About

Everett E. Vokes, MD, is the John E. Ultmann Distinguished Service Professor and Chair of the Department of Medicine at the University of Chicago, as well as physician-in-chief at the University of Chicago Medicine. He earned his medical degree at the University of Bonn Medical School in Germany and completed his clinical training in Australia and the United States, including a fellowship in hematology-oncology at the University of Chicago. Dr. Vokes is a clinical and translational investigator focusing on the biology and treatment of lung and head and neck cancers, with particular interest in the interaction of chemotherapy and radiation, as well as the integration of targeted and immune-based agents. He has established the clinical and intellectual basis for national trials investigating concomitant chemoradiotherapy and multispecialty care approaches, leading clinical and translational research both at the university and nationally. Dr. Vokes is a member of several professional organizations, including the American Society of Clinical Oncology, the American Association for Cancer Research, and the International Association for the Study of Lung Cancer. He is an elected member of the American Society of Clinical Investigation and the American Association of Professors, and serves on editorial boards of multiple oncology journals. His prolific publication record includes over 80 book chapters and 500 papers in prominent journals, and he has presented his work at numerous medical congresses.

Research topics

• Internal medicine
• Oncology
• Medicine
• Radiology
• Biology
• Chemistry
• Nuclear medicine
• Immunology
• Cancer research
• Surgery

Selected publications

• Integrated analysis of stemness-associated immune modulatory circuits in squamous cell carcinomas

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-06

  articleOpen access

  ABSTRACT Emerging evidence indicates that a subset of cancer cells enriched for stemness-related gene signatures possess distinct immunomodulatory capacities, enabling these tumor-initiating stem cells (tSCs) to more effectively evade or resist anti-tumor immunity. Despite these advances, the tSC-specific molecular circuits orchestrating their specialized immune privilege program are not well defined. Here, in squamous cell carcinomas of the skin and oral cavity, we comprehensively delineate the unique immune-evasive properties of tSCs and dissect the transcriptional regulation shaping their immunomodulatory programs. By integrating transcriptome profiling, chromatin landscape mapping, genetic perturbation, and single-cell RNA sequencing, we found that the tSC-specific immune program is broadly governed by SOX2, a stemness-associated transcription factor. We demonstrate that SOX2 enables tSCs to sustain immature tumor-associated neutrophils (TANs) and subsequently trigger these myeloid cells to foster the development of tumor-associated macrophages (TAMs). This SOX2-directed tSC-TAN-TAM axis establishes a localized immunosuppressive niche for protecting tSC. SIGNIFICANCE Here, we uncover SOX2 as a master regulator that orchestrates conserved immune modulatory circuits in tSCs to sustain pro-tumor myeloid cell states. These findings place tSCs at the apex of immune landscape remodeling, asserting a central role of stemness-associated program in organizing the immunosuppressive tumor microenvironment.

  PublisherOA PDFDOI

• Circulating tumor HPV-DNA dynamics and neoadjuvant chemotherapy with or without nivolumab in viral-mediated oropharyngeal cancer.

