About

Georgia Marie Beasley is an Associate Professor of Surgery and an Associate Professor in Medicine at Duke University. She is a member of the Duke Cancer Institute and is based in Durham, North Carolina. Her professional roles involve contributions to the fields of surgery and medicine, with a focus on cancer research. She is affiliated with the Duke Department of Surgery and is involved in academic and clinical activities related to biostatistics and bioinformatics, contributing to the university's research and educational missions.

Research topics

• Cancer research
• Biology
• Medicine
• Immunology
• Oncology
• Internal medicine
• Cell biology
• Computer Science
• World Wide Web
• Biochemistry
• Bioinformatics
• Virology

Selected publications

• Abstract 4146: Melanocytic transcriptional state is an independent marker of survival in metastatic melanoma

  Cancer Research · 2026-04-03

  article

  Abstract Introduction: Advanced cutaneous melanoma shows substantial heterogeneity in clinical outcomes, even among patients classified within the same clinical stage. Understanding the molecular drivers underlying this heterogeneity is critical for advancing treatment strategies. Previous studies have identified distinct melanoma transcriptomic states - Tirosh et al. and Balderson et al. have agreed on a four-subtype model defining “Undifferentiated”, “Neural Crest”, “Transitory”, and “Melanocytic” states. However, their biological and clinical relevance remains unclear. Here we profiled in-transit melanoma (ITM) using digital spatial RNA profiling to associate melanoma transcriptomic states with overall survival (OS) and acral melanoma (AM) status. Methods: Digital spatial profiling (Nanostring GeoMx Whole Transcriptome Atlas) was performed across a tissue microarray constructed from patients with ITM diagnosed from 1990-2020. After filtering poor quality areas of interest (AOIs), we processed the data using noise correction and quantile normalization. We applied Principal Component Analysis (PCA) to define melanoma subtype signatures by ranking genes contributing to each of the first four PCs. We performed gene set enrichment analysis using GSEA with significance defined as an adjusted p-value < 0.05. Association between gene or gene-set expression and OS was evaluated using optimal expression cutoffs to define high and low groups, with a minimum group size of 20%. Cox proportional hazards models were then used to assess survival differences between groups. Results: We analyzed a cohort of 84 patients (116 AOIs) with ITM passing QC. PCA of transcriptional profiles revealed distinct transcriptional states. The PC1 axis differentiated Transitory from Undifferentiated melanoma, PC2 reflected immune cell infiltration, PC3 corresponded to stromal cells and Neural crest-like melanoma, and PC4 associated with Melanocytic melanoma. We derived gene sets from the PCA results and associated the expression of each gene set with OS. Across a cohort of treatment-naïve ITM, high expression of the melanocytic state conferred a median overall survival difference of 7.59 years (melanocytic ‘high’=5.16 years vs ‘low’=12.75 years, log-rank p=0.0024) and independently associated with poor survival in multivariate analysis. AMs showed higher melanocytic state gene expression compared to non-acral cases. These findings were validated in external datasets, supporting that the melanocytic state predicts poor prognosis. Conclusion: The melanocytic transcriptional state was independently associated with worse overall survival in patients with metastatic melanoma and was enriched in acral melanoma, suggesting that assessment of the melanocytic state may have value for clinical risk stratification. Citation Format: Ziyin Huang, Kristen E. Rhodin, Rami Al-Rohil, Viviana Geron, Arul M. Chinnaiyan, Margaret H. O'Connor, Christina Vadala Angeles, Smita K. Nair, Georgia M. Beasley, Matthew K. Iyer. Melanocytic transcriptional state is an independent marker of survival in metastatic melanoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4146.

