Introduction
Metastatic solid tumors remain a significant therapeutic challenge across cancer types, particularly when patients develop resistance to conventional treatments ( 1 – 3 ). Despite advancements in chemotherapy, targeted therapy, and immune checkpoint inhibitors (ICIs), many patients with advanced prostate adenocarcinoma, melanoma, triple-negative breast cancer (TNBC), or urothelial carcinoma ultimately experience disease progression and death ( 4 ).
Like fluorodeoxyglucose-positron emission tomography (FDG-PET) for other solid tumors, the emergence of prostate-specific membrane antigen-positron emission tomography/computed tomography (PSMA-PET/CT) for prostate cancer (PCa) has enabled earlier detection of oligometastatic recurrence, opening the door for metastasis-directed therapy ( 5 , 6 ). Yet even with advanced imaging and focal interventions like stereotactic body radiation therapy, robotic surgical excision, or focal ablation, long-term disease control is typically elusive, especially when patients have exhausted standard-of-care (SOC) options such as androgen deprivation therapy (ADT), radiopharmaceuticals, and taxane-chemotherapy ( 7 , 8 ).
Similarly, while immune checkpoint inhibitors have transformed the treatment landscape for metastatic melanoma, some patients demonstrate primary or acquired resistance, and overall response rates remain low for most indications ( 9 , 10 ). Recent clinical studies have shown that combination checkpoint inhibitor therapy can extend overall survival to 15–20 months in some patients; yet, durable responses are limited and treatment failures common ( 11 , 12 ). This is particularly devastating in those with high disease burden or rapid clinical decline. In breast and urothelial cancers, diseases for which response rates to immunotherapy remain modest, new strategies are urgently needed ( 13 – 15 ).
Chimeric antigen receptor T-cell (CAR-T) therapy represents a promising therapeutic development, although autoimmune-type toxicities may be dose-limiting ( 16 ). Moreover, to date, no CAR-T product targeting non-B-cell tumor types has been approved in the United States of America; however, China has approved a CAR-T therapy for gastric malignancies targeting Claudin18.2, a tight-junction protein that is highly overexpressed in gastrointestinal cancers while showing relatively restricted expression in healthy tissues ( 17 ). Although this is a significant breakthrough, the lack of appropriate and comprehensive cell surface targets on most solid tumor types remains a substantial limitation to the CAR-T approach.
In contrast, dendritic cell (DC) immunotherapy offers a highly personalized, more physiological approach by stimulating the adaptive immune system through direct tumor-specific antigen presentation ( 18 ). Existing DC-based strategies have used defined peptides, tumor lysates, or tumor-derived nucleic acids as antigen sources, with varying approaches to DC activation and maturation. For example, Sipuleucel-T utilizes autologous antigen-presenting cells activated ex vivo with a fusion protein composed of prostatic acid phosphatase and granulocyte-macrophage colony-stimulating factor (GM-CSF), thereby directing the immune response toward a shared prostate tumor antigen rather than the patient-specific tumor antigen repertoire ( 19 ). CreaVax-RCC instead sensitizes autologous DCs with tumor lysate and keyhole limpet hemocyanin, whereas APCEDEN utilizes whole-tumor lysate-loaded DCs matured with polyinosinic:polycytidylic acid ( 20 – 22 ). Although these strategies facilitate antigen presentation and DC activation, they are not expected to engage the multi-enzyme aminoacyl-tRNA synthetase (mARS) complex because they were not specifically designed to provide homologous antigenic information simultaneously to the major histocompatibility complex (MHC) class I and II pathways.
Recent mechanistic discoveries suggest that simultaneous presentation of homologous MHC class I and class II-associated antigenic sequences may engage the mARS complex, providing an additional mechanism for DC-mediated immune polarization ( 23 – 26 ). This 1.5-MDa complex within the endosomes of the DC compares peptide sequences associated with MHC class I and II compartments. When sufficient antigenic homology is detected, conformational changes within the mARS complex promote the release of aminoacyl-tRNA synthetase complex-interacting multifunctional protein 1 (AIMP1/p43), a mediator required for interleukin 12 production and downstream T helper 1 (Th1) polarization in experimental models ( 25 ). This mechanistic framework provides the rationale for homologous “double-loading,” in which DCs are supplied with patient-specific tumor mRNA and tumor lysate to provide overlapping antigenic information through MHC class I and II pathways. By contrast with single-antigen or single-source antigen-loading strategies, double loading is designed to engage this mARS-associated pathway and promote a broader, Th1-based antitumor immune response ( 25 , 27 – 31 ). Clinical trials of double-loaded DCs for aggressive solid malignancies, including glioblastoma ( NCT04552886 ) and pancreatic ductal adenocarcinoma ( NCT04157127 ), have reported encouraging preliminary findings ( 32 ).
