Nishant Agrawal
· ProfessorVerifiedUniversity of Chicago · Pharmacology
Active 2001–2025
About
Nishant Agrawal is a Professor at the University of Chicago in the Department of Surgery. His lab is devoted to the study of the genetics and molecular diagnostics of head and neck cancer. His research has described the genomic landscape of head and neck squamous cell carcinoma, esophageal cancer, and medullary thyroid cancer, and has developed assays using tumor DNA as a biomarker in saliva and plasma. His work focuses on applying cancer genetics to design diagnostic approaches aimed at reducing morbidity and mortality from head and neck cancer. Dr. Agrawal's background includes education and training at Johns Hopkins University, where he completed a residency in Otolaryngology-Head and Neck Surgery, a post-doctoral fellowship in Molecular Genetics, and a fellowship in Head and Neck Surgical Oncology. His research activities are supported by multiple NIH grants, and he has contributed to the understanding of molecular alterations in various cancers, including head and neck, thyroid, and salivary gland tumors. He has also been involved in clinical trials and the development of liquid biopsy platforms for cancer detection and monitoring.
Research topics
- Medicine
- Genetics
- Biology
- Computational biology
- Computer Security
- Internal medicine
- Computer Science
- Pathology
- Intensive care medicine
- Risk analysis (engineering)
- Gastroenterology
- Nursing
- Physical therapy
- Evolutionary biology
- Family medicine
- Surgery
- Microbiology
- Medical emergency
- Cancer research
- Bioinformatics
Selected publications
Oral Oncology · 2025-07-28
erratumInternational Journal of Radiation Oncology*Biology*Physics · 2025-09-01
article2025-08-01
preprintOpen accessSenior author<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>
Journal of Pediatric Surgery · 2025-07-17 · 1 citations
articleLaboratory Investigation · 2025-03-01
articleOpen accessClinical Cancer Research · 2025-05-27 · 7 citations
articleOpen accessSenior authorPURPOSE: Human papillomavirus-associated (HPV+) oropharyngeal carcinoma is associated with excellent survival, yet treatment drives substantial toxicity. Improved biomarkers are needed to select patients for de-escalated treatment. Circulating tumor HPV DNA (ctHPV-DNA) represents a promising noninvasive biomarker to gauge treatment response and surveil for disease recurrence. PATIENTS AND METHODS: A prospective biomarker clinical trial of response-stratified de-escalation was conducted. Eligible patients with non-metastatic HPV+ oropharyngeal carcinoma received neoadjuvant chemotherapy, followed by risk/response-stratified de-escalation with transoral robotic surgery, de-escalated radiation with or without chemotherapy to 50 Gy, or standard chemoradiation to 70 Gy. Deep response (≥50% tumor shrinkage per RECIST v1.1) qualified patients for de-escalation. ctHPV-DNA was measured using HPV-SEQ in plasma at baseline, during neoadjuvant chemotherapy, radiation, and following treatment. The primary endpoint was the correlation of ctHPV-DNA kinetics and radiographic response. RESULTS: Forty-six eligible patients were enrolled, and 488 ctHPV-DNA samples were analyzed (median 11 per patient). The median follow-up was 30 months, and five recurrences were observed (10.9%). Baseline ctHPV-DNA was detected in 95% of evaluable patients. Rapid early ctHPV-DNA clearance after one cycle of neoadjuvant therapy (≥95% reduction) predicted radiographic deep response (P = 0.04). Detection of ctHPV-DNA 3 months or later after treatment was associated with worse progression-free and overall survival (P < 0.001). Sensitivity, specificity, and positive and negative predictive values of longitudinal ctHPV-DNA were 100%. The longest lead time from positive ctHPV-DNA to detection of recurrent disease was 25 months. CONCLUSIONS: Rapid early clearance of ctHPV-DNA during neoadjuvant therapy demonstrates utility in predicting response to treatment. Detectable ctHPV-DNA following treatment is predictive of both disease recurrence and worse survival.
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.
2025-08-01
supplementary-materialsOpen accessSenior author<p>Supplementary Table 1. Representativeness of Study Participants.</p>
Journal of Clinical Oncology · 2025-05-28 · 1 citations
article6091 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
Abstract 2199 PDCD10 as a driver of oral squamous cell carcinoma tumorigenesis and progression
Journal of Biological Chemistry · 2025-05-01
articleOpen accessINTRODUCTION Oral cavity squamous cell carcinoma (OCSCC) is the most common subtype of head and neck cancer, the seventh most prevalent type of cancer worldwide. With few targeted therapies, OCSCC causes substantial morbidity and mortality. Thus, it is crucial to identify suitable therapeutic targets for this disease. PDCD10 is a multifaceted adaptor protein shown to be overexpressed in several solid malignancies including HNSCC and is thought to be involved in pathways related to cell survival, migration, differentiation, and senescence.
Recent grants
NIH · $2.5M · 2012
NIH · $437k · 2014
NIH · $52.7M · 2019
Somatic Mutations in Tissue and Saliva as Prognostic and Screening Biomarkers for Oral Premalignancy
NIH · $1.9M · 2020–2026
Multi-analyte Approach for Earlier Detection of Cancers in Non Plasma Biofluids
NIH · $5.8M · 2018–2028
Frequent coauthors
- 279 shared
Bert Vogelstein
Howard Hughes Medical Institute
- 277 shared
Kenneth W. Kinzler
Johns Hopkins University
- 257 shared
Chetan Bettegowda
Johns Hopkins Medicine
- 215 shared
Nickolas Papadopoulos
University of Baltimore
- 125 shared
Luis A. Díaz
- 124 shared
Yuxuan Wang
Johns Hopkins University
- 123 shared
Joseph A. Califano
University of California, San Diego
- 122 shared
Victor E. Velculescu
University of Baltimore
Education
- 2009
M.D.
University of Chicago
- 2005
B.S.
University of Illinois at Urbana-Champaign
Awards & honors
- Marvin Harold Cheiten Award (1st in class), Rutgers Universi…
- Johns Hopkins University School of Medicine Scholarship
- Owsei Temkin Scholarship, Johns Hopkins University
- Richard Westcott Appleton Scholarship, Johns Hopkins Univers…
- George T Nager Award for Excellence in Teaching, Johns Hopki…
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