Macrophages are not "background" immune cells in cancer—they are architects of the tumor microenvironment (TME). From shaping inflammatory tone and remodeling extracellular matrix to orchestrating angiogenesis, immune suppression, and therapy resistance, tumor-associated macrophages (TAMs) can decide whether antitumor immunity ignites—or fizzles out.

At Creative Biolabs, we build disease-relevant, modular macrophage platforms for oncology teams who need actionable answers—fast and with experimental rigor.

Why Macrophages Matter in Cancer Biology

In many solid tumors and hematologic malignancies, macrophages accumulate through monocyte recruitment and local expansion, then adopt phenotypes shaped by hypoxia, lactate, cytokines, lipids, tumor debris, and stromal signals. A simplified view divides TAMs into "M1-like" (pro-inflammatory, antigen-presenting) and "M2-like" (immunosuppressive, pro-angiogenic), but real tumors contain multiple TAM states spanning interferon responses, lipid metabolism programs, wound-healing signatures, phagocytic/efferocytic states, and antigen-presentation-high subsets.

Fig.1 Functions of macrophages in cancers.^1,2

Creative Biolabs provides a full range of professional services for macrophage study in cancer with our highly experienced team. For more information on the role of macrophage in cancer, please click on the links below.

• Macrophage in Lung Cancer
• Macrophage in Liver Cancer
• Macrophage in Glioblastoma
• Macrophage in Breast Cancer
• Macrophage in Colorectal Cancer
• Macrophage in Pancreatic Cancer
• Macrophage in Gastric Cancer

What We Offer

Creative Biolabs offers a comprehensive cancer macrophage research solution centered on tumor relevance, mechanism-driven insights, and scalable study design.

Disease-Relevant Model Library

• Human PBMC-derived monocytes → M0 macrophages → controlled polarization and TAM-like conditioning
• Mouse bone marrow-derived macrophages (BMDMs) and tissue macrophage preparations where appropriate
• Tumor-conditioned macrophages generated using tumor cell–derived factors, exosomes, and defined cytokine cocktails
• THP-1-derived macrophage models for standardized, high-throughput workflows
• RAW 264.7-based macrophage platforms for murine mechanistic and screening studies
• Tumor microenvironment modules
• Macrophage–tumor spheroid infiltration assays
• Macrophage–tumor organoid co-culture for immune exclusion/infiltration and secretome mapping
• ECM-tunable systems to model stiff/desmoplastic environments (especially relevant in the pancreas and certain breast tumors)

Mechanism-Focused TAM Phenotyping

We design phenotyping panels around your hypothesis and modality, typically combining:

• Lineage and activation markers
• Antigen presentation and co-stimulation modules
• Fc receptor profiling for antibody and ADC programs
• Scavenger receptors and efferocytosis-associated signatures
• Chemokine receptor modules tied to recruitment and trafficking
• qPCR panels for rapid iteration
• Bulk RNA-seq for pathway-level quantification

Functional Assays for Cancer Programs

Our oncology macrophage suites commonly include:

• Phagocytosis & antibody-dependent cellular phagocytosis (ADCP)
  • Target-specific opsonization setups for antibody programs
  • Fc dependency mapping and Fcγ receptor involvement studies
• Efferocytosis and debris handling
  • Apoptotic cell clearance as a driver of immunosuppressive rewiring
  • Downstream cytokine skewing and metabolic shifts
• Antigen processing & presentation
  • MHC-associated presentation metrics
  • Co-stimulation / co-inhibition balance
  • T-cell activation consequences in macrophage–T cell co-culture
• Migration, chemotaxis & invasion support
  • Chemokine-driven migration modules (including recruitment-relevant axes)
  • Matrix invasion support readouts tied to metastatic potential
• Secretome profiling
  • Cytokines, chemokines, growth factors, and lipid mediator-adjacent signatures
  • Multi-timepoint mapping to capture early vs late macrophage programming

Candidate Evaluation: TAM-Targeting, Reprogramming, and Combinations

We support multiple oncology modalities:

• Small molecules and biologics that modulate macrophage pathways
• Antibodies affecting macrophage checkpoints or Fc signaling
• Nanoparticle or liposome systems designed for myeloid targeting
• Combination logic studies (e.g., macrophage modulation plus T-cell–directed immunotherapies)

Workflow

Manipulation of TAMs to Improve Cancer Therapy

• TAM depletion

Increasing evidence indicates that TAMs may influence the efficacy of anticancer therapies. Therefore, TAM depletion is one choice to manipulate TAMs. For instance, 1) trabectedin, a DNA-damaging agent approved for the treatment of soft tissue carcinomas, may rely on its ability to kill TAMs rather than tumor cells. 2) Trabectedin administration can reduce tumor growth even when drug-resistant carcinomas have been transplanted in immunocompetent mice, an occurrence correlating with reduced TAM density. 3) Docetaxel depletes immunosuppressive TAMs and drives concomitant expansion of antitumor myeloid cells. 4) Since CSF-1/CSF-1R signalings axis is essential for macrophage survival, inhibition of CSF-1/CSF-1R signaling is an effective approach to deplete TAM.

