Oncology Evaluation Services

Where conventional patient-derived 3D culture expands tumor cells alone in animal-derived matrix, this service reconstructs the microenvironment: tumor cells together with immune cells, cancer-associated fibroblasts and endothelial cells, in defined synthetic hydrogels or decellularized ECM, under static, air–liquid interface or dynamic perfusion culture selected by endpoint.

Applied to: immune checkpoint inhibitor evaluation in autologous immune-competent models; CAR-T trafficking and solid tumor penetration under perfusion; bispecific T-cell bridging efficiency in 3D; CAF-directed and anti-angiogenic agents in vascularized configurations; resistance, invasion and matrix remodeling biology.

Model Panel: clinically annotated patient-derived models across breast (TNBC, HR+/HER2−, HER2+), colorectal (primary and hepatic metastasis, MSI-H/dMMR vs MSS), pancreatic (desmoplastic, chemo-resistant, with stromal density scoring), ovarian (high-grade serous, platinum-resistant, HRD status) and melanoma (BRAF V600, NRAS, PD-L1 expression).

Endpoints: flow cytometry, live-cell and confocal imaging, cytokine profiling, spatial transcriptomics, with viability, morphology and marker-expression QC at each passage and inter-replicate CV reported with every dataset.

Where It Stops: throughput is medium - this is deep mechanistic and immuno-oncology work, not primary sensitivity screening, for which conventional high-throughput 3D expansion remains the appropriate and complementary tool. Microvascular networks are available on MPS-based configurations and are preliminary rather than a full vascular bed. Model establishment success rate and expansion timeline are reported per case before assay initiation, because they are case-dependent.

The tissue-context layer, applied to the delivery problem. Minced tumor tissue is combined with a collagen matrix on a permeable membrane support, fed by diffusion from below with the upper surface exposed to the gas phase. Stroma, native matrix and endogenous CD45⁺ immune populations - CD8⁺ T cells, regulatory T cells, macrophages - are carried over from the source tissue rather than reconstituted from purified components.

Applied to: ADC penetration depth through dense stroma as a function of DAR and payload hydrophobicity; free payload release kinetics; cytotoxic potency mapped against where the molecule actually reached; bystander activity; effects on the local immune compartment; and ADC–checkpoint inhibitor combination arms.

Endpoints: target antigen characterization at assay start by IHC and immunofluorescence; binding and internalization with labelled material; penetration by three orthogonal routes - confocal imaging of labelled ADC, mass spectrometry imaging of unlabeled payload, and IHC on sectioned fragments; free payload quantification by LC-MS/MS in tissue and medium, with method performance established in matched matrix at feasibility.

Where It Stops: low throughput, technically demanding, and gated by fresh resected tissue availability within a defined collection window. Dosing and readout commonly run 7–14 days from establishment; the assay window is set so the populations relevant to your endpoint are present throughout, not to the maximum achievable duration. Not a screening tool.

The functional immunology layer. Patient-derived 3D tumor microtissues are paired with defined immune effector populations to generate data on immune-mediated killing, cytokine response and effector phenotype - with 3D architecture retained, so that chemotaxis, matrix penetration and target engagement are represented rather than bypassed.

Effector modules:

• T cell (CD8⁺, CD4⁺, CAR-T, TCR-T) - checkpoint inhibitor evaluation, adoptive cell therapy penetration and cytotoxicity, tumor-reactive T-cell expansion. Readouts include proliferation, CD107a degranulation, IFN-γ/TNF-α/IL-2 profiling, granzyme B and perforin, and exhaustion phenotyping (PD-1, TIM-3, LAG-3, TIGIT).
• Macrophage / TAM - polarization under 3D oxygen and metabolite gradients, phagocytosis-directed agents including CD47-axis antibodies and CSF-1R inhibitors, and macrophage-derived suppression of T-cell access.
• NK cell - ADCC quantification, CAR-NK potency against solid tumor models, and combination strategies including NKG2D ligand upregulation and IL-15 support. Not MHC-restricted, which makes allogeneic healthy-donor NK a practical effector source; KIR–HLA relationships are accounted for in donor selection.
• Dendritic cell - vaccine and neoantigen-driven maturation, TGF-β-mediated suppression of antigen presentation, and DC-directed checkpoint regulation in three-way DC–T–tumor configurations.

Where It Stops: allogeneic T-cell configurations carry alloreactive killing unrelated to the mechanism under test, so antigen-specific endpoints require autologous or HLA-matched material - which extends the timeline substantially and depends on matched availability. Tumor-reactive responses are not detected in every donor–tumor pair; where a reactivity threshold matters to the program, the interpretation of a negative result is agreed at Stage 1 rather than after the fact.