Macrophages are dynamic architects of the tumor microenvironment (TME) in gastric cancer. From early inflammation-driven remodeling to advanced invasion, angiogenesis, immune suppression, and peritoneal dissemination, tumor-associated macrophages (TAMs) continuously shape how gastric tumors evolve and how experimental therapies perform in preclinical models.

At Creative Biolabs, we provide an end-to-end, gastric cancer-focused macrophage toolkit spanning primary cell sourcing, polarization & phenotyping, TAM functional assays, immune-oncology co-culture systems, 3D organoid/spheroid platforms, multi-omics profiling, and in vivo validation workflows.

Overview of Macrophages in Gastric Cancer

Within gastric tumors, macrophages often become one of the most abundant immune populations, and their plasticity makes them both a powerful research target and a major confounder in model translation. Key macrophage-linked mechanisms frequently observed in gastric cancer research include:

• Immune suppression and T-cell exclusion via inhibitory cytokines/chemokines, metabolic competition, and checkpoint ligand expression.
• Angiogenesis and stromal remodeling, supporting invasion and altered drug penetration.
• Epithelial-myeloid crosstalk that enhances EMT-like programs, tumor stemness, and therapy tolerance.
• Metastasis support, especially in peritoneal spread, where macrophages influence adhesion, survival in ascites, and niche formation.

The Interplay Between Macrophages and GC

In the GC microenvironment, cross-talk between TAMs and tumor cells has been shown to extremely conduce to the progression of GC. Tumor cells can secrete a few cytokines and growth factors that mediate the M2 polarization of macrophages, such as prostaglandin E2 (PGE2), interleukin-6 (IL-6), and colony-stimulating factor-1 (CSF-1). M2 TAMs can secrete epidermal growth factor (EGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), hyperglycemic factor (HGF), and vascular endothelial growth factor (VEGF) to stimulate the progression of tumors.

In gastritis and gastric cancers, marked infiltrating macrophages are recruited by epithelium-derived chemokines and cytokines, leading to secretion of a few pro-inflammatory cytokines like tumor necrosis factor (TNFα) and stimulation of tumor growth. Activated macrophages are reported to produce nitric oxide synthase (NOS) and/or reactive oxygen species (ROS) that lead to epigenetic changes in the gastric epithelial cells. M2 TAMs can be reprogrammed into M1 TAMs by interfering with the interactive signals, resulting in a shift in the immune microenvironment.

Our Gastric Cancer–Focused Macrophage Service Portfolio

Creative Biolabs helps you move from macrophage "observations" to actionable conclusions, using gastric cancer-relevant models, functional validation, and data packages designed for real decisions. Below is a structured view of our core offerings.

Macrophage Sourcing, Differentiation, and Gastric-TME Conditioning

We support multiple macrophage sources to match different stages of R&D:

• Primary human monocyte-derived macrophages (MDMs) from donor-diverse PBMCs (fresh or cryopreserved workflows)
• iPSC-derived macrophages for consistency, genetic control, and scalable screening
• Myeloid cell lines (e.g., THP-1-derived macrophage-like cells) for rapid, high-throughput feasibility work
• Mouse macrophage preparations for in vivo-aligned mechanistic panels (where appropriate for your model design)

Macrophage Polarization, Phenotyping, and Multidimensional Scoring

We build macrophage states that reflect your hypothesis, then validate them with orthogonal readouts.

• Flow cytometry/high-parameter cytometry: macrophage identity, activation, and polarization markers
• Cytokine profiling (ELISA or multiplex) for functional secretome signatures
• Transcriptomic profiling (bulk or single-cell options based on project needs)
• Signal transduction panels (phospho-protein pathways relevant to activation/reprogramming)
• Metabolic characterization (glycolysis/respiration–aligned readouts when your mechanism suggests metabolic rewiring)

TAM Functional Assays

Phenotype is a snapshot; function is what drives outcomes. Our TAM functional modules include:

• Phagocytosis and efferocytosis panels
• Chemotaxis and recruitment assays
• Antigen presentation and co-stimulation readouts
• Pro-angiogenic activity readouts through macrophage secretome profiling and endothelial response assays
• Immunosuppressive function tests (impact on T-cell activation, proliferation, cytokine production)

These modules can be assembled into a program that mirrors your candidate's expected mechanism—particularly valuable for macrophage reprogramming strategies.

Macrophage–Tumor Interaction Assays

We quantify how macrophages influence tumor behavior and how tumors reshape macrophages.

