Hallmarks of a genomically distinct subclass of head and neck cancer.

Autor: Muijlwijk T; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands.; Amsterdam Institute for Infection and Immunity, Cancer Immunology, Amsterdam, The Netherlands., Nauta IH; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands., van der Lee A; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands.; Amsterdam Institute for Infection and Immunity, Cancer Immunology, Amsterdam, The Netherlands., Grünewald KJT; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands., Brink A; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands., Ganzevles SH; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands.; Amsterdam Institute for Infection and Immunity, Cancer Immunology, Amsterdam, The Netherlands., Baatenburg de Jong RJ; Erasmus University Medical Center, Otorhinolaryngology / Head and Neck Surgery, Rotterdam, Netherlands., Atanesyan L; MRC Holland, Oncogenetics, Amsterdam, The Netherlands., Savola S; MRC Holland, Oncogenetics, Amsterdam, The Netherlands., van de Wiel MA; Amsterdam UMC, Epidemiology & Data Science, Amsterdam Public Health Research Institute, Amsterdam, The Netherlands., Peferoen LAN; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands.; Amsterdam UMC, location Vrije Universiteit Amsterdam, Pathology, Amsterdam, The Netherlands.; Academic Center for Dentistry, Maxillofacial Surgery/ Oral Pathology, Amsterdam, The Netherlands., Bloemena E; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands.; Amsterdam UMC, location Vrije Universiteit Amsterdam, Pathology, Amsterdam, The Netherlands.; Academic Center for Dentistry, Maxillofacial Surgery/ Oral Pathology, Amsterdam, The Netherlands., van de Ven R; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands.; Amsterdam Institute for Infection and Immunity, Cancer Immunology, Amsterdam, The Netherlands., Leemans CR; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands., Poell JB; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands. j.poell@amsterdamumc.nl.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands. j.poell@amsterdamumc.nl., Brakenhoff RH; Amsterdam UMC, location Vrije Universiteit Amsterdam, Otolaryngology / Head and Neck Surgery, Amsterdam, The Netherlands. rh.brakenhoff@amsterdamumc.nl.; Cancer Center Amsterdam, Cancer Biology and Immunology, Amsterdam, The Netherlands. rh.brakenhoff@amsterdamumc.nl.
Jazyk: angličtina
Zdroj: Nature communications [Nat Commun] 2024 Oct 20; Vol. 15 (1), pp. 9060. Date of Electronic Publication: 2024 Oct 20.
DOI: 10.1038/s41467-024-53390-3
Abstrakt: Cancer is caused by an accumulation of somatic mutations and copy number alterations (CNAs). Besides mutations, these copy number changes are key characteristics of cancer development. Nonetheless, some tumors show hardly any CNAs, a remarkable phenomenon in oncogenesis. Head and neck squamous cell carcinomas (HNSCCs) arise by either exposure to carcinogens, or infection with the human papillomavirus (HPV). HPV-negative HNSCCs are generally characterized by many CNAs and frequent mutations in CDKN2A, TP53, FAT1, and NOTCH1. Here, we present the hallmarks of the distinct subgroup of HPV-negative HNSCC with no or few CNAs (CNA-quiet) by genetic profiling of 802 oral cavity squamous cell carcinomas (OCSCCs). In total, 73 OCSCC (9.1%) are classified as CNA-quiet and 729 as CNA-other. The CNA-quiet group is characterized by wild-type TP53, frequent CASP8 and HRAS mutations, and a less immunosuppressed tumor immune microenvironment with lower density of regulatory T cells. Patients with CNA-quiet OCSCC are older, more often women, less frequently current smokers, and have a better 5-year overall survival compared to CNA-other OCSCC. This study demonstrates that CNA-quiet OCSCC should be considered as a distinct, clinically relevant subclass. Given the clinical characteristics, the patient group with these tumors will rapidly increase in the aging population.
(© 2024. The Author(s).)
Databáze: MEDLINE
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