  Journal of Clinical Oncology · 2025-05-28 · 1 citations

  article

  6091 Background: Human papillomavirus-associated (HPV+) oropharyngeal carcinoma (OPC) is linked to favorable survival outcomes, prompting efforts to de-intensify treatment strategies. Circulating tumor HPV-DNA (ctHPV-DNA) is a promising biomarker for assessing treatment response and guiding de-escalation strategies. This study evaluates how patient characteristics influence ctHPV-DNA dynamics during neoadjuvant therapy across two de-escalation clinical trials. Methods: Patients with non-metastatic HPV+ OPC enrolled across two trials of neoadjuvant carboplatin/paclitaxel (NCT04572100) or carboplatin/ nab -paclitaxel/nivolumab (OPTIMA II, NCT03107182), with ctHPV-DNA available at baseline and post-neoadjuvant, were eligible. All participants received three cycles of neoadjuvant therapy followed by response-adapted de-escalated locoregional treatment. ctHPV-DNA values (copies per ml plasma) were measured at baseline and after 2-3 cycles of neoadjuvant therapy, and percentage reductions were calculated. We defined “ctHPV-DNA clearance” as ≥ 95% reduction from baseline and compared data distribution between patients who achieved clearance and those who did not using Kruskal-Wallis, Pearson’s χ2, or Fisher’s exact tests. Overall survival (OS) and progression free survival (PFS) probabilities were compared using log-rank test. Results: The study included 84 patients . The mean age was 60.9 years. 93% of patients with neoadjuvant nivolumab/chemotherapy achieved ctHPV-DNA clearance compared to 82% with chemotherapy alone, p =0.298. Patients with T1-T2 tumors (AJCC 8 th edition) were significantly more likely to achieve ctHPV-DNA clearance compared to those with T3-T4 tumors ( p =0.0254). Age, race/ethnicity, smoking history, tumor site (e.g., tonsil), and risk group were not significantly associated with ctHPV-DNA clearance rates. ctHPV-DNA clearance by cycle 2-3 of neoadjuvant therapy predicted radiographic response per RECIST v1.1 ( p =0.001), and significantly improved OS ( p =0.025) and PFS ( p <0.001). Survival outcomes were similar across OPTIMA II and NCT04572100 as previously reported. Conclusions: Earlier T-stage tumors were associated with rapid ctHPV-DNA clearance by cycle 2 with a trend towards higher clearance rate with neoadjuvant nivolumab/chemotherapy. Rapid clearance predicts radiographic response, OS, and PFS, supporting ctHPV-DNA as a useful biomarker for treatment monitoring with neoadjuvant treatment in HPV+ OPC. Clinical trial information: NCT03107182 . ctHPV-DNA % reduction between baseline and follow up at cycle 2-3. ≥ 95% reductionN (%) < 95% reductionN (%) p Age, (mean ± sd) 60.4 ± 10 61.3 ± 8.5 0.656 Gender (Male) 59 (86.8) 9 (13.2) 1 Race (Caucasian) 54 (86) 9 (14) 0.583 Risk (High) 34 (92) 3 (8) 0.309 T1 stage 12 (75) 4 (25) 0.0254 T2 stage 30 (97) 1 (3) T3 stage 8 (89) 1 (11) T4 stage 3 (60) 2 (40) Tumor shrinkage (median %, range) -64.2 (-23, -100) -42 (-14, -71) 0.001

  PublisherDOI

• Supplementary Table S3 from A Randomized Multi-institutional Phase II Trial of Everolimus as Adjuvant Therapy in Patients with Locally Advanced Squamous Cell Cancer of the Head and Neck

  2025-11-25

  articleOpen access

  <p>Adverse events at least possibly related to study drug by NIH-NCI Common Terminology Criteria for Adverse Events (CTCAE), version. 4.0.</p>

  PublisherDOI

• Spurn the Scorecard: Personalized Dose Constraints for Head and Neck Radiotherapy to Minimize Treatment Toxicity

  International Journal of Radiation Oncology*Biology*Physics · 2025-09-01

  article
  PublisherDOI

• Supplementary Table S1 from A Randomized Multi-institutional Phase II Trial of Everolimus as Adjuvant Therapy in Patients with Locally Advanced Squamous Cell Cancer of the Head and Neck

  2025-11-25

  articleOpen access

  <p>List of all observed somatic mutations in TP53.</p>

  PublisherDOI

• A Randomized Multi-institutional Phase II Trial of Everolimus as Adjuvant Therapy in Patients with Locally Advanced Squamous Cell Cancer of the Head and Neck.