All patients in this case series received double-loaded DC therapy through a standardized three-phase Immunocine™ Dendritic Cell therapy (IDCT) protocol outside the framework of formal clinical trials. The patients first received 5 micrograms/kg of granulocyte colony-stimulating factor (G-CSF), filgrastim subcutaneously daily over five consecutive days to mobilize white blood cells, concurrent with biopsy to harvest tumor antigens. Apheresis was then performed to collect peripheral blood mononuclear cells for DC production. Monocytes were isolated and differentiated ex-vivo into DCs using a combination of 0.5 ml of GM-CSF stock solution at 2ug/mL (Miltenyi 170-076-136), for a final media concentration 20 ng/ml, and 0.5 mL of Interleukin 4 (IL-4) stock solution at 1ug/mL (Miltenyi 170-076-135), resulting in a final media concentration of 10 ng/ml. Cells were cultured in a final total volume of 50 mL CTS AIM-V media supplemented with 10% inactivated autologous plasma media per T225 flask over a 6-day incubation period. The resulting DCs were then “double-loaded” with patient-specific tumor mRNA and lysate matured with a proinflammatory cytokine cocktail by the method of Decker et al. (2006), enabling tumor-specific antigen presentation via both MHC class I and II pathways ( 34 ). Total tumor mRNA was amplified according to the method of Slagter-Jager et al, with technical modifications to enhance fidelity and reproducibility ( 33 ). Final DC products underwent in-house and external quality-control assessment. For cell enumeration and dosing determination, acridine orange/propidium iodide fluorescence was measured using a LUNA™ Stem automated cell counter (Logos Biosystems). Cell viability was additionally assessed by 7-aminoactinomycin D staining during flow cytometric analysis, while DC identity was evaluated primarily by CD11c and MHC class II (HLA-DR) expression. Additional phenotypic markers and patient-specific viability results are provided in Supplementary Table 1 . Aliquots of the final DC products were also submitted for independent flow cytometric validation to Diagnóstico Molecular de Leucemias y Terapias Celulares, a laboratory accredited by the Entidad Mexicana de Acreditación. Antigen loading was assessed by direct sequencing of the final cellular product. Each injection contained approximately 5–7 million mature DCs, with individual doses ranging from 1.5-20.6 million cells; patient-specific cell yields and administered doses are provided in Supplementary Table 2 . Patients then received three image-guided perilymphatic injections every two weeks over the course of six weeks, typically adjacent to lymph nodes most adjacent to the tumor site. 180 micrograms of pegylated interferon-alpha (IFN2a) was co-administered intramuscularly with each IDCT injection in either the right or left deltoid throughout the six-week treatment period. Some patients also continued systemic therapy, such as tamoxifen or checkpoint inhibitors, concurrent with the immunotherapy protocol. Informed consent was obtained from all of the patients for treatment and for publication of this case series, including all accompanying images. Ethics approval was granted by COFEPRIS (Comisión Federal para la Protección contra Riesgos Sanitarios; Federal Committee for Protection from Sanitary Risks) based on FDA clinical trials for other tumor histologies (Clinical Trial # NCT04157127 , Clinical Trial Date 2020-08-03).
This first-time report case series presents five patients with metastatic solid tumors, all having failed standard therapies, who subsequently experienced a complete response following treatment with a doubly-loaded autologous DC therapy. The approach incorporates advances in DC preparation utilizing antigen loading and administration techniques that have shown promise in other malignancies, but have not been previously reported in metastatic prostate, melanoma, breast, or urothelial carcinoma ( 34 – 36 ). These five cases are drawn from the first 80 patients, 82% of whom had stage IV cancer after failing at least one line of SOC therapy. In this cohort, an objective response rate of 74% was observed, and 39% of patients achieved either no evidence of disease (NED) or long-term stability (>2 years).
Case reports and results
Prostate adenocarcinoma
A 62-year-old White male with no smoking history and only occasional alcohol use underwent robot-assisted radical prostatectomy with extended pelvic lymph node dissection for PCa in September 2019. Pathology revealed intraductal adenocarcinoma, Gleason 4 + 3 with 10% tertiary pattern 5, extensive left neurovascular bundle extra-prostatic extension, bilateral seminal vesicle invasion and bilateral microscopic pelvic nodal involvement, 3 nodes-left, 2-right. Postoperative prostate-specific antigen (PSA) declined to 0.04 ng/mL but rose to 0.06 ng/mL two months later. Imaging was initially negative. The patient underwent adjuvant pelvic proton radiation at 6 months post-op, and after eighteen months of ADT exhibited undetectable PSA.
