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. Author manuscript; available in PMC: 2022 Jun 30.
Published in final edited form as: Oncogene. 2006 Jul 31;26(6):822–835. doi: 10.1038/sj.onc.1209847

Figure 2.

Figure 2

CoAA gene amplification is independent of CCND1. Quantitative real-time PCR analysis of CoAA (primers P6) and CCND1 (primers P14) was performed using genomic DNA from non-small cell lung carcinomas (NSCLC), squamous cell skin cancers, lymphomas, and lung cancer cell lines. Each PCR was normalized by a single copy gene, thyroid hormone receptor alpha (TRa). Serial dilution of normal human genomic DNA was used as standard (Supplemental Figure S4). Data shown represent mean of duplicate PCR as the fold increase of each gene. The experiments were repeated a minimum of twice with representative data shown. Normal genomic DNA control is indicated as N. Lung cancers include squamous cell lung carcinoma (1, 2, 3, 5, 6, 17, 18, 19, 20) and adenocarcinoma (4, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16). Lymphomas include follicular lymphoma (1, 2, 3, 4, 5, 6, 7, 8, 9), and large B cell lymphoma (10, 11, 12).