Esophageal cancer, primarily comprising the squamous cell carcinoma (ESCC) and adenocarcinoma (EAC) subtypes, is the sixth leading cause of cancer deaths globally. In addition to many well-established endogenous and exogenous risk factors, there is emerging evidence for the etiologic role of infectious agents in esophageal cancer, although these associations are incompletely understood. Here, we review the currently available literature on the relationship between infectious agents and esophageal cancer. By far, human papilloma virus (HPV), particularly HPV 16 and 18, have the strongest etiologic association with ESCC. Less robust is the association of high-risk HPV (hr-HPV) with EAC. Although H. pylori has been implicated in the development of EAC via increased acid reflux, decreased lower esophageal sphincter tone, and the resultant Barrett’s metaplasia–dysplasia–adenocarcinoma pathway, some hypothesize based on epidemiological trends that H. pylori may in fact be a protective factor. In rare cases, EBV can cause esophageal lymphoepithelial carcinoma. Several other agents including HSV, polyomaviruses, and Candida are associated with esophageal cancer to varying degrees. In summary, while several studies, including those conflicting with each other, implicate several infectious agents, the evidence is weak, at best. Clearly, further work is needed to help solidify clear etiologies that will help facilitate prevention and treatment.

Lung cancer remains the leading cause of cancer-related death in the US and worldwide. Recent advances in molecular profiling and targeted therapies have revolutionized the management of non-small cell lung cancer (NSCLC), particularly in oncogene-driven subtypes. These therapies selectively target key molecular alterations in EGFR, ALK, KRAS, ROS1, MET, RET, ERBB2 (HER2), BRAF V600E, and NTRK, resulting in substantial improvements in survival rates and quality of life for lung cancer patients. However, disparities in molecular diagnostics and precision treatments persist, disproportionately affecting minority patients. These inequities include underrepresentation in clinical trials, disparities in molecular testing, and barriers to treatment access. The limited participation of racial and ethnic minorities in landmark clinical trials raises concerns about the generalizability of findings and their applicability to diverse populations. In this review, we examine the current landscape of molecular diagnosis and precision medicine in minority patients with oncogene-driven lung cancer, highlighting challenges, opportunities, and future directions for achieving equity in precision oncology. Additionally, we discuss differences in the prevalence of oncologic driver mutations across populations and emphasize the urgent need for greater diversity in clinical research. Addressing these gaps is critical to improving survival outcomes and ensuring equitable access to personalized lung cancer care for all patients.