (blue) revealing frequent chromosomal deletions in Chr. 3p, 9p, 14q, 16q, and amplification of Chr. 3q, 8q, 12p, 12q, 18q as major feature of NPC (n = 99 tumors). b Average chromosomal gain (red) and loss (blue) frequencies among different NPC subtypes (n = 99 tumors). Violin plots show the kernel probability density of the data at different values. Inside boxplots represent median levels, first and third percentiles. Whiskers indicate 1.5× inter-quartile range (IQR) extending from the hinges. Points above the upper and lower whiskers represent the outliers (>1.5× IQR). Statistical significance was calculated using two-sided t-test. No significant subtype-specific difference on either gain or loss was observed (p > 0.05), except EC vs. SC on chromosomal gain frequencies (p = 0.039). 55 EC, 24 MESC and 17 SC tumors were analyzed. c Top frequent CNVs identified from this cohort revealing common and subtype-specific driver mutational pathways of NPC. CNVs involving in G1-S transition, NF-κB signaling, receptor tyrosine kinase (RTK), chromatin remodeling, microtubule polymerization, mitosis regulation, DNA repair, and EMT/invasion were suggested as NPC oncogenic drivers. Information of subtype, sample type, WHO subtype, gender, age of diagnosis, tumor stage, node classification, metastasis, and smoking status are shown at the bottom. 99 tumor samples were used for CNV identification. d Subtype-specific chromosomal gains (red) and deletions (blue). Chromosomal amplifications of Chr. 1q, 5p, 7p, 15q, 17q, 20q, 21q, 22q and deletions in Chr. 5q, 13q exhibited significant differences among NPC subtypes. Important subtype-specific CNVs are indicated at top and bottom region. e Subtype-specific aberrant cancer driver pathways and networks in EC and SC subtypes. Important signaling pathways, including microtubule polymerization, mitosis regulation, NF-κB signaling, and EMT/invasion, were suggested to contribute to NPC subtype specificity.