Pfeiffer

t(14;18) Translocation and BCL2 Expression in the Pfeiffer Cell Line

Chromosomal rearrangements can alter genome organization and gene expression. In leukemia, nuclear positioning of fusion genes from chromosomal translocations can exacerbate gene expression, but this is understudied in lymphoma. Garimberti et al. explored genome organization in lymphoma cells Pfeiffer with the t(14;18)(q32;q21) rearrangement, which overexpresses the BCL2 gene, using fluorescence in situ hybridization (FISH) to map chromosome territories and translocated genes in the Pfeiffer cell line.

The t(14;18) translocation in the Pfeiffer cell line was confirmed by FISH. Due to the limited extent of the translocated portion from chromosome 14, der(18) was undetectable with whole chromosome painting (WCP) (Fig. 1A). However, using both WCP and bacterial artificial clone (BAC) probes, they clearly identified der(14) and the IGH::BCL2 gene fusion (Fig. 1). This translocation correlates with BCL2 expression in the Pfeiffer cell line and in lymphoma patients (Fig. 2). RNA-seq data from the Cancer Cell Line Encyclopedia (CCLE) showed high BCL2 expression in diffuse large B-cell lymphoma lines, including Pfeiffer, and low expression in whole blood and non-cancerous tissue (Fig. 2A). BCL2 expression in Pfeiffer cells was also confirmed by in-house reverse transcription (RT) PCR (Fig. 1E). Additionally, BCL2 expression was significantly higher in follicular lymphoma patients with t(14;18) compared to those without, based on publicly available data (GSE16131) (Fig. 2B).

RNA-seq Analysis Reveals the Hub Genes of Paclitaxel Inhibition on Adriamycin Resistant DLBCL Cells

40% of patients with diffuse large B-cell lymphoma (DLBCL) are insensitive to first-line chemotherapy, in which Adriamycin is the main drug. The previous work showed that Paclitaxel may be a therapeutic for Adriamycin-resistant DLBCL. Here, Hong et al. sought to elucidate the molecular mechanisms by which Paclitaxel treats Adriamycin-resistant DLBCL using RNA-seq and network analysis. CCK-8 assay results showed that Paclitaxel and Adriamycin significantly inhibited Pfeiffer and Pfeiffer/ADM cell proliferation in a dose- and time-dependent manner (Fig. 3). The IC₅₀ of Paclitaxel in Pfeiffer/ADM cells was 0.4912 ± 0.0230 μmol/L, significantly lower than Adriamycin (1.3256 ± 0.0328 μmol/L), indicating that the sensitivity of Paclitaxel was higher (Fig. 4). RNA sequencing results identified 971 differentially expressed genes (DEGs), which included 519 upregulated and 452 downregulated genes (Fig. 5).