• Common 2D designs
• Direct co-culture
• Transwell co-culture
• Conditioned media exchange and time-course secretome mapping
• Tumor-killing or tumor-protection assays under macrophage influence
• Myeloid-mediated drug response modulation (how TAMs change apparent potency)

If you are screening candidates, we can implement dose-response designs with macrophage context.

Our Other Featured Services

• Macrophage Isolation and Culture Service
• Macrophage Polarization Assay
• Macrophage Polarization Phenotype Identification Service
• Macrophage Characterization Service
• Macrophage Reprogramming Service
• Macrophage Engineering Service for Drug Delivery
• Macrophage Marker Development Service

Integrated Platforms at a Glance

Therapeutic Strategies Targeting Macrophages in Gastric Cancer

Macrophage-directed strategies in gastric cancer research typically fall into four categories. We can configure assays around any of these directions.

• Block recruitment and TAM accumulation: Chemokine axes and recruitment signals to reduce pro-tumor macrophage influx.
• Deplete TAMs or specific subpopulations: Macrophage survival pathways and depletion tools; critical to measure rebound and compensatory myeloid shifts.
• Reprogram macrophage state: Shift tumor-supportive programs toward anti-tumor functions; requires multidimensional scoring to avoid superficial "marker-only" conclusions.
• Enhance macrophage effector functions: Phagocytosis competence, antigen presentation, and synergy with adaptive immunity in co-culture settings.

Workflow: How We Run Gastric Cancer Macrophage Projects

Step 1: Scientific alignment (goal→model→endpoints)

• Target hypothesis and mechanism assumptions
• Candidate type (small molecule, biologic, nanoparticle, gene modulation, etc.)
• Choice of macrophage source and conditioning logic
• Selection of endpoints tied to your go/no-go criteria

Step 2: Model build & QC

• Cell sourcing and differentiation
• Polarization/education using gastric-TME mimics
• Baseline phenotyping/QC to ensure reproducibility and interpretability

Step 3: Functional testing (single assays→integrated panels)

• TAM functional modules
• Tumor co-culture panels (2D/3D)
• IO tri-culture when your pathway intersects immune suppression or killing

Step 4: Data integration & interpretation package

• Raw data + processed summaries
• Polarization/function scoring logic

Deliverables You Can Use Immediately

Creative Biolabs is committed to being your most trusted partner, empowering your breakthroughs with our leading-edge technologies and services.

• Highly customizable: We work closely with our clients to design and optimize experimental protocols tailored to your specific research needs.
• High-quality cell sources: All primary cells undergo rigorous quality control to ensure high purity and viability.
• Multi-dimensional detection platforms: We provide a one-stop shop for comprehensive analysis, from genes and proteins to cellular functions.
• Experienced expert team: Our scientists will provide you with professional technical support and in-depth data interpretation.

Related Products

To support study continuity, we can also provide research-use materials such as:

Scientific Resources

Q & A

Q: Which macrophage source is best for gastric cancer studies—primary MDMs, iPSC macrophages, or cell lines?

A: It depends on your decision point. For translational relevance and donor diversity, primary human MDMs are often the best choice. If you need batch consistency, genetic control, or repeated large screening campaigns, iPSC-derived macrophages are excellent. Cell-line–derived macrophage-like models can be useful for early feasibility and throughput, but we typically recommend validating key findings in primary or iPSC systems before drawing mechanistic conclusions.

Q: What endpoints are most informative for macrophage impact in gastric cancer models?

A: The most decision-relevant endpoints usually include a combination of: (1) macrophage phenotype + secretome, (2) suppression/effector function, and (3) tumor behavior outputs such as invasion, survival under immune pressure, or drug response shifts. For 3D models, infiltration depth and spatial distribution can be as informative as cytokines.

Q: We have our own gastric cancer cell line or engineered tumor cells. Can you use them?

A: Yes. Using your own tumor cells often strengthens program continuity. We'll align culture conditions, labeling strategy, and co-culture design to preserve the biology you care about while ensuring the macrophage component remains interpretable and reproducible.

Q: Can you analyze macrophage subsets from our tumor tissues or ascites samples?

A: In many cases, yes. We can profile macrophage populations using flow/IHC/IF and integrate subset patterns with your study endpoints. Sample handling and feasibility depend on specimen type, preservation, and study goals, so we'll propose a practical analysis plan once we understand your sample logistics.

Q: How do we start?

A: Send a short project brief—your target hypothesis, modality, preferred model type, and desired endpoints. Our scientific team will propose a tailored gastric cancer macrophage study design with a transparent workflow, deliverables list, and quotation.

Share your target, modality, and endpoints—our scientists will map a gastric cancer macrophage plan optimized for your program.