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Author Notes:

Corresponding author: Curtis R. Pickering, PhD, Department of Head and Neck Surgery, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030; crpickering@mdanderson.org

Frederico O. Gleber-Netto: Acquisition, analysis, or interpretation of the data; drafting of the article; and statistical analysis.

Mei Zhao: Acquisition, analysis, or interpretation of the data.

Sanchit Trivedi: Acquisition, analysis, or interpretation of the data.

Jiping Wang: Acquisition, analysis, or interpretation of the data.

Samar Jasser: Acquisition, analysis, or interpretation of the data.

Christina McDowell: Acquisition, analysis, or interpretation of the data.

Humam Kadara: Acquisition, analysis, or interpretation of the data.

Jiexin Zhang: Acquisition, analysis, or interpretation of the data.

Jing Wang: Acquisition, analysis, or interpretation of the data.

William N. William, Jr: Acquisition, analysis, or interpretation of the data.

J. Jack Lee: Acquisition, analysis, or interpretation of the data.

Minh Ly Nguyen: Critical revision of the article for important intellectual content.

Sara I. Pai: Acquisition, analysis, or interpretation of the data and critical revision of the article for important intellectual content.

Heather M. Walline: Acquisition, analysis, or interpretation of the data.

Dong M. Shin: Acquisition, analysis, or interpretation of the data and critical revision of the article for important intellectual content.

Robert L. Ferris: Critical revision of the article for important intellectual content.

Thomas E. Carey: Conception or design; acquisition, analysis, or interpretation of the data; and critical revision of the article for important intellectual content.

Jeffrey N. Myers: Conception or design; acquisition, analysis, or interpretation of the data; and critical revision of the article for important intellectual content.

Curtis R. Pickering: Conception or design; acquisition, analysis, or interpretation of the data; and drafting of the article.

Robert L. Ferris reports working on an advisory board and a clinical trial for Astra-Zeneca/MedImmune and receiving research funding from the company, working on an advisory board for Lilly, working on an advisory board and a clinical trial for Bristol-Myers Squibb and receiving research funding from the company, working on an advisory board and a clinical trial for Merck, working on an advisory board for Pfizer, and receiving research funding from VentiRx Pharmaceuticals outside the submitted work.

Subjects:

Research Funding:

This study was funded by the Head and Neck Cancer Specialized Program of Research Excellence Human Immunodeficiency Virus Supplement Consortium (the National Cancer Institute) and the American Recovery and Reinvestment Act through the following grants: P50 CA097248 to the University of Michigan; University of Michigan Cancer Center Core Grant P30 CA46592; 5P50 CA097007 to The University of Texas MD Anderson Cancer Center; P50 CA097190 to the University of Pittsburgh; P50 DE019032 and 3P50 DE019032-14S2 to Johns Hopkins University; and P50 CA128613 to Emory University.

Sarah I. Pai is supported by grant 1R01 DE025340.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Oncology
  • head and neck cancer
  • human immunodeficiency virus (HIV)
  • human papillomavirus (HPV)
  • mutation
  • TP53 gene
  • HUMAN-PAPILLOMAVIRUS
  • P53-MEDIATED APOPTOSIS
  • CIGARETTE-SMOKING
  • UNITED-STATES
  • BREAST-CANCER
  • HIV PATIENTS
  • P53
  • POPULATION
  • INFECTION
  • HIV/AIDS

Distinct pattern of TP53 mutations in human immunodeficiency virus-related head and neck squamous cell carcinoma

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Journal Title:

Cancer

Volume:

Volume 124, Number 1

Publisher:

, Pages 84-94

Type of Work:

Article | Post-print: After Peer Review

Abstract:

BACKGROUND: Human immunodeficiency virus–infected individuals (HIVIIs) have a higher incidence of head and neck squamous cell carcinoma (HNSCC), and clinical and histopathological differences have been observed in their tumors in comparison with those of HNSCC patients without a human immunodeficiency virus (HIV) infection. The reasons for these differences are not clear, and molecular differences between HIV-related HNSCC and non–HIV-related HNSCC may exist. This study compared the mutational patterns of HIV-related HNSCC and non–HIV-related HNSCC. METHODS: The DNA of 20 samples of HIV-related HNSCCs and 32 samples of non–HIV-related HNSCCs was sequenced. DNA libraries covering exons of 18 genes frequently mutated in HNSCC (AJUBA, CASP8, CCND1, CDKN2A, EGFR, FAT1, FBXW7, HLA-A, HRAS, KEAP1, NFE2L2, NOTCH1, NOTCH2, NSD1, PIK3CA, TGFBR2, TP53, and TP63) were prepared and sequenced on an Ion Personal Genome Machine sequencer. DNA sequencing data were analyzed with Ion Reporter software. The human papillomavirus (HPV) status of the tumor samples was assessed with in situ hybridization, the MassARRAY HPV multiplex polymerase chain reaction assay, and p16 immunostaining. Mutation calls were compared among the studied groups. RESULTS: HIV-related HNSCC revealed a distinct pattern of mutations in comparison with non–HIV-related HNSCC. TP53 mutation frequencies were significantly lower in HIV-related HNSCC. Mutations in HIV+ patients tended to be TpC>T nucleotide changes for all mutated genes but especially for TP53. CONCLUSIONS: HNSCC in HIVIIs presents a distinct pattern of genetic mutations, particularly in the TP53 gene. HIV-related HNSCC may have a distinct biology, and an effect of the HIV virus on the pathogenesis of these tumors should not be ruled out. Cancer 2018;124:84-94.

Copyright information:

© 2017 American Cancer Society

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