  UNC Libraries · 2025-09-30

  articleOpen access

  PURPOSE: Investigate whether adjuvant everolimus, an mTOR inhibitor, improves progression-free survival (PFS) in advanced-stage head and neck squamous cell carcinoma (HNSCC) and provide outcomes related to correlative biological factors associated with disease control. PATIENTS AND METHODS: This was a prospective, randomized, double-blind phase II trial of patients with advanced-stage HNSCC from 13 institutions who were confirmed disease-free post-definitive therapy and enrolled between December 2010 and March 2015. Patients received adjuvant everolimus or placebo daily (10 mg, oral) for a maximum of 1 year. p16 IHC as a surrogate marker for human papillomavirus infection and whole-exome sequencing were performed. Cox proportional hazard models estimated hazard rates. Log-rank tests evaluated differences in survival. The primary endpoint was PFS. Secondary endpoints and objectives included overall survival (OS) and toxicity assessment. RESULTS: 52 patients [median (range) age, 58 (37-76) years; 43 men (83%), 9 women (17%)] were randomized to placebo (n = 24) or everolimus (n = 28). PFS favored everolimus, but was not significant [log-rank P = 0.093; HR = 0.44; 95% confidence interval (CI), 0.17-1.17]. There was no difference in OS (P = 0.29; HR = 0.57; 95% CI, 0.20-16.2). Everolimus resulted in significant improvement in PFS for p16-negative patients (n = 31; P = 0.031; HR = 0.26; 95% CI, 0.07-0.97), although subgroup analysis showed no difference for p16-positive patients (n = 21; P = 0.93). Further, PFS was significantly higher in TP53-mutated (TP53mut) patients treated with everolimus compared with placebo (log-rank P = 0.027; HR = 0.24; 95% CI, 0.06-0.95). No treatment difference was seen in patients with TP53 wild-type tumors (P = 0.79). CONCLUSIONS: p16-negative and TP53mut patients may benefit from adjuvant treatment with everolimus.

  PublisherDOI

• Supplemental Table 3 from Early Dynamics of Circulating Tumor HPV-DNA with Neoadjuvant Chemotherapy and Response-Adapted De-escalation in Human Papillomavirus–Associated Oropharyngeal Cancer

  2025-08-01

  preprintOpen access

  <p>Supplemental Table 3. Discordance between deep radiographic response (>50% tumor shrinkage per RECIST v1.1) and rapid ctHPV-DNA clearance (≥95% reduction) after 1 cycle.</p>

  PublisherDOI

• Tumor-initiating stem cells fine-tune the plasticity of neutrophils to sculpt a protective niche

  Cancer Cell · 2025-12-04 · 2 citations

  articleOpen access

  ) signaling in TANs, which can disrupt the interferon response and prevent the interferon-induced anti-tumor functions in TANs. By fine-tuning the plasticity of neutrophils, tSCs shape neutrophil heterogeneity and sculpt a protective micro-niche to survive from immunotherapy and drive cancer relapse.

  PublisherDOI

• Supplementary Table 1 from Early Dynamics of Circulating Tumor HPV-DNA with Neoadjuvant Chemotherapy and Response-Adapted De-escalation in Human Papillomavirus–Associated Oropharyngeal Cancer

  2025-08-01

  supplementary-materialsOpen access

  <p>Supplementary Table 1. Representativeness of Study Participants.</p>

  PublisherDOI

• Corrigendum to “Analysis of AI foundation model features decodes the histopathologic landscape of HPV-positive head and neck squamous cell carcinomas”. [Oral Oncol. 163 (2025) 107207]

  Oral Oncology · 2025-07-28

  erratum
  PublisherDOI

Recent grants

• NIH Grant P50DE011921

  NIH · $8.6M · 2002

• NIH Grant U01CA063187

  NIH · $2.1M · 2001

Frequent coauthors

• Ezra E.W. Cohen

  Tempus Labs (United States)

  487 shared

• Daniel J. Haraf

  University of Chicago

  454 shared

• James E. Herndon

  Duke University

  324 shared

• Ravi Salgia

  City of Hope

  291 shared

• Ralph R. Weichselbaum

  University of Chicago

  282 shared

• Kerstin Stenson

  268 shared

• Waun Ki Hong

  242 shared

• Jay S. Cooper

  R&D Systems (United States)

  235 shared

Awards & honors

• Elected member of the American Society of Clinical Investiga…
• Elected member of the American Association of Professors