Gregory Daniels
· M.D., Ph.D.VerifiedUniversity of California, San Diego · Hematology and Medical Oncology
Active 1988–2026
About
Gregory Daniels is a Clinical Professor of Medicine at UCSD, with a focus on melanoma. His research involves understanding the link between autoimmunity and tumor immunity to develop more effective and less toxic vaccines and immune stimulatory approaches for patients with melanoma. He coordinates the clinical program in melanoma at UCSD and has contributed to research on early predictors of immunotherapy response, immune-related adverse effects, and the immune parameters in cancer patients. His educational background includes a PhD in Cancer Biology from Stanford University and an MD from USC School of Medicine. His training also includes residency and fellowship at Mayo Clinic, Rochester, MN, in Medicine and Medical Oncology.
Research topics
- Medicine
- Internal medicine
- Oncology
- Dermatology
- Cancer research
- Immunology
- Physics
- Ophthalmology
- Endocrinology
Selected publications
npj Precision Oncology · 2026-01-24 · 1 citations
articleOpen accessCirculating tumor DNA (ctDNA)-based response assessment is appealing but limited by conventional analytical thresholds. We utilized a whole genome sequencing based, tumor-informed ultrasensitive ctDNA assay which tracked ~1800 somatic mutations to analyze 227 longitudinal plasma samples from 39 patients with advanced/metastatic cancers receiving immune checkpoint inhibitors (ICIs). ctDNA was detected from 2.0-239,315 PPM (median limit of detection: 1.77 PPM), with 33% of positive detections below 100 PPM. Early molecular response, defined as >50% ctDNA reduction or sustained ctDNA negativity from baseline to first follow-up, strongly predicted improved progression-free survival (PFS) (hazard ratio (HR) = 0.09, 95% CI: 0.02-0.39, p = 0.001) and was independently prognostic of PFS. Molecular complete response (mCR), defined as any ctDNA clearance, predicted overall survival and PFS, with 1-year PFS of 87% in mCR patients versus 16% in non-mCR patients (HR = 0.14, 95% CI: 0.04-0.50, p = 0.003). The high-sensitivity ctDNA monitoring may enable precise, real-time evaluation of ICI response to guide clinical decision-making.
2025-10-01
articleOpen access<p>Figure S5 shows Kaplan-Meier curves depicting progression-free survival for patients treated with nelitolimod 2 mg or 8 mg in combination with pembrolizumab 200 mg. The figure illustrates time-to-event data for each dose group.</p>
Antigenic cancer persister cells survive direct T cell attack
bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-17 · 2 citations
preprintOpen accessSummary Drug-tolerant persister cancer cells were first reported fifteen years ago as a quiescent, reversible cell state which tolerates unattenuated cytotoxic drug stress. It remains unknown whether a similar phenomenon contributes to immune evasion. Here we report a persister state which survives weeks of direct cytotoxic T lymphocyte (CTL) attack. In contrast to previously known immune evasion mechanisms that avoid immune attack, antigenic persister cells robustly activate CTLs which deliver Granzyme B, secrete IFNγ, and induce tryptophan starvation resulting in apoptosis initiation. Instead of dying, persister cells paradoxically leverage apoptotic caspase activity to avoid inflammatory death. Furthermore, persister cells acquire mutations and epigenetic changes which enable outgrowth of CTL-resistant cells. Persister cell features are enriched in inflamed tumors which regressed during immunotherapy in vivo and in surgically resected human melanoma tissue under immune stress ex vivo . These findings reveal a persister cell state which is a barrier to immune-mediated tumor clearance. Graphical abstract
2025-10-01
articleOpen access<p>Figure S6 shows transcriptomic data from paired tumor biopsies collected at baseline and on therapy from patients treated with nelitolimod 2 mg plus pembrolizumab 200 mg. The figure displays consistent and durable increases in the expression of gene signatures representing immune cell density and upregulation of functional signatures.</p>
2025-10-01
articleOpen access<p>Figure S1 shows the treatment schema with nelitolimod 2 mg or 8 mg and pembrolizumab 200 mg. Nelitolimod was administered weekly for 4 weeks, followed by one dose every 3 weeks for up to 22 doses.</p>
2025-10-01
articleOpen access<p>Figure S2 shows detailed response and treatment duration data for patients with anti–PD-1/PD-L1–naive melanoma treated with nelitolimod 2 mg plus pembrolizumab 200 mg. The figure illustrated patterns of tumor response over time.</p>
2025-10-01
articleOpen access<p>Table S3 reports PFS for patients with anti–PD-1/PD-L1–naive melanoma who received nelitolimod 2 mg or 8 mg and pembrolizumab 200 mg (intention-to-treat).</p>
2025-10-01
articleOpen access<p>Table S2 describes the representativeness of study participants.</p>
2025-10-01
articleOpen access<p>Table S1 shows additional exclusion criteria of this study.</p>
Regular and Young Investigator Award Abstracts · 2025-11-01
articleOpen access
Frequent coauthors
- 139 shared
René González
University of Colorado Anschutz Medical Campus
- 131 shared
John A. Thompson
University of Washington
- 121 shared
Robert H.I. Andtbacka
HiFiBiO Therapeutics (United States)
- 118 shared
Merrick I. Ross
The University of Texas MD Anderson Cancer Center
- 116 shared
Brian Gastman
- 114 shared
April K.S. Salama
Duke Medical Center
- 113 shared
Susan M. Swetter
- 113 shared
Anthony J. Olszanski
Fox Chase Cancer Center
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