Six months later, while still on ADT, the patient’s PSA rose to 0.53 ng/mL. Castrate-resistant PCa recurred sequentially in multiple areas: the right perirectal side wall followed by a sub-diaphragmatic implant, a common iliac lymph node, and a substernal lymph node. All were managed with focal ablation, using laser, cryotherapy, or irreversible electroporation. Each time the oligo-metastatic lesions were successfully ablated as determined by both PSMA-PET/CT scanning and magnetic resonance imaging (MRI), however, the PSA did not decline substantially, despite combination ADT + androgen receptor inhibitor. Chemotherapy was considered but was withheld due to COVID pandemic-era concerns for immune compromise.
Eleven months later, PSA rose to 73 ng/mL and PSMA-PET/CT revealed multiple mediastinal metastases, verified on MRI with gadolinium ( Figures 1A, C, E ). Circulating tumor cell (CTC) count was 4/mL and the patient’s PSA peaked at 140 ng/mL. Treatment with a combination of Po Salicinum plus topical and sub-lingual Gc protein-derived macrophage activating factor was used while the patient was being qualified for IDCT. Two months later, following the initial IDCT injection to the right inguinal region adjacent to the right inguinal lymph nodes, the patient’s PSA declined to 7.8 ng/mL. PSA subsequently decreased to 2.5 ng/mL after the second injection to the bilateral inguinal regions, to 0.7 ng/mL before the third injection, and to 0.6 ng/mL following the third injection in the bilateral axillary region adjacent to the axillary lymph nodes. The prognostic WREN PROSTest, a machine-learning based, 27-gene qPCR liquid biopsy with a diagnostic cutoff of ≥50/100, returned 7/100, consistent with disease control ( 37 , 38 ).
Treatment was well tolerated, with only minimal adverse events (AEs) of back pain during filgrastim and 24 hours of myalgias with IFN2a. Repeat PSMA-PET/CT showed resolution of all lesions ( Figures 1B, D, F ) except one faint internal mammary lymph node ( Figure 1F ), which was cryo-ablated. At the six-month follow-up, the patient remains in near-complete remission, without biochemical evidence of progression.
Melanoma
A 39-year-old White male with a history of cutaneous melanoma, previously treated with complete surgical resection with negative margins, presented with progressive respiratory symptoms including wheezing and dyspnea. He had a prior history of smoking and alcohol use, but reported cessation of both at the time of evaluation. Chest X-ray revealed a lower left lobe mass, and a computed tomography (CT)-guided biopsy confirmed metastatic melanoma with immunohistochemistry positive for SOX10 and focal S100, consistent with melanocytic origin.
Staging CT scans 6 months later revealed a left lower lobe mass of 4.69cm in greatest dimension with satellite nodular opacities along the major fissure, scattered nodular pleural thickening with extension into paraspinal soft tissues at T10, and mediastinal/hilar lymphadenopathy ( Figures 2A, C ). CT of abdomen, pelvis, and neck revealed left supraclavicular lymphadenopathy, but no other metastases.
The patient received checkpoint inhibitor therapy with ipilimumab (3mg/kg) and nivolumab (1mg/kg) every three weeks for two cycles, yet experienced rapid clinical deterioration from Eastern Cooperative Oncology Group (ECOG) 0 to ECOG 3–4 over a four-week period. Repeat imaging confirmed progressive disease with a 29% increase in the primary left lower lobe mass, from 4.69 to 5.8 cm, and worsening lymphadenopathy across multiple sites indicating primary ICI resistance.
Two months later, the patient received IDCT injections to the left supraclavicular region adjacent to the left supraclavicular lymph nodes. There were minimal AEs, such as mild fatigue, diarrhea, and changes in hair color, however, no AE required discontinuation of therapy. CT post-treatment revealed a reduction of primary lung mass to 2.9 cm, and no new lesions were identified ( Figure 2B, D ). Multiple biopsies confirmed the absence of viable tumor. A month following treatment, the patient demonstrated an ECOG 0 status with resumption of modified physical activities, and three to five months following treatment, patient regained pre-diagnosis activity levels.
