Annals

Annals Reports (3)

Edited by Edited by Annals of the New York Academy of Sciences editorial staff
Explore the Table of Contents
Annals Reports (3)

Published: December 2014

Volume 1333

Learn More

Cumulative findings from many research groups have identified new signaling mechanisms associated with head and neck squamous cell carcinoma (HNSCC), a disease with significant morbidity and mortality. This Annals volume presents a report that summarizes these findings, including discussion of aberrant NOTCH, PI3K, STAT3, immune recognition, oxidative pathway, and regulation of cell cycle and cell death. The genomic landscape of head and neck cancers has been shown to differ depending on human papillomavirus (HPV) status. This report discusses studies that are examining the integration of HPV into genomic regions, as well as the epigenetic alterations that occur in response to HPV infection, and how these may help reveal new biomarker and treatment predictors. The characterization of premalignant lesions is also highlighted, as is evidence indicating that the surgical removal of these lesions is associated with better clinical outcomes.

The advancement of next-generation sequencing technologies now enables the landscape of genetic alterations in HNSCCs to be deciphered. This volume also includes a report that describes the mutation spectrum discovered in HNSCCs, especially HPV-associated and/or tobacco smoke exposure–associated HNSCCs. Related research is described from two independent investigators and from the Cancer Genome Atlas. Emphasis is placed on the therapeutic implications of genes frequently altered in HNSCCs and their corresponding pathways, with a particular focus on recent findings of Notch signaling pathway activation in HNSCC. Also discussed is the application of integrated genomic pathway–based analysis for precision cancer therapy in HNSCC.

The third report presented in this volume explores the class of adhesion G protein–coupled receptors (aGPCRs)—the second largest family of GPCRs. All aGPCRs but one (GPR123) contain a GPCR autoproteolysis–inducing (GAIN) domain that mediates autoproteolytic cleavage at the GPCR autoproteolysis site motif to generate N- and a C-terminal fragments (NTF and CTF, respectively) during protein maturation. Subsequently, the NTF and CTF are associated noncovalently as a heterodimer at the plasma membrane. While the biological function of the GAIN domain–mediated autocleavage is not fully understood, mounting evidence suggests that the NTF and CTF possess distinct biological activities in addition to their function as a receptor unit. Recent advances in understanding the biological functions, signaling mechanisms, and disease associations of the aGPCRs are discussed.