  PublisherDOI

• Tumor-infiltrating lymphocyte therapy in metastatic vulvar melanoma: A case report and review of the literature

  SSRN Electronic Journal · 2026-01-01

  preprintOpen access
  PublisherDOI

• Tumor-infiltrating lymphocyte therapy in metastatic vulvar melanoma: A case report and review of the literature

  Gynecologic Oncology Reports · 2026-04-15

  articleOpen access

  BACKGROUND: Vulvar melanoma is a rare and aggressive malignancy comprising less than 1% of all melanomas in women. Despite advances in immune checkpoint blockade, durable responses remain limited, and treatment of refractory disease poses a major challenge. Tumor-infiltrating lymphocyte (TIL) therapy has emerged as a promising option for patients with metastatic mucosal melanoma resistant to standard immunotherapy. CASE: We report a 48-year-old woman diagnosed with multifocal, unresectable vulvar melanoma who initially received ipilimumab and nivolumab, but discontinued due to immune-related colitis and progression of disease. She subsequently developed pulmonary, hepatic, and nodal metastases and underwent palliative vulvectomy for symptomatic relief. Following left inguinal lymph node harvest and autologous TIL expansion, she received lymphodepleting chemotherapy, TIL (lifileucel) infusion, and adjuvant interleukin-2 therapy. Her treatment course was notable for transient transaminitis, rash, and reversible encephalopathy. Follow-up PET-CT demonstrated a partial metabolic response with resolution of hepatic lesions and decreased pulmonary nodularity. CONCLUSION: This case highlights the potential clinical benefit of TIL therapy in metastatic vulvar melanoma following checkpoint inhibitor failure, supporting its consideration as an emerging therapeutic option in this rare gynecologic malignancy.

  PublisherDOI

• Biosafety analysis from the skin cancer cohorts in the IGNYTE clinical trial of RP1.

  Journal of Clinical Oncology · 2025-05-28

  article

  9534 Background: RP1 (vusolimogene oderparepvec) is an HSV–based oncolytic immunotherapy administered intratumorally. RP1 + nivolumab (nivo) has demonstrated deep, durable responses with favorable safety in advanced melanoma. We report biodistribution and shedding data from the skin cancer cohorts of the IGNYTE trial (NCT03767348) . Methods: Following RP1 injection into superficial and/or deep lesions, injection sites were covered with occlusive dressings. Injection sites, dressings and mucosa were swabbed, and blood and urine were collected pre-dose, during treatment, and at follow-up visits. Samples were assessed for RP1 DNA by qPCR. Swab samples positive for RP1 DNA were further assessed by TCID50 assay for live RP1. Results: The highest incidence of RP1 DNA was from injection-sites where RP1 was detected in ~35% of samples for up to 15 days post-injection. Blood samples showed the presence of low copy numbers of RP1 DNA (122/1573 [7.8%]) in ~20% (53/274) of pts during or after RP1 treatment. The highest levels were detected in blood within 6 hours of injection and decreased thereafter. RP1 was only very rarely detected and at low copy number in urine samples (3/1976 [0.2%]) from 0.7% (2/273) pts at 15 days post-injection, with all subsequent samples testing negative. RP1 DNA was detected on injection-site dressing exteriors less often (9.5% of 1114 samples) than from injection sites (18.4% of 1947 samples), demonstrating that the dressings act as a barrier to RP1. RP1 DNA was rarely present on oral mucosa (0.9% of 2052 samples). At follow-up (30-100 days post last dose), RP1 DNA was detected only at injection-sites. All available samples were negative for live RP1 by TCID50. Eight swab samples from 7 pts were collected from suspected herpetic infections but all tested negative for live RP1. There were no reports of systemic herpetic infections in pts, nor of transmission to contacts. Conclusions: RP1 DNA was primarily detected on the surface of injected lesions for up to 15 days, with no live RP1 being detected at 30, 60 and 100 days post the last RP1 dose. Collectively, these data demonstrate that RP1 is rapidly cleared from blood and urine, with negligible likelihood of environmental dissemination or transfer to contacts, and that the use of occlusive dressings contains RP1.Defining the biodistribution and shedding of RP1 is relevant to the education of healthcare providers and to the development of best practices for the proper administration, handling and clean down. Clinical trial information: NCT03767348 .

