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Review

The Golden Hamster: A Valuable Model for Designing Cancer Therapies

by
Mahmoud Singer
1,*,
David K. Imagawa
2,
Michael Alexander
2 and
Nadine Abi-Jaoudeh
1,*
1
Department of Radiological Sciences, School of Medicine, University of California, Irvine, CA 92617, USA
2
Department of Surgery, University of California Irvine, Orange, CA 92697, USA
*
Authors to whom correspondence should be addressed.
Therapeutics 2025, 2(3), 10; https://doi.org/10.3390/therapeutics2030010
Submission received: 5 May 2025 / Revised: 8 June 2025 / Accepted: 16 June 2025 / Published: 20 June 2025
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Abstract

:
Animal models are indispensable in biomedical research, offering critical insights into disease mechanisms and therapeutic strategies. However, existing models often inadequately replicate human pathophysiology, leading to discrepancies between preclinical and clinical outcomes. Despite their contributions, many models exhibit significant limitations, especially concerning cancer and infectious diseases. Inaccurate modeling of human biological responses can result in failed clinical trials, escalated research costs, and delays in developing effective treatments. The golden hamster (Mesocricetus auratus) has emerged as a viable model, particularly in cancer and infectious disease research. Sharing physiological and immunological profiles similar to humans, the golden hamster offers distinct advantages over other rodent models, such as mice and rats. This review explores the benefits of using golden hamsters in cancer research, highlighting their contributions to scientific advancements while also addressing the limitations due to incomplete immunological and molecular knowledge about this species.

1. Introduction

Animal models are fundamental in biomedical research by helping researchers understand disease mechanisms and contributing to the development as well as perfection of therapeutic interventions [1,2,3]. One of the major challenges in preclinical and clinical research is the use of unsuitable animal models that fail to accurately replicate human physiology, pathology, and drug responses. This can lead to misleading results, ineffective treatments, and even harmful consequences when therapies move to human trials [2]. A major limitation of animal models is their inherent biological differences from humans. Even genetically similar species, such as primates, differ significantly in metabolism, immune system function, and organ structure [4,5]. Rodents, which are widely used in preclinical research, process drugs differently due to variations in liver enzyme activity, leading to inaccurate predictions of drug efficacy and toxicity. Many drugs that show promising results in animal models fail during human clinical trials [4,6,7].
According to studies, approximately 90% of drugs that pass preclinical animal testing fail in human trials because of a lack of efficacy or unexpected toxicity [6]. For example, treatments for neurodegenerative diseases such as Alzheimer’s and Parkinson’s often show success in mouse models but fail in humans because rodent brains do not fully replicate human neurobiology [8,9]. Using inappropriate animal models raises ethical concerns, as it subjects animals to unnecessary suffering while providing limited scientific benefits. Additionally, the high failure rate of animal-tested drugs results in significant financial losses for pharmaceutical companies and research institutions, increasing the cost of drug development [10,11]. Certain diseases, especially those related to human-specific conditions (such as psychiatric disorders, cancer metastasis, and autoimmune diseases), do not have accurate animal equivalents. For example, small animals like mice do not naturally develop many human cancers or replicate the complexity of human immune responses, making them poor models for immunotherapy research [11,12,13].
To address these challenges, alternative models are explored, such as human organoids, microfluidic “organ-on-a-chip” systems, and AI-driven drug discovery methods [14,15]. These innovations aim to provide more accurate, ethical, and cost-effective alternatives to traditional animal testing, potentially improving the reliability of preclinical research [16]. However, relying on mice and rats as preclinical models has shown incompatible results with the complex interactions that are found in humans [16,17].
Golden hamsters provide unique advantages in specific research areas, especially in oncology and infectious diseases. Their susceptibility to human-like tumor growth and a wide range of viral and bacterial pathogens makes them invaluable in translational medicine [18]. There are several strains of hamsters used as animal models in biomedical research, each with unique physiological and genetic characteristics suited for different studies. The Syrian hamster (Mesocricetus auratus) is a valuable animal model for infectious diseases (such as SARS-CoV-2 and leishmaniasis) and cancer research (such as Leukemia [18,19,20,21]. The Chinese hamster (Cricetulus griseus) is widely utilized in genetic and biopharmaceutical research, particularly for producing recombinant proteins in Chinese hamster ovary (CHO) cells [22]. Other strains, such as the Armenian hamster (Cricetulus migratorius) and the Djungarian hamster (Phodopus sungorus), have been employed in circadian rhythm, metabolic, and neurobiological studies [23]. The choice of hamster strain depends on the research focus, as differences in immune response, metabolism, and susceptibility to diseases can significantly impact study outcomes [24]. In our study, we focus only on the Syrian golden hamster (Mesocricetus auratus) as the new optional strain for cancer research.