• Inhibition of circulating monocyte recruitment into the tumor

Inhibition of circulating monocyte recruitment into the tumor is an alternative approach to selectively deplete TAMs. As TAM recruitment is CCL2-dependent in most cancer types, this inhibition can be effectively achieved by interfering with CCL2-CCR2 signaling. Studies have shown that antibody-mediated blockade of CCL2 inhibited monocyte recruitment to primary breast tumors and metastatic sites in the lungs, leading to reduced tumor growth and improved survival. However, interruption of anti-CCL2 therapy caused a rapid rebound of monocyte infiltration in tumors, correlating with accelerated metastatic relapse.

• Reprogramming of TAMs

Functional reprogramming of TAMs to enhance their antitumor properties while limiting the protumor ones is the most attractive strategy for cancer therapy. TAMs represent the major source of IL-10. Previous studies have shown that the inhibition of IL-10 signaling in a mouse model of mammary carcinoma can significantly improve the efficacy of chemotherapy. Moreover, inhibition of IL-10 signaling closely phenocopied the effects of CSF-1R blockade in the same system, highlighting the possibility of alternative and more targeted therapies directed against the protumor functions of TAMs. The observed therapeutic effects relied at least partially on direct repurposing of TAMs towards immunostimulatory functions, likely including direct activation of NK and T cells by IFNα administration

Creative Biolabs' Cancer Macrophage Study Solutions

Below are "package-style" solutions that many oncology teams adopt for speed and clarity. Each is modular—expandable with additional tumor types, donors, and omics layers.

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

• Oncology-first macrophage thinking: We design experiments around the tumor microenvironment, not generic macrophage activation.
• Modular study construction: Start with a tight core panel, then scale into co-culture, 3D, single-cell, and in vivo-aligned modules without losing comparability.
• Multi-modal integration: Phenotype + function + secretome + transcriptome, analyzed under a unified framework.
• QC and reproducibility focus: Cell quality, activation baselines, batch controls, and standardized reporting built into every run.
• Communication that accelerates decisions: Clear endpoints, interpretable plots, and "what this means" summaries aligned with program milestones.

Related Products

Curated, assay-ready tools that plug into cancer macrophage workflows. (Availability may vary by project design.)

Scientific Resources

Q & A

Q: Can you accommodate custom tumor-derived materials (e.g., supernatants, exosomes, patient-derived inputs)?

A: Yes. Many cancer macrophage studies become more predictive when macrophages are conditioned using project-specific tumor materials. We incorporate these inputs into standardized conditioning pipelines with appropriate controls to maintain interpretability. The goal is to preserve tumor realism while keeping your dataset clean and decision-oriented.

Q: How do you model recruitment vs local macrophage expansion?

A: We use recruitment modules (chemotaxis assays driven by tumor-conditioned media and recruitment-linked chemokine axes) and pair them with differentiation follow-through (monocyte-to-macrophage state tracking).

Q: Can you model TAM biology beyond simple M1 vs M2 polarization?

A: Yes. Because tumor-associated macrophages rarely fit a binary label, we generate TAM-like states using tumor-conditioned media, defined cytokine cocktails, metabolic and hypoxia-mimetic pressures, or tumor-education co-cultures, and then characterize them with multi-dimensional phenotyping (flow marker panels, transcriptional signatures, secretome profiling) combined with functional assays (phagocytosis, chemotaxis, immunosuppression/activation readouts).

Q: Can you run macrophage–tumor co-culture and tri-culture models?

A: We support direct co-cultures to capture contact-dependent effects (including phagocytosis and tumor cell modulation), transwell formats to isolate paracrine signaling and migration, and tri-cultures that include T cells or NK cells to evaluate macrophage-driven suppression or immune activation, and we tailor endpoints to your question.

Creative Biolabs will assemble a goal-driven macrophage study plan—from model design to multi-modal readouts—so you can move forward with confidence.

References

1. Duan, Zhaojun, and Yunping Luo. "Targeting macrophages in cancer immunotherapy." Signal transduction and targeted therapy 6.1 (2021): 127. https://doi.org/10.1038/s41392-021-00506-6
2. Distributed under Open Access license CC BY 4.0, without modification.