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Tumor Neoantigen-Mediated Specific DC-T Cells
Tumor development can be described as cumulative genetic errors. When the human body is chronically exposed to harmful substances such as chemicals, radiation and viruses, or affected by intrinsic factors including genetics and aging, these triggers gradually induce genetic abnormalities. Eventually, cells lose normal growth regulation and proliferate uncontrollably, progressing into tumors.
Genetic abnormalities stem from accumulated gene mutations, analogous to faulty code in cellular operating programs, falling into three core categories:
1. Activation of Proto-Oncogenes
Normal "accelerator genes" go out of control and overstimulate cell division
2. Inactivation of Tumor Suppressor Genes
Growth-inhibiting brake genes fail and lose regulatory function
3. Cumulative Overlap of Multiple Genetic Defects
A single gene mutation rarely causes cancer. Malignant tumors only develop after concurrent activation of multiple proto-oncogenes and loss of tumor suppressor function
Human genetic research remains limited; numerous undiscovered proto-oncogenes and tumor suppressors exist, and many unknown multi-site mutations can generate novel oncogenes.
Major cancer treatments include surgery, radiotherapy, chemotherapy, targeted therapy, immunotherapy, endocrine therapy and interventional therapy. Immunotherapy saw rapid advancement after the advent of CAR-T. From 2013 to 2017, overseas pharmaceutical companies invested heavily in CAR-T research for solid tumors with disappointing outcomes. Between 2016 and 2025, Chinese scholars conducted extensive innovative CAR-T studies yet failed to break through solid tumor barriers. In addition, global research on CAR-NK has largely stagnated.
Current CAR-T can only target known proto-oncogenes or tumor suppressors, with an extremely limited pool of selectable targets. For malignant tumors, intervention against just one or a handful of targets is insufficient. We need to identify abundant precise targets for combined therapy to achieve disease control. Imagine a bucket with dozens of leaks draining water: patching only the largest hole cannot solve the problem; all leaks must be sealed as much as possible.
The human immune system naturally recognizes and eliminates foreign pathogens, which carry distinct non-self antigens that allow immune cells to quickly distinguish self from invaders. Tumors are hard to cure because they originate from mutated autologous cells lacking unique specific markers. Most tumor-associated antigens are highly expressed on tumors yet also present in healthy tissues, creating two critical dilemmas: either the immune system ignores tumors as normal tissue, or over-activates and attacks tissues indiscriminately, triggering cytokine storms.
Identifying tumor-specific neoantigens equips tumor cells with exclusive markers to guide precise immune attack, a worldwide bottleneck in oncology. NsDC-T cell therapy delivers a viable solution to this challenge.
The workflow of NsDC-T cell therapy: perform whole-gene sequencing on patient tumor, peritumoral and normal tissues, apply bioinformatic algorithms to screen all mutation-derived tumor antigens, and direct immune cells to eliminate all pathogenic targets simultaneously for tumor control or eradication.
1. Higher Precision 2. Superior Safety 3. Fully Personalized Customization 4. Broader Target Coverage 5. Improved Overall Efficacy
CAR-T refers to genetically engineered T cells with potent cytotoxicity but high risk of cytokine storms. It demonstrates outstanding efficacy against hematological malignancies, yet performs poorly in solid tumors. Dense, irregular solid tumor architecture plus CAR-T’s single-target design prevents deep infiltration into tumor masses. NsDC-T recognizes multiple antigen sites, enabling three-dimensional tumor clearance from outer layers inward, with mild side effects and repeatable administration.
1. Broader Functional Coverage
NsDC-T incorporates all capabilities of the WT1-DC vaccine while possessing powerful tumor-killing effects absent from WT1-DC.
2. More Active Immunological Mode of Action
A WT1-DC vaccine acts like a landmine fuse, only triggering defense when tumor cells pass through. NsDC-T resembles a missile battery equipped with phased array radar, releasing large quantities of immune cells that actively track circulating tumor cells.
3. Far More Abundant Available Targets
According to the latest Japanese WT1 publications and public data, WT1 only contains two usable antigen epitopes (WT1-1: WAPVLDFAPPGASAYGSL; WT1-2: CYTWNQMNL), limited to two synthetic peptides. Beyond these two epitopes, NsDC-T conducts full patient gene sequencing and comparative bioinformatic analysis to screen additional, more precise neoantigens for custom peptide synthesis.
1. Specimen Submission
2. Genetic Sequencing Test (7–14 days)
3. Target Antigen Analysis (3–5 days)
4. Peptide Design & Analysis (3–5 days)
5. Custom Peptide Synthesis (30–60 days)
6. NsDC-T Cell Manufacturing (13–15 days)
1. Case: Stage IIIA Left Lung Adenocarcinoma
Mr. Zheng, 82 years old, diagnosed with left lung adenocarcinoma (Stage IIIA, poorly differentiated with neuroendocrine differentiation, EGFR/ALK/ROS1 negative). Previous treatments: chemotherapy (albumin-bound paclitaxel + carboplatin), proton heavy ion therapy, immune checkpoint inhibitors.
Received a total of 8 combined immunotherapy sessions starting July 14, 2025; treatment is ongoing.
Treatment dates:
2025: Jul 14, Aug 8, Aug 22, Oct 18, Nov 12, Dec 4
2026: Jan 14, Mar 28
Key tumor markers declined continuously and turned negative post-treatment.
2. Case: Stage IVA Moderate-Poorly Differentiated Transverse Colon Adenocarcinoma
Ms. Qian, 79 years old, diagnosed with moderately-poorly differentiated transverse colon adenocarcinoma (pT4aN2aM1a Stage IVA, KRAS mutant, MSS) with multiple liver metastases. Previous treatments: right hemicolectomy + hepatic ablation, secondary surgery for intestinal obstruction, mFOLFOX6 chemotherapy.
Received a total of 8 combined immunotherapy sessions starting November 14, 2025; treatment is ongoing.
Treatment dates:
2025: Nov 14, Nov 21, Dec 10, Dec 29
2026: Jan 15, Feb 6, Mar 12, Mar 30
Key tumor markers rose transiently early on then dropped sustainably throughout treatment.
