Editorial on the Research TopicCongruities between cancer and infectious diseases: Lessons to be learned from these distinct yet analogous fields It is a very well-established fact that cancer is a multifactorial disease involving innumerable complex cellular signaling pathways (Wu et al., 2018). These pathways are mainly regulated by oncogenes and tumor suppressor genes (Lee and Muller, 2010). Recent studies show that microRNAs (miRNAs) and associated RNA-induced silencing complex (RISC) also play a major role in oncogenesis (Yoo et al., 2011;Santhekadur and Kumar, 2019;Santhekadur et al., 2012). Infectious diseases are serious health disorders, and they are mainly caused by various unicellular or multicellular organisms such as bacteria, viruses, and fungi (Prasad et al., 2022;Joséet al., 2020). Infectious human viruses like human papillomavirus (HPV) cause cervical cancer; Epstein-Barr virus (EBV) is known to cause nasopharyngeal cancer and Burkitt lymphoma. Liver-associated human viruses like hepatitis B virus (HBV) and hepatitis C virus (HCV) cause hepatitis and induce hepatocellular carcinoma (Liao, 2006). Bacteria, namely, Helicobacter pylori, are also known to cause gastric cancer (Prasad et al., 2022). Some of the fungal secondary metabolites and toxic chemicals are known to trigger mutations and initiate cancer growth and development (Ekwomadu et al., 2022). Fungal origin environmental toxins like aflatoxin and ochratoxin are known carcinogens and activate inflammation and carcinogenesis (Shiragannavar et al., 2021;Vamadevaiah and Santhekadur, 2022) (Felizardo andCamara, 2013). Inflammation is a major contributor and a well-known hallmark of almost all of the infectious diseases and carcinogenesis. Inflammatory cytokines like tumor necrosis factor alpha (TNF-a) and transcription factor nuclear factor kappa B (NF-kB) act as master regulators of inflammation-associated infectious Frontiers in Cellular and Infection Microbiology frontiersin.org 01