Table 1 Preclinical studies with single-agent lenalidomide in NHL

Gandhi et al. [11]

Namalwa CSN.70 (Burkitt lymphoma) cells

• Len inhibited proliferation of B-cell lymphoma cells and interfered with Gab1 phosphorylation and adaptor protein complex assembly.

Reddy et al. [14]

Rtx-resistant cell lines created from Raji (Burkitt lymphoma) cells

• Len improved Rtx anti-tumor activity and partially overcame Rtx resistance by augmenting ADCC.

Verhelle et al. [50]

Namalwa (Burkitt lymphoma) and normal CD34+ progenitor cells

• Len plus pomalidomide inhibited proliferation of malignant B cells while expanding population of normal CD34+ progenitor cells.

Zhu et al. [12]

Raji (Burkitt lymphoma), K562 (CLL), PC-3 (prostate cancer), and PBMC cells

• Len plus pomalidomide induced apoptosis through NK cell activation.

Gaidarova et al. [51]

MCL and PBMC (healthy donor) cells

• Len enhanced anti-tumor effects of γδ T-cells against MCL.

Zhang LH et al. [52]

MCL, DLBCL, and FL cells

• Len induced direct anti-proliferative effects against each NHL subtype.

• Len inhibited high vascular endothelial growth factor levels seen in cell lines.

• These effects were associated with increased expression of tumor suppressor proteins p21 and SPARC.

Escoubet-Losachet al. [53]

Namalwa (Burkitt lymphoma) and LP-1 (MM) cells

• Len plus pomalidomide induced p21 WAF-1 expression in lymphoma and MM through an LSD1-mediated epigenetic mechanism.

Ramsay et al. [17]

FL, DLBCL, and TmL cells (fresh samples)

• FL cells induced T-cell immunological synapse dysfunction that were repaired with len.