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Key Insights | Tumor Models: Growth, Metastasis, and Recurrence Models

Introduction

Animal tumor models are simple, cost-effective, and widely used in biomedical research. Depending on the specific research objectives, what are the common types of tumor models? We will now introduce them one by one.

 

I. Tumor Growth Models

Concept: The malignancy of a tumor depends on its capacity for unlimited proliferation; accordingly, most clinically used drugs target tumor growth to achieve antitumor effects. Consequently, tumor‑growth models constitute a simple yet crucial preclinical approach for evaluating a drug’s efficacy in vivo.

Features: Immune-deficient mice are commonly used, including both subcutaneous and orthotopic tumor models.

 

Subcutaneous growth pattern

Tumor-bearing mice are established by implanting tumors subcutaneously in the axillary region of the forelimb or on the back.

Advantages: This model is easy to establish and its detection methods are simple and cost-effective, enabling straightforward and intuitive acquisition of key data such as animal body weight, tumor growth curves (based on tumor volume), tumor weight, and tumor inhibition rates. It also supports relevant analyses of tissue and biofluid samples, making it widely applicable in biomedical research and drug development.

Disadvantages: Due to the mutual interactions between tumor cells and stromal cells, this model cannot accurately simulate in vivo tumor growth.

For example: Tumor cells, or tumor cells combined with a certain concentration of Matrigel, are inoculated into the axillary region of the mouse’s forelimb or into the subcutaneous tissue of the back, after which a subcutaneous tumor can be established (as shown in Figure 1).

Figure 1. Subcutaneous melanoma tumor

In-situ growth model

Tumor implantation is performed in the native organs or tissues of mice; for example, in a murine orthotopic breast cancer model, tumors are typically implanted in the fourth mammary pad.

Advantages: In situ growth more accurately mimics the tumor microenvironment in vivo, providing a model that enables precise prediction of drug efficacy.

Disadvantages: Compared with subcutaneous tumor implantation, orthotopic tumor implantation is more complex and technically demanding, and typically requires techniques such as magnetic resonance imaging, fluorescence‑based imaging, or bioluminescence in vivo imaging to monitor tumor growth.

For example: Tumor cells stably expressing luciferase, or tumor cells co‑implanted with a defined concentration of Matrigel, are inoculated at the original anatomical site corresponding to the clinical lesion; thereafter, bioluminescence in vivo imaging can be used to monitor tumor location and relative size (as shown in Figure 2).

Figure 2. In vivo imaging system for small animals and the in situ prostate cancer tumor imaged by it.

II. Tumor Metastasis Models

Concept: Tumor metastasis is the leading cause of cancer-related mortality; in many patients, death results from metastatic spread. Common sites of metastasis include the lungs, liver, and lymph nodes [4]. Tumor metastasis models can replicate part or all of the metastatic process, facilitating research into tumor metastasis and the evaluation of anti‑metastatic drug efficacy, among other applications.

Features: Tumor metastasis models typically employ immunodeficient mice, with inoculation sites ranging from the subcutaneous, intraperitoneal, and intrathoracic compartments to orthotopic or ectopic locations, thereby mimicking stages such as tumor cell infiltration, migration, and subsequent outgrowth in distant organs. Alternatively, injection can be directed along specific vascular pathways—such as the tail vein or the left ventricle—to establish metastatic foci directly in target organs. Based on the organ‑specific tropism of tumor cells, common target organs include the liver, lungs, bone, and lymph nodes. Monitoring of initial tumor growth and subsequent metastatic progression often relies on bioluminescence imaging and other in vivo techniques.

For example, highly malignant tumors with strong metastatic potential can exhibit marked metastasis even when implanted subcutaneously (as shown in Figure 3).

Figure 3. Subcutaneous pulmonary metastasis of breast cancer

Typical tumors can be established by orthotopic injection to generate an orthotopic tumor, which may then give rise to metastatic lesions via the vasculature or lymphatics; alternatively, they can be directly metastasized to the lungs, among other sites, through tail vein injection (as shown in Figure 4).

Figure 4. Pulmonary metastasis of breast cancer via the tail vein

III. Tumor Recurrence Model

Concept: Even after cancer treatment—whether radiotherapy, chemotherapy, or surgery—minimally residual lesions and tumor cells may persist, or tumor cells may enter a dormant state. Over time following treatment, these cells can resume proliferation and growth, leading to recurrence. Tumor recurrence and metastasis models closely mimic the clinical scenario of cancer relapse and metastasis after surgical resection, providing a more reliable and efficient platform for the development of anti‑cancer therapeutics.

Features: This model builds upon the growth or metastasis paradigm by first administering chemoradiotherapy or surgery as a staged treatment, followed by monitoring for tumor recurrence at the primary site or in metastatic lesions. Combined with bioluminescence imaging and other techniques, it enables tracking of tumor recurrence and subsequent metastasis.

For example: In situ breast cancer tumors induced in mouse mammary fat pads can exhibit significant recurrence and metastasis within three weeks after surgical resection (as shown in Figure 5).

Figure 5. Orthotopic Recurrence and Metastasis Model of Breast Cancer

 

IV. Systemic Tumor Models

Concept: For non-solid tumors such as leukemia and lymphoma, although they possess the ability to form subcutaneous xenografts, this does not closely reflect the clinical reality. Therefore, for these non‑solid tumors, tumor cells are typically injected via the tail vein to facilitate their homing to specific organs—such as the spleen or bone marrow—thereby establishing a systemic tumor model.

Features: Tumor cells enter the bloodstream or the lymphatic system and, after circulating, infiltrate organs and tissues such as the liver, spleen, kidneys, brain, and lungs. This closely mirrors clinical manifestations and allows for a more accurate assessment of therapeutic efficacy. Such models typically also rely on techniques like fluorescence‑based imaging to monitor tumor cell distribution, growth, and metastasis.

For example: Injecting leukemia tumor cells via the tail vein into FVB/NJ mice that have undergone X-ray irradiation can establish a murine leukemia model, which induces splenomegaly and other phenotypes (as shown in Figure 6).


Figure 6. Splenomegaly induced in a leukemia mouse model

 

That’s all for this episode’s valuable insights. We hope it was helpful to you all.

 

Aniphe BioLab can provide you with tumor animal model generation and pharmacological efficacy evaluation services. We will select the most suitable animal models based on your experimental objectives and application scope, and we can also tailor personalized efficacy assessment services to meet your specific needs.

Using small-animal in vivo imaging technology, we can monitor tumor status in real time with high precision. Feel free to call for more information!

 

References:

[1] Tamura K. Development of cell-cycle checkpoint therapy for solid tumors[J]. Japanese Journal of Clinical Oncology, 2015, 45(12):1097-1102.

[2] Wu J, Yu L, Yang F, et al. Optimization of 2-(3-(arylalkyl amino carbonyl) phenyl)-3-(2-methoxyphenyl)-4-thiazolidinone derivatives as potent antitumor growth and metastasis agents.[J]. European Journal of Medicinal Chemistry, 2014: 340-351.

[3] He Y, Peng S, Wang J, et al. Ailanthone targets p23 to overcome MDV3100 resistance in castration-resistant prostate cancer[J].Nature Communications, 2016, 7: 13122.

[4] Schroeder A, Heller D A, Winslow M M, et al. Treating metastatic cancer with nanotechnology[J]. Nature Reviews Cancer, 2012, 12(1):39-50.

[5] Cui H W, Peng S, Gu X Z, et al. Synthesis and biological evaluation of D-ring fused 1, 2, 3-thiadiazole dehydroepi and rosterone derivatives as antitumor agents[J]. European journal of medicinal chemistry, 2016, 111: 126-137.

[6] Li J, Zhang T, Yang F, et al. Inhibition of breast cancer progression by a novel histone deacetylase inhibitor, LW479, by down‐regulating EGFR expression[J]. British journal of pharmacology, 2015, 172(15): 3817-3830.

[7] Zhang T, Chen Y, Li J, et al. Antitumor action of a novel histone deacetylase inhibitor, YF479, in breast cancer[J]. Neoplasia, 2014, 16(8): 665-677.

[8] Wang X, Lin Q, Lv F, et al. LG-362B targets PML-RARα and blocks ATRA resistance of acute promyelocytic leukemia[J]. Leukemia, 2016.

 

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