MyD88's function in the emergence and growth of tumors

Abstract MyD88 was initially discovered to be upregulated during interleukin (IL)-6-induced myeloid differentiation in the 1990s. Subsequent studies have identified it as a typical adapter for inflammatory signaling pathways downstream of members of the Toll-like receptor (TLR) and IL-1 receptor families. MyD88 is profoundly involved in the NF-κB and its associated signaling pathways, which contribute to the proliferation and survival of B cells. The downstream products of MyD88's involvement in the pathway also define it as a key link of the inflammatory pathway. This suggests that MyD88 plays a vital role in the emergence and growth of both hematologic and solid tumors. In this review, we focus on the role of MyD88 in signaling pathways and explore its impact on tumors.