  PublisherDOI

• RP1 Combined With Nivolumab in Advanced Anti–PD-1–Failed Melanoma (IGNYTE)

  Journal of Clinical Oncology · 2025-07-08 · 30 citations

  articleOpen access

  PURPOSE Effective treatment options for melanoma after immune checkpoint blockade failure are limited. RP1 (vusolimogene oderparepvec) is a herpes simplex virus type 1–based oncolytic immunotherapy, here evaluated in combination with nivolumab in anti–PD-1–failed melanoma. METHODS Patients had advanced melanoma that had confirmed progression on anti–PD-1 (≥8 weeks, last prior treatment). RP1 was administered intratumorally (≤8 doses, ≤10 mL/dose; additional doses allowed) with nivolumab (≤2 years). The objective response rate (ORR) was assessed by independent central review using Response Evaluation Criteria in Solid Tumors version 1.1. RESULTS Of 140 patients enrolled, 48.6% had stage IVM1b/c/d disease, 65.7% had primary anti–PD-1 resistance, 56.4% were PD-L1 negative, and 46.4% received prior anti–PD-1 and anti–cytotoxic T-lymphocyte antigen-4 therapy (43.6% in combination and 2.9% sequentially). Confirmed ORR (95% CI) was 32.9% (95% CI, 25.2% to 41.3%; 15.0% complete response). Responses occurred with similar frequency, depth, duration, and kinetics for injected and noninjected, including visceral lesions. The median (95% CI) duration of response was 33.7 (95% CI, 14.1 to not reached) months. Overall survival rates (95% CI) at 1 and 2 years were 75.3% (95% CI, 66.9% to 81.9%) and 63.3% (95% CI, 53.6% to 71.5%), respectively. Biomarker analysis demonstrated broad immune activation associated with response, including increased CD8 + T-cell infiltration and PD-L1 expression. Treatment-related adverse event rates were 77.1% grade 1/2, 9.3% grade 3, 3.6% grade 4, and no grade 5 events. CONCLUSION RP1 combined with nivolumab provided deep and durable systemic responses in patients with anti–PD-1–failed melanoma, including those with poor prognostic factors. The safety profile was favorable, with mostly grade 1/2 adverse events.

  PublisherDOI

• Supplementary Data from GLI2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating WNT and Prostaglandin Signaling

  2025-05-02

  preprintOpen access

  <p>Supplementary Figures and Tables</p>

  PublisherDOI

• Lymph node excision (LNEx) for patients with stage III melanoma with one clinically positive node: Excision of Lymph Node trial (EXCILYNT).

  Journal of Clinical Oncology · 2025-05-28

  article

  TPS9608 Background: When melanoma metastases are detected clinically in regional lymph nodes (cLNs) without distant metastasis, standard surgical management is therapeutic lymph node dissection (TLND), which can cause lifelong lymphedema, delay return of function, and reduce quality of life (QOL). Among patients with cLN, 40-50% have metastasis confined to just 1 LN. The goal of this trial is to test a limited lymph node excision (LNEx) for patients with 1 cLN. In a multicenter retrospective analysis of 21 patients treated with LNEx rather than TLND, only 1 (4.8%) developed a LN recurrence in the same node basin, prior to distant disease (same node basin-only recurrence: sNBoR) over ~3 years. Also, only 1 (4.8%) developed lymphedema. To provide more precise estimates of sNBoR and lymphedema rates in a prospective study, and to collect data on HRQOL and return to normal activity after surgery, the EXCILyNT trial was initiated in 2024. The primary hypothesis is that LNEx will provide regional control, with sNBoR of ≤5% at 3 years. The secondary hypothesis is that LNEx will induce lymphedema in ≤6% at 3 years. Exploratory objectives are to assess overall morbidity and HRQOL, to identify features of tumors that may most accurately identify patients with only 1 pathologic LN, and to estimate overall DFS, MSS, and overall survival rates. Methods: EXCILyNT is a multicenter, phase II clinical trial for patients with 1 cLN, enrolled on either of two cohorts. All are treated surgically with LNEx: those undergoing surgery first (cohort 1) and those treated with neoadjuvant systemic therapy prior to LNEx (cohort 2). Participants on cohort 2 may receive standard of care neoadjuvant therapy or may be concurrently enrolled in a clinical trial of neoadjuvant therapy, as long as that trial does not mandate TLND. Major eligibility criteria: informed consent, age ≥18 years, ECOG PS 0-2, confirmed metastatic melanoma to only 1 cLN in the axilla, groin, or iliac basin; able to undergo LNEx. The following are excluded: prior LND or radiation therapy of the cLN basin; in-transit or satellite metastases within 1 year; distant metastasis; pre-existing lymphedema that precludes assessment of lymphedema; systemic or intratumoral therapy within 3 months of enrollment. Correlative studies include: evaluation of tumor-involved nodes for immune infiltrates, tumor cell proliferation rates, and somatic mutations; serum collection for cell-free tumor DNA; Health-related quality of life (HRQOL) surveys, FACT-M and Work Productivity and Activity (WPAI) Questionnaire: General health (WPAI:GH) V2.0. The target sample size of 60 eligible participants is chosen to estimate the 3-year rate of sNBoR with an upper CI precision of 7.5% (upper CI limit of 12.5%) using a one-sided Clopper-Pearson exact test. Enrollment is planned to include 7 centers. Thus far, 12 of planned 60 patients have been enrolled at the first 2 centers. Clinical trial information: NCT05839912 .