Parallel case: desmoplastic melanoma
A 33-year-old White male with no history of smoking or alcohol use underwent a sub-total resection of a desmoplastic melanoma of the lower lip, bilateral neck dissection, and reconstruction using a radial forearm free flap. Pathology revealed an 11mm desmoplastic melanoma ulceration, neurotropism, and 11 mitoses/mm 2 . Within six months, despite adjuvant pembrolizumab, the patient experienced local recurrence with tumor involving almost the entire reconstructed lip flap, indicative of acquired ICI resistance. Imaging showed a 4.9×2.9×5.6cm mass with mandibular periosteal involvement and cervical lymphadenopathy ( Figures 3A, C, E ).
Five months after receiving IDCT injections to the neck adjacent to the cervical lymph nodes, imaging documented mass reduction to 3.36×1.35×2.4cm with complete lymph node resolution ( Figures 3B, D, F ). 18 months post-treatment, the patient ceased ICI and fully resumed all activities and personal pursuits. Over 28 months post-treatment, the most recent imaging studies show that the patient remains in complete remission with NED.
Triple-negative breast cancer
A 58-year-old White female, with a 12-pack-year smoking history but reported cessation of 10 years at the time of evaluation, who had been diagnosed with TNBC in 2021 and had been treated with anthracycline+taxane-based chemotherapy, underwent lumpectomy and right axillary lymph node dissection revealing 11/12 positive nodes in 2022. Pathology from the mass excised from the right breast revealed recurrent invasive ductal carcinoma, Nottingham grade 3 (3 + 3 + 2), with margin involvement (≥12 mm) and lymphovascular invasion. Thus, the patient received adjuvant radiotherapy and several rounds of platinum-based chemotherapy.
In July 2024, staging workup demonstrated hypermetabolic right axillary/subpectoral and right cervical (5B) nodes (SUVmax 2.9-4.1) on PET/CT (images not shown). Fine-needle aspiration of the right cervical node confirmed metastatic adenocarcinoma, SOX10+/CKAE1/3+, ER/PR/HER2 negative, AR negative. Baseline laboratory results demonstrated lactate dehydrogenase (LDH) 293 U/L, D-dimer markedly elevated, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) elevated, and neutrophil-to-lymphocyte ratio (NLR) ~5.0. Traditional tumor markers (CA 27-29, CA 15-3) remained within normal ranges and a Northstar genomic assay showed a methylation score of 370, consistent with high tumor burden.
In September 2024, the patient initiated IDCT therapy to the inguinal region adjacent to the inguinal lymph nodes. Serial labs demonstrated significant biologic response: LDH declined to 193 U/L, NLR improved to 2.4, CRP and ESR normalized, and CA 27–29 remained stable. At six-month follow-up, the patient reported ECOG 0–1 performance status and preserved quality of life. Objective markers indicated metabolic and immune improvement, despite tumor markers remaining uninformative.
By September 2025, the patient achieved complete remission with negative PET/CT scans (images not shown). LDH normalized, CA 27–29 and CA 15–3 remained stable within normal limits, and blood counts/metabolic panels were preserved. The patient remains ECOG 0 performance status with an excellent quality of life and NED, with no adjuvant chemotherapy or ICI.
Urothelial carcinoma
A 62-year-old White male with no history of tobacco or alcohol use and a complex oncologic history presented with two concurrent malignancies: metastatic urothelial cancer-bladder primary and multiple myeloma in remission for three years after autologous hematopoietic stem cell transplantation followed by daratumumab maintenance therapy.
During hospitalization for colitis, the patient was found to have microhematuria on cystoscopy, and transurethral resection of bladder tumor revealed invasive high-grade, T2b urothelial carcinoma of the bladder, with a high proliferation index (Ki-67 at 90%). FDG-PET/CT showed no evidence of FDG-avid metastatic disease; thus, the patient opted for bladder-preservation and chemotherapy rather than a radical cystectomy.
Four months later, the patient experienced disease progression and clinical deterioration. FDG-PET/CT demonstrated aggressive metastatic spread with multiple left hilar lymph node metastases-the largest measuring 2.4×1.6cm with SUV of 6.6, malignant left pleural effusion, and a left pleural lesion ( Figures 4A, C, E ). A pleural catheter was placed to drain the effusion due to dyspnea. Laboratory studies revealed severe anemia (hemoglobin 8.2g/dL, red blood cell (RBC) 2.59million/µL, hematocrit 26.5%, mean corpuscular volume 102.3fL) with nucleated RBCs. Liver function rests showed significant dysfunction, with low albumin (2.2g/dL), elevated alkaline phosphatase (299U/L), and transaminases (ALT 118U/L, AST 80U/L).