2. The Necessity for a Reliable Animal Model

2.1. Limitations

The commonly used animal models, such as mice and rats, show marked differences with humans in immune system function, genetic composition, and metabolic processes. These differences manifest in different responses and outcomes during infectious diseases and tumors when compared to humans [25]. Due to these disparities, results are often misleading and do not accurately reflect human experiences, hindering the ability to translate research findings. For instance, mice are naturally resistant to certain human-specific pathogens, such as HIV, Shigella flexneri and Plasmodium falciparum. The resistance is dependent on how the pathogen co-evolves and adapts to the host-selected animal model [26,27,28,29].
The complexity of human cancers, encompassing tumor heterogeneity and microenvironment interactions, poses a significant challenge for animal models [30]. Classic xenograft models lack a complete immune system; in contrast, the mutations in genetically modified mouse models may not perfectly reflect those in human cancers. The existing animal models of tumor angiogenesis or metastasis are not without their limitations and controversies [31]. Some laboratory mice strains are susceptible or resistant to cancer-causing viruses, which requires the search for alternative animal models [32,33]. These models do not reflect the pathophysiology in humans. The principle of 3Rs (replacement, reduction and refinement) causes ethical concerns about animal welfare, which limits the use of highly intrusive experiments on mammals and other species [6,34,35].

2.2. Current Alternatives

Human-derived organoid and 3D culture systems are easy solutions that offer a promising alternative because they closely mimic the structure and diseases of human tissue in a lab setting [36,37]. Implementing these systems enables a sharper analysis of drug efficacy and patient responses, leading to improved drug-testing methods and the creation of truly personalized medicine through detailed data analysis [38,39,40]. However, the accuracy of organoid models in representing pathogen-associated cancers needs improvement; current research aims to enhance their predictive capabilities and better reflect the complexities of these diseases [40,41]. To that end, artificial intelligence (AI) simulations and computer models are being used to complement animal studies, which may lead to a reduction in the number of animals used in research [42,43].
The rapid analytical speed offers a considerable edge over the slower pace of traditional methods. Although in-silico models have advanced, the inherent complexities of living systems necessitate animal experimentation to verify results and account for the countless in vivo variables that can lead to discrepancies [44,45]. The close genetic and physiological kinship between non-human primates and humans makes them invaluable for infectious disease research; subtle physiological similarities allow for more effective testing of new medicines and vaccines. Ethical, logistical, and cost issues limit their use [46,47]. Progress in genetic engineering has resulted in the development of mice with human components, known as humanized mice [48,49]. Although these models improve the relevance of preclinical data, accurately replicating human immune responses remains challenging, especially in immune-related processes [50,51]. Given the aforementioned limitations and existing alternatives, the optimal animal model should ideally exhibit unique characteristics to facilitate translation between preclinical and clinical studies to ensure a smooth transition. These unique characteristics include (1) closer physiology to humans; (2) possessing a closer resemblance to the human immunological mechanism; (3) a tumor microenvironment of similar nature; (4) similar genetic expression and metabolic profiles; (5) logistically feasibility; and (6) availability in large numbers.

3. Unique Biological Similarity Between Hamsters and Humans

3.1. Anatomical and Physiological Advantages of the Syrian Hamster

Although NOD scid gamma (NSG) mice serve as a widely used animal model for human tumor xenografts [52], they are susceptible to infections, leading to inaccurate results when studying cancer and its treatment [53]. Moreover, it has polymorphism in the SIRP-alpha gene which impacts macrophages and immune cells, which influences studying the immune response to tumors [54]. The Syrian hamster’s cheek pouch, an immune-privileged site lacking lymphatic drainage, leaving systemic immune function unaffected, enables long-term engraftment of human tumor xenografts without the need for immunosuppression medications [55]. The cheek pouch’s thin, translucent, and easily accessible structure enables non-invasive in vivo imaging in hamster (such as angiogenesis, tumor progression, and intravital microscopy) studies, which is less invasive than surgical implantation in the internal organs of mice [56,57]. The tumor microenvironment may be manipulated with greater ease, and vascularization and tumor–host interactions can be observed in real time [58,59]. Hamsters exhibit greater robustness compared to NSG mice, necessitating less stringent pathogen-free conditions, potentially resulting in reduced husbandry expenses [60]. Comparative limitations of hamsters versus NSG mice are less genetically tractable (fewer transgenic lines, genetic tools), less standardized with no established protocols nor widespread use, and not as well-characterized for long-term tumor growth and metastasis studies [61,62,63]. Comparisons between the hamster cheek pouch, NSG and humanized mice models are summarized in Table 1.
This feature has been exploited to study myofibrosarcoma (MFS-l) and melanotic melanoma (ME-l), which retain drug sensitivity profiles mirroring human tumors [55,64]. Unlike murine models, hamster pancreatic ductal adenocarcinomas exhibit 99% homology in sonic hedgehog (SHH) signaling pathways with humans, driving desmoplastic stromal reactions identical to those in clinical specimens [65]. Hamster’s cancer cell lines that can be used in cancer research are summarized in Table 2.

3.2. Lung: Similarities and Differences

The anatomical similarities between the lungs of golden hamsters and humans make hamsters a good model for respiratory research. Hamsters and humans both have lobed structures, but have different lobe numbers [86]. Like humans, hamsters have a bronchial tree branching from the trachea into progressively smaller bronchi and finally bronchioles, culminating in alveoli where gas exchange occurs [87]. Both species have alveoli lined with epithelial cells and surrounded by capillaries for gas exchange. These structural similarities aid researchers in studying disease processes such as viral infections [88].
In cancer research, hamster lungs exhibit a unique similarity to human lungs not found in other animal models; specifically, their capacity to develop lung tumors that closely resemble the histopathological subtypes and metastatic patterns observed in human non-small cell lung cancer (NSCLC), including adenocarcinoma [87,89,90]. The induction of lung cancer in Syrian hamsters by chemical carcinogens, such as N-nitrosobis(2-oxopropyl)amine (BOP), demonstrates histological and molecular similarities to human NSCLC. Specifically, these models replicate the overexpression of cyclooxygenase-2 (COX-2) and nuclear factor kappa B (NF-κB), key components of human lung cancer pathogenesis [59].
Moreover, the metastatic frequencies and distribution patterns of primary NSCLCs in hamsters closely resemble those observed in human patients, a characteristic not consistently replicated in murine or rat models [91]. Hamsters’ immunological compatibility and similar tumor biology make their lung model suitable for preclinical lung cancer research [59].

3.3. Pancreas: Similarities and Differences

Human and hamster pancreases are anatomically similar. Both species’ pancreases are compact and located in the upper abdomen, near the posterior abdominal wall [92]. Both hamsters and human pancreases have a higher content of adipose tissue at the pancreatic tail [93]. This structural organization is not commonly observed in other rodent models, such as mice and rats, allowing improved comparative studies of localized pancreatic functions and pathologies [93]. Despite similarities, the pancreatic anatomy differs between hamsters and humans. The hamster pancreas comprises three lobes: gastric, splenic, and duodenal, with an average weight of approximately 0.46 g or 0.4-0.5% of total body weight [94]. The human pancreas is divided by head, body, and tail. Hamsters possess a gastric lobe in their pancreas unique to them compared to all other species [92]. Islet cell distribution also varies between species. In hamsters, the islet cell distribution varies across the pancreatic most ubiquitous in the tail [95] unlike the organized structure seen in humans [92].
Human pancreatic cancer’s progression and key genetic mutations (like KRAS and TP53) are closely mirrored in golden Syrian hamsters [18]. The histological presentation of well-differentiated ductal adenocarcinomas resulting from pancreatic cancer induction or transplantation in golden hamsters closely mirrors that observed in human pancreatic cancer. These neoplasms show invasive growth and metastatic potential, specifically to lymph nodes and the liver, thereby replicating the metastatic spread seen in human disease [96,97]. Orthotopic pancreatic cancer cell transplantation in hamsters produces higher metastasis (e.g., 100% in liver and lungs in some models) than in mice, exhibiting human-like ascites, cachexia, and local invasion [59]. Additionally, hamster pancreatic cancer cell lines, such as HaP-T1 which is described in Table 2, exhibit epithelial traits and express a nearly identical (99%) N-terminal sonic hedgehog (SHH) to that of humans, thus inducing desmoplasia—characteristic of human pancreatic cancers [59]. Analysis of pancreatic cancer in hamsters reveals the expression of blood group-related antigens and tumor-associated markers (A, B, H, Le(b), Le(y), Le(x), and TAG-7) in both primary and orthotopic hamster pancreatic cancer cells, mirroring patterns observed in human pancreatic cancers [97]. This antigenic profile shows that the model is useful for studying human tumor biology and the immune system’s response [97]. Hamster models present advantages in the study of acute pancreatitis, exhibiting parallels with human responses to ethanol and fatty acids to induce pancreatitis, and the comparable alterations in lipid metabolism [93]. The usage of metformin was found to protect from harmful metabolic changes and insulin resistance that can subsequently lead to pancreatic cancer [98].
The common similarities between humans and hamsters open an avenue for testing the pancreatic cancer virotherapy. The sequential administration of engineered oncolytic viruses to express the immunostimulatory cytokine oncostatin M or IL-12 produces a significantly enhanced antitumor effect in the Syrian hamster model of pancreatic cancer [99,100]. Also, research using the hamster animal model has explored using therapy (such as Angiostatin) to treat pancreatic cancer that metastasizes to the liver [101].

3.4. Liver: Similarities and Differences

Hamster livers, though small, possess a remarkable functionality relative to their body size, proving advantageous for experimental studies involving tissue biopsies or surgical procedures [102,103]. Conversely, the larger size and more intricate vascular system of human livers present challenges for experimental models yet offer a greater physiological capacity [102,103]. Both golden hamsters and humans share similar hepatic lobular architecture, including sinusoids, bile ducts, and hepatocytes organized to facilitate metabolic and detoxification processes [104,105]. However, the hepatic segments are larger and divided into clear segments as opposed to hamsters [106,107]. Both species exhibit similar lipid metabolism characteristics, including lipoprotein synthesis, processing, and recycling. This characteristic makes hamsters a suitable model for atherosclerosis [108,109,110]. However, newborn hamsters have a significantly faster rate of cholesterol synthesis in their livers than humans, because of the difference in developmental metabolic needs [111].
Golden hamsters, through chemically induced models, show similar histological, molecular, and pathological progression to human liver cancer. Hamsters exposed to hepatocarcinogens such as diethylnitrosamine (DEN) or streptozotocin develop HCC, which is poorly differentiated, exhibits frequent mitosis, and expresses AFP—a biomarker also elevated in human HCC [59]. The development of invasive HCC from pre-neoplastic lesions, such as hyperplastic nodules, fatty metamorphosis, and bile duct proliferation, closely mirrors the stages of human hepatocarcinogenesis, encompassing initial toxic injury, subsequent regenerative hyperplasia, and ultimately, malignant transformation [112]. Recently, chemical carcinogens like N-methyl-N-nitrosourea (MNU) and carbon tetrachloride (CCl4) have been employed to induce liver tumors in hamsters, which has provided insights into the pathological and molecular progression of liver cancer similar to humans [18,59]. The advancements in genetic engineering, such as CRISPR/Cas9, have allowed for the development of gene-targeted knockout hamster models (e.g., TP53, KCNQ1, IL2RG), which can further elucidate the genetic keystones of liver cancer and support translational research for new therapies [18].

3.5. Gastrointestinal Tract: Similarities and Differences

Hamsters and humans, like mice and many other mammals, share a dominant gut microbiota consisting primarily of Firmicutes and Bacteroidetes phyla at the highest taxonomic level [113]. The proportions, however, vary between hamsters and humans. Hamsters show a strong Firmicutes dominance (92.6%), while humans have a more balanced Firmicutes and Bacteroidetes population [114]. Even with this distinction, both humans and hamsters share many of the same key bacterial families and genera, such as Erysipelotrichaceae, Ruminococcaceae, and Lactobacillaceae [115]. While both hamsters and humans rely on pancreatic amylase in their small intestines to digest starch, the process’s effectiveness varies depending on their respective diets and evolutionary adaptations [116] (Table 3). In both hamsters and humans, microbial fermentation of undigested nutrients takes place, but the location differs; in hamsters, it primarily occurs in the cecum pouch of their large intestine, while in humans, with their reduced cecum, fermentation happens mainly in the colon [117]. While both species share a similar gastrointestinal structure, including a stomach, small intestine, cecum, and colon, human stomachs consist of a single glandular pouch, unlike the compartmentalized stomachs of hamsters, which have a non-glandular forestomach and a glandular region. The human cecum is small; the hamster’s is large and essential to fermentation [116]. Similar carbohydrate fermentation and metabolic processes in humans and hamsters are reflected in the presence of shared bacterial genera, including Ruminococcus and Lactobacillus [118].
The Syrian hamster exhibits a strong congruence with human gastrointestinal (GI) tract cancers regarding tumorigenesis, histopathology, and progression [18,59]. Both human and hamster GI tract cancers can express similar tumor-associated antigens, such as those with blood group specificities (A, B, H, Leb, Lex, Ley), and markers like CA 125, TAG-72, and 17-1A [119]. Human and hamster cancers, especially oral and gastric, exhibit analogous histological characteristics and pathological mechanisms. For example, hamster models of oral squamous cell carcinoma and gastric adenocarcinoma display similar cellular abnormalities, differentiation patterns, and progression from chronic inflammation or precancerous lesions to invasive cancer, mirroring human observations [59,120].

4. Golden Syrian Hamsters in Cancer Research

The use of hamsters in cancer research is selected over mice, due to their unique biological traits and heightened sensitivity to carcinogens, making them exceptionally useful for evaluating therapies, especially immunotherapies [59].
Hamsters are highly susceptible to chemically induced cancers, facilitating carcinogenesis studies [102]. For example, the DMBA (7,12-dimethylbenz[a]anthracen)-induced cheek pouch model of oral squamous cell carcinoma is similar to those of human cancer, starting with normal cells progressing to hyperplasia, then dysplasia, and finally carcinoma. This immunoprivileged site allows tumor growth without rejection, facilitating studies on several carcinogenic pathways, such as oncogene activation (Egfr, Myc, Hras), loss of tumor suppressor (p53, p16), Wnt/β-catenin pathway dysregulation, mirroring of the human oral cancer and chemopreventive agent testing (e.g., rosmarinic acid, black raspberries) [121].
The application of CRISPR/Cas9 technology has broadened the utility of hamsters through the generation of knockout (KO) models that display human-like cancer characteristics [122], such as the TP53 KO hamster that develops aggressive acute myelogenous leukemia (AML), the KCNQ1 KO hamster that exhibits gastric neoplasia, and IL2RG KO that enables human tumor xenograft studies for immunodeficient studies [59].
In cancer therapy, the Syrian hamster is suitable for testing the oncolytic virotherapy in immunocompetent animals. The viral replication, tumor-specific T-cell infiltration, and prolonged-survival post-human adenovirus (Adv) treatment (e.g., Delta-24-RGD) is promising as an appropriate model for glioma and pancreatic cancer [59,123]. Hamsters can be used in combination therapies for cancers such as the sequential administration of oncolytic adenovirus and vaccinia virus (VV) for kidney cancer models [59]. Immunologically, the immune response of hamster’s natural killer cells to vaccinia virus administration mirrors human responses, aiding in the study of the immune mechanism and optimization of immunotherapy [59,124], (Table 4).
The tumor immune microenvironment (TIME), metastasis development and tumor-stroma interactions are akin to humans, facilitating their study [59]. The intraperitoneal injection of SHPC6 cancer cells forms disseminated nodules mimicking advanced human pancreatic cancer metastasis [125].

5. Immunological Connections Between Hamsters and Human

Immune System Parallels and Divergences

Hamsters possess omental milky spots—lymphoid structures rich in macrophages—that mimic human peritoneal immune surveillance and cancer metastasis [59]. However, key immune markers diverge, while ribosomal protein L18 (RPL18) serves as a stable reference gene for qRT-PCR, and assays for cytokines like IFN-γ and IL-6 require species-specific validation [126].
The immunology of golden hamsters shows remarkable similarities to that of humans, especially concerning cytokine function and adaptive immunity [20,127]. Hamsters exhibit biological responsiveness to human cytokines like GM-CSF, IL-12, IL-21, and IL-2, thus facilitating direct evaluation of cytokine therapies without species-specific adjustments [128]. The administration of oncolytic viruses expressing human IL-12 or IL-2 in hamster models resulted in significant anti-tumor immune responses, evidenced by interferon-γ production and CD8+ T-cell infiltration, thus corroborating observations from human clinical trials [59,128]. Furthermore, hamsters demonstrate Th1/Th2 immune polarization comparable to humans when dealing with infections [127]. In hamsters with hookworm infections, the initial inflammatory response (Th1, IFN-γ) gives way to a Th2-driven response (IL-4, IL-10) as the infection develops, a pattern consistent with human parasitic diseases [129]. Their adaptability is key to studying chronic infection immune modulation. The hamster’s immune system provides a close analog to human responses to viral pathogens. Hamsters infected with SARS-CoV-2 experience cytokine storms with high levels of IFN-γ, IL-6, and IL-17A—inflammatory mediators also seen in humans—and maintain memory B and T cells for weeks afterward [130,131]. Similar to human immunity, these memory cells protect against cancer and reinfection. The cytokine functionality in cancers is similar in hamsters as in humans, such as in GM-CSF, IL-2, IL-21 and IL-2, with shared cytokine pathways (IFN-α and TNF-α) in colorectal cancer specifically [59]. In pancreatic cancer, Syrian hamsters showed similar CD4+ and CD8+ T cell infiltration in the human tumor microenvironment, and local delivery of IL-2 via oncolytic adenoviruses [132]. Furthermore, hamsters exhibit human-like lymphoproliferative responses and organ-specific immune activation, such as splenomegaly and lung mononuclear cell infiltration during viral clearance [133]. The ability to support adenovirus replication in liver and human tumor xenografts in immunocompetent settings further validates their translational applicability [58,134].

6. Limitations with Hamster Research

Despite their advantages, golden hamsters are not a perfect animal model because of gaps in immunological understanding:
(a)
Limited Immunological Tools and Reagents: Compared to mice and rats, fewer antibodies and immunological assays are commercially available for hamsters because of limited studies determining the functionality and expression of these markers, thus hampering detailed immune response analyses [20].
Several studies have used anti-mouse or anti-rat CD markers to investigate the immune cell infiltration in the target organ of hamsters [135,136,137,138]. Similarly, while the immune metabolome has been extensively studied in humans and mice, it remains distinct and relatively unexplored in hamsters [139,140]. For that reason, we illustrate the comparisons of amino acid compositions of CD4 (Figure 1) and CD8a (Figure 2) antigens between hamsters and different species (humans, mice and rats) based on amino acid polarity, to prove that the expected antigenic similarity is not enough to rely on the cross-reactive antibodies or similar immune reaction to build the mechanism and understand disease pathogenesis. The amino acid sequence of CD4 and CD8a showed a low abundance of conserved continuous sequences, making it unexpected to have a common antigenic determinant for finding multi-species antibodies.
To overcome this limitation, studies should be addressed to identify the unique epitopes in surface antigens expressed on hamsters’ immune cells, such as CD3, CD4, and CD8a. From these effective epitopes, we can identify suitable antibody paratopes to be designed and manufactured later on. A confirmational functional assay will be needed to ensure the antigenic functionality in terms of expression; for example, CD69 expression in hamsters is related to early T-cell activation, which is similar to humans and mice.
Understanding immune mechanisms in hamsters could enhance their use in preclinical research, potentially offering greater benefits for studying diseases compared to other commonly used animal models.
(b)
Incomplete Genome Annotation: Hamster genome sequencing has been achieved, but functional annotation of immune-related genes remains incomplete, restricting genetic manipulation capabilities. This limitation may be addressed firstly by employing long-read sequencing to improve the contiguity and accuracy of the genome assembly [141]. Second, the application of RNA-Seq across multiple tissues and developmental time points enables a detailed characterization of the transcriptome and enhances gene annotation through the identification of a wide range of transcripts. The third objective is to use comparative genomics to predict gene structures by aligning hamster sequences against the well-annotated genomes of related species like mice and rats. This method improves annotation accuracy through the utilization of conserved genomic features [141]. Fourthly, bioinformatics tools will be utilized to functionally annotate predicted genes and elucidate gene roles and interactions based on domain content and homology [139]. Finally, experimental validation of gene models by CRISPR/cas9 knockouts and RT-PCR will be required to confirm the functions, and structure will be needed.
(c)
Uncharacterized Immune System Components: Certain immune mechanisms, such as cytokine interactions and T-cell responses, are not fully understood in hamsters, making it difficult to extrapolate findings directly to humans. Comparative analysis of immune responses in simplified experimental models (human and murine) and corresponding disease states may elucidate cytokine/chemokine secretion patterns. Analysis of diverse trials across various cancers and infectious disease models, stratified by disease severity, will elucidate the patterns of immune mediator secretion, including source, target cells, concentrations, and biological effects.
(d)
Unknown ability to correlate with human outcomes: Usually, nine out of ten drugs that appear promising in animal studies fail in human clinical trials. By characterizing the immune response and performing genomic annotation, we can better understand the disparities between human and murine models, thereby improving the translation of hamster study results to human outcomes.
(e)
Lack of Standardization: The disease outcomes can be influenced by variables such as inoculation dose and volume, requiring careful experimental design for reproducibility and comparison across studies [142]. Once fundamental biological data from hamsters, including immune mechanisms, available immunological CD markers, cytokine/chemokine secretion, genomic annotation, and metabolic processes, are established, subsequent cancer research will benefit from enhanced standardization and reproducibility.

7. Conclusions

Syrian hamsters bridge critical gaps in cancer research by combining immunocompetence, human-like carcinogenesis, and viral permissiveness. Golden hamsters have significantly contributed to advancements in cancer and infectious disease research, (Figure 3). Their unique biological traits make them a valuable model for studying tumor biology, viral pathogenesis, and bacterial infections. However, the incomplete immunological and molecular knowledge of hamsters presents challenges in fully utilizing their potential as a model. Several studies are using the hamster antibodies based on cross-creative antibodies without verification of these antibodies’ binding specificities or comparable functionalities, which makes the data generated misleading and deceptive. For greater utilization of hamsters in biomedical research, these limitations must be addressed by further genetic and immunological studies, leading to better therapeutic strategies and disease management.

Author Contributions

M.S., D.K.I., M.A. and N.A.-J. contribute to Conceptualization, investigation, writing of this manuscript, editing and review of this manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. CD4 antigen sequence across species. (a) Amino acid comparison between golden hamsters versus humans, mice and rats; the highlighted blue are the amino acids that have charge. The underlined red part is the intercellular domain responsible for signal transduction inside the cells, while the rest (non-underline) is the transmembrane domain (exposed part). (b) The percentage of similarity between them, where the highest similarity (64.6%) is between a hamster’s CD4 and rat’s CD4. Darker color means more similarity between each 2 animal models.
Figure 1. CD4 antigen sequence across species. (a) Amino acid comparison between golden hamsters versus humans, mice and rats; the highlighted blue are the amino acids that have charge. The underlined red part is the intercellular domain responsible for signal transduction inside the cells, while the rest (non-underline) is the transmembrane domain (exposed part). (b) The percentage of similarity between them, where the highest similarity (64.6%) is between a hamster’s CD4 and rat’s CD4. Darker color means more similarity between each 2 animal models.
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Figure 2. CD8a antigen sequence across species. (a) Amino acid comparison between golden hamsters versus humans, mice and rats; the highlighted blue are the amino acids that have charge. The underlined red part is the intercellular domain responsible for signal transduction inside the cells, while the rest (non-underline) is the transmembrane domain (exposed part). (b) Percentage of similarity between them, where the highest similarity (62.65%) is between a hamster’s CD4 and rat’s CD8a.
Figure 2. CD8a antigen sequence across species. (a) Amino acid comparison between golden hamsters versus humans, mice and rats; the highlighted blue are the amino acids that have charge. The underlined red part is the intercellular domain responsible for signal transduction inside the cells, while the rest (non-underline) is the transmembrane domain (exposed part). (b) Percentage of similarity between them, where the highest similarity (62.65%) is between a hamster’s CD4 and rat’s CD8a.
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Figure 3. Benefits and challenges in cancer and infectious disease research. The figure was created by Biorender online licensed software.
Figure 3. Benefits and challenges in cancer and infectious disease research. The figure was created by Biorender online licensed software.
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Table 1. Comparison between hamster check pouch, NSG and humanized mice models.
Table 1. Comparison between hamster check pouch, NSG and humanized mice models.
FeatureHamster Cheek PouchNSG MiceHumanized Mice
Immune systemLocal immune privilegeFully immunodeficientEngrafted human immune cells
Imaging accessExcellentLimitedLimited
Tumour-immune interactionMinimalAbsentHuman-like
Cost and simplicityLow and simpleModerateHigh and complex
Immunotherapy researchNoNoYes
Tumour microenvironment studyAppropriate for local interaction and angiogenesisModerateAppropriate with immune aspect
StandardizationLess standardHighModerate (but variable)
Table 2. Hamster cell lines used in cancer research.
Table 2. Hamster cell lines used in cancer research.
Cell LineOrigin/TissueSpeciesApplication and Similarity to Human CancerRef.
BHK-21Baby
Hamster
Kidney
fibroblasts		Syrian hamster
-
Virus-induced tumorigenesis (parallels in human cancers (e.g., HPV, EBV, HBV). Transformed by various viruses, including simian virus 40 (SV40), to study viral replication and oncogenesis.
-
Mimics loss of replicative senescence in cancer, cancer instability, virus-driven cancers like HPV or HBV-associated cancers, early events in oncogenic transformation.
[66,67,68,69,70]
HaKKidney
carcinoma		Syrian hamsterTransformation studies, tumorigenesis, anchorage-independent growth, alteration in cell cycle checkpoint and response to DNA damaging agents. [71,72]
HapT1Pancreatic adenocarcinomaSyrian hamster
-
Pancreatic cancer models, and immunotherapy research.
-
Sharing features to human PDAC such as desmoplastic stroma, tumor invasion, PDAC invasion, PDAC’s inflammation, immunosuppressive tumor microenvironment and poor immune recognition.
[73,74,75]
HTCHepatoma tissue cultureRat (Rattus norvegicus)
-
Genotoxicity testing, drug metabolism studies.
-
Mimic genomic instability that drives liver cancer, inflammation-induced hepatocarcinogenesis, reflected deregulated cell cycle, chronic exposure to carcinogens.
[76,77,78,79,80]
CHO-K1Ovary
epithelial line		Chinese hamster
-
Biopharmaceutical production, gene expression studies.