  PublisherDOI

• ASO Visual Abstract: Circulating Tumor DNA in High-Risk Stage II/III Cutaneous Melanoma: A Feasibility Study

  Annals of Surgical Oncology · 2025-05-11

  articleSenior author
  PublisherDOI

• Development of Entrustable Professional Activities for Complex General Surgical Oncology

  Annals of Surgical Oncology · 2025-11-05 · 2 citations

  article
  PublisherDOI

• Data from GLI2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating WNT and Prostaglandin Signaling

  2025-05-02 · 1 citations

  preprintOpen access

  <div>Abstract<p>Therapeutic resistance to immune checkpoint blockade has been commonly linked to the process of mesenchymal transformation (MT) and remains a prevalent obstacle across many cancer types. An improved mechanistic understanding for MT-mediated immune evasion promises to lead to more effective combination therapeutic regimens. Herein, we identified the hedgehog transcription factor, GLI2, as a key node of tumor-mediated immune evasion and immunotherapy resistance during MT. GLI2 generated an immunotolerant tumor microenvironment through the upregulation of WNT ligand production and increased prostaglandin synthesis. This pathway drove the recruitment, viability, and function of granulocytic myeloid-derived suppressor cells while also impairing type I conventional dendritic cell, CD8<sup>+</sup> T-cell, and NK cell functionality. Pharmacologic inhibition of EP2/EP4 prostaglandin receptor signaling or WNT ligand secretion each reversed a subset of the immunomodulatory effects of GLI2 and prevented primary and adaptive resistance to anti–PD-1 immunotherapy, respectively. A transcriptional GLI2 signature correlated with resistance to anti–PD-1 immunotherapy in patients with stage IV melanoma. Together, these findings provide a translational roadmap to direct combination immunotherapies in the clinic.</p><p><b>Significance:</b> WNT and prostaglandin signaling generate an immunotolerant environment in GLI2-active tumors and can be targeted as a component of immunotherapeutic combination strategies to overcome resistance in tumors exhibiting mesenchymal plasticity.</p></div>

  PublisherDOI

Recent grants

• PVSRIPO in melanoma

  NIH · $794k · 2020–2025

• PVSRIPO in melanoma

  NIH · $251k · 2020–2025

Frequent coauthors

• Douglas S. Tyler

  Kuwait Petroleum Corporation (Kuwait)

  140 shared

• Jonathan S. Zager

  Moffitt Cancer Center

  71 shared

• Christina K. Augustine

  Durham VA Medical Center

  58 shared

• April K.S. Salama

  Duke Medical Center

  55 shared

• Brent A. Hanks

  Duke University

  49 shared

• Paul J. Mosca

  Duke Medical Center

  46 shared

• James C. Padussis

  University of Nebraska Medical Center

  43 shared

• Kristen E. Rhodin

  Duke Medical Center

  38 shared

Education

• surgical oncology fellowship

  Ohio State University Hospital

  2017

• general surgery residnecy, Surgery

  Duke University Hospital

  2015

• MHSc

  Duke University School of Medicine

  2012

• MD

  Duke University School of Medicine

  2008

• BA

  Duke University

  2001