Faced with limited SOC options, the patient underwent IDCT, receiving three injections to the right inguinal region adjacent to the right inguinal lymph nodes. Imaging three months post-treatment revealed complete resolution of the pleural effusion and lymphadenopathy ( Figures 4B, D, F ). At 18-month follow-up, the patient remained in complete remission with NED on cross-sectional imaging or cystoscopic examination. The patient’s physical condition and quality of life have significantly improved, and the patient has returned to normal daily activities. Treatment-related AEs were minimal (grade 1-2), with patient experiencing only mild flu-like symptoms after the first injection and transient fatigue.
Discussion
This case series demonstrates a pattern of complete and short- to intermediate-duration responses to IDCT across four distinct metastatic solid tumors: prostate adenocarcinoma, malignant melanoma, TNBC, and urothelial carcinoma. All patients received available conventional therapies, yet each experienced recurrence or progression to advanced stage disease. After exhausting all SOC options, each patient achieved clinically complete, or near-complete, remission with IDCT.
In contrast to conventional treatments for metastatic cancer, which often carry significant toxicity profiles that heavily impact patients’ quality of life, IDCT was well-tolerated in all cases. For example, immune checkpoint inhibitors commonly induce thyroid dysfunction, with a median onset of approximately 5.3 weeks following treatment initiation ( 39 ). Following treatment, the patient with PCa remains in biochemical remission at 6 months. The patients with melanomas have sustained complete remission well beyond two years, well exceeding the 6-month survival for patients with poor ECOG performance and high disease burden ( 10 ). The breast and bladder cancer patients have remained in complete remission for 12–18 months, far longer than the historical benchmarks for endocrine or salvage therapy in these settings ( 40 ). These timeframes are significant because durable responses in stage 4 disease, especially in checkpoint-refractory, chemotherapy-refractory, radiotherapy-refractory, hormone-refractory, or heavily pretreated patients, are uncommon outside of select immunotherapy responders ( 41 ).
Each case in this case series carried clinicopathological features typically associated with poor responsiveness to immunotherapy. The PCa case had castration-resistant disease, with low mutational burden, high tumor burden, and androgen receptor-independent clones that are known to acquire immune escape mechanisms ( 41 , 42 ). The melanoma cases had both forms of checkpoint inhibitor failure- one demonstrating primary resistance, and the other acquired resistance during adjuvant therapy ( 12 , 41 ). The breast cancer case involved heavily pretreated, poorly differentiated TNBC, a subtype often regarded as immunologically “cold” due to sparse tumor infiltrating lymphocytes (TILs), high systemic inflammation, and impaired antigen presentation ( 15 , 43 ). The urothelial carcinoma case exhibited multiple immune-suppressive features, including visceral pleural metastases with malignant effusion, reduced functional status, concurrent multiple myeloma, and a history of immunosuppressive treatments including stem cell transplantation, radiation, and daratumumab maintenance ( 40 , 44 ). Collectively, these features would be expected to confer a low likelihood of meaningful response to immunotherapy. The observation that each patient achieved complete or near-complete remission suggests that double-loaded DC therapy may be capable of overcoming diverse resistance mechanisms across tumor types, including immunologically “cold” microenvironments and checkpoint-refractory disease.
While ICIs have revolutionized the treatment of melanoma and some bladder and breast cancers, many patients experience primary or acquired resistance ( 9 ). In PCa, for which immunotherapy is less well established, standard management often includes radiation and ADT, but outcomes remain poor once metastases recur ( 42 , 45 ). Similarly, patients with TNBC, who relapse after standard chemotherapy, often have limited therapeutic options, and although immune checkpoint inhibitors have shown some activity, most patients ultimately develop resistance and poor outcomes ( 43 ). Checkpoint inhibitors work by lifting immune suppression, but they require pre-existing TILs or endogenous tumor-specific T-cells to be effective ( 46 ). In “cold” tumors lacking TILs, the immune system may never have received the right signals to generate a response. By supplying activated, antigen-loaded DCs, the therapy may prime the immune system to recognize and attack tumor antigens, turning “cold” tumors hot and enabling checkpoint inhibitors to work when previously ineffective.
The therapy employed was built upon lessons learned from prior limitations in DC treatment design. Traditional DC therapies frequently underperform due to suboptimal antigen loading and lack of adequate costimulatory signals ( 4 , 23 ). Previous DC therapy trials in solid tumors yielded limited success, often due to weak antigen presentation, poor T-cell activation, and unabated tumor-induced immunosuppression ( 47 ). Th1 may have been limited by failure to activate the mARS complex, promote AIMP1 release, and expand key effector subsets ( 29 , 48 ). By contrast, the IDCT protocol employs dual antigen loading with tumor mRNA to facilitate MHC Class I presentation and tumor lysate to facilitate MHC Class II presentation, combined with ex-vivo DC maturation with cytokines, image-guided injection near tumor-draining lymph nodes, and adjuvant type I interferon. Combining DC vaccination with strategic injection near lymphatic drainage sites and type I interferon results in potent immune responses capable of reversing immune escape mechanisms and overcoming ICI resistance ( 49 ).
This case series is limited by its small, heterogeneous sample and retrospective observational design, precluding definitive conclusions regarding treatment efficacy. Its primary purpose was to demonstrate the potential applicability of this therapeutic approach across multiple tumor types rather than to establish efficacy within any single malignancy. Because treatment was administered outside traditional FDA-approved frameworks and all patients were sufficiently well to travel, the findings may also be subject to selection bias and limited generalizability. Although the outcomes are encouraging, larger prospective studies and well-designed clinical trials are needed to confirm these observations.
Conclusion
This case series describes complete or near-complete responses following IDCT in five patients with advanced, treatment-refractory solid tumors and provides preliminary observations supporting further evaluation of this therapeutic approach. Patients with metastatic prostate adenocarcinoma, malignant melanoma, TNBC, and urothelial carcinoma achieved prolonged disease control despite prior failure of multiple standard therapies and adverse immunologic prognostic features, including ICI resistance and immunosuppressive treatments.
Although these findings are observational, the consistency of responses, long-term remission, and stability across tumor types justifies further investigation of this approach. Controlled clinical trials are warranted to evaluate efficacy and define optimal combination strategies. In an era increasingly defined by precision oncology, this approach represents a compelling strategy for transforming immune-inert tumors into targets of effective immune attack and may offer new hope to patients with limited therapeutic options.
Acknowledgments
The authors thank Janet Maendel, ND, and Nasha Winters, ND, for their significant contributions to improving patients’ nutritional status and optimizing immune function; Bernadette Greenwood for coordinating consultations and communications; and the Prostate Cancer Foundation for supporting prostate cancer research.
Funding Statement
The author(s) declared that financial support was received for this work and/or its publication. JAJ received funding for prostate cancer research from the Prostate Cancer Foundation-Challenge Grant-VALOR award 3100027501-7200, but not for publication of the current case series.
Footnotes
Edited by: Kwak Jong-Young , Ajou University, Republic of Korea
Reviewed by: Sivapar V. Mathan , University of Delhi, India
Shukoofeh Torabi , Kashan University of Medical Sciences, Iran
Yeganeh Mehrani , University of Guelph, Canada
Ethics statement
The studies involving humans were approved by Mexican Health Authorities Hospitals Galenia and Amerimed Immunocine COFEPRIS Criogenia y Biotecnología SAPI de CV. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article. Written informed consent was obtained from the participant/patient(s) for the publication of this case report.
Author contributions
JAJ: Supervision, Visualization, Writing – original draft. AA: Visualization, Writing – review & editing. WD: Conceptualization, Writing – review & editing. LF: Data Curation, Writing – review & editing. GV: Data Curation, Writing – review & editing. RG: Investigation, Methodology, Writing – review & editing. EA: Formal analysis, Writing – review & editing. AZ: Formal analysis, Writing – review & editing. RH: Formal analysis, Writing – review and editing. SJN: Supervision, Writing – review & editing. SH-R: Data Curation, Resources, Writing – review & editing. PZ: Writing – review & editing. DAS: Validation, Writing – review & editing. AK: Validation, Writing – review & editing. LT: Resources, Writing – review & editing. DG: Writing- review & editing. MH: Conceptualization, Project administration, Writing – review & editing.
Conflict of interest
Authors LF, GV, EA, SN, and MH are full-time employees of Immunocine Cancer Center. RG, AZ, and SH-R are consultants of Immunocine Cancer Center.
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
The author WD declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.
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Supplementary material
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fimmu.2026.1886898/full#supplementary-material
Specific dendritic cell identity and viability markers for the individual cases.
Additional information about the DC treatment.
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Associated Data
Supplementary Materials
Specific dendritic cell identity and viability markers for the individual cases.
Additional information about the DC treatment.