The effects of MYC on tumor immunity and immunotherapy

Abstract

The oncogene MYC is dysregulated in a host of human cancers, and as an important point of convergence in multitudinous oncogenic signaling pathways, it plays a crucial role in tumor immune regulation in the tumor immune microenvironment (TIME). Specifically, MYC promotes the expression of immunosuppressive factors and inhibits the expression of immune activation regulators. Undoubtedly, a therapeutic strategy that targets MYC can initiate a new era of cancer treatment. In this review, we summarize the essential role of the MYC signaling pathway in tumor immunity and the development status of MYC-related therapies, including therapeutic strategies targeting MYC and combined MYC-based immunotherapy. These studies have reported extraordinary insights into the translational application of MYC in cancer treatment and are conducive to the emergence of more effective immunotherapies for cancer.

Single‐cell sequencing of head and neck carcinoma: Transcriptional landscape and prognostic model based on malignant epithelial cell features

“…Notably, the EMT process plays a pivotal role in the invasion and metastasis of HNSCC, 9,28 and MYC, being aberrantly expressed in various tumors, acts as a nexus in many cancer-associated signaling pathways, exerting a critical influence on the tumor and its immune microenvironment. 29,30 Our findings underscore the potential pivotal roles of these pathways in HNSCC, offering new avenues for future therapeutic strategies, yet their precise mechanisms warrant further exploration.…”

Distinct peripheral T-cell and NK-cell profiles in HGBL-MYC/BCL2 vs patients with DLBCL NOS

“…For example, MYC contributes to evading both innate and adaptive antitumor immune responses in the tumor microenvironment, as we and others have reviewed before. 30 , 31 , 32 This is suggested by experimental and clinical evidence that the overexpression of lymphoma-intrinsic MYC and subsequent target genes clinically associates with less favorable responses toward the CD20 × CD3 bispecific antibody glofitamab in patients with BCL. 33 Possibly, the exhausted T cells observed in our study may be more pronounced in the tumor microenvironment of patients with MYC rearrangement.…”

Impact of programmed death‐ligand 1 (PD‐L1) positivity on clinical and molecular features of patients with metastatic gastric cancer

“…Furthermore, therapeutic targeting of RICTOR and MYC amplifications, which were significantly enriched in tumors with PD-L1 CPS ≥5, previously demonstrated synergistic effects in several cancer types other than GC. [28][29][30][31] By contrast, tumors with a PD-L1 CPS <5 were significantly enriched in RHOA mutations, which were previously associated with genomically stable and diffuse subtypes, 8,32 requiring further development of treatment strategies for these patients. Collectively, we believe that combining ICIs with other targeted agents would be particularly beneficial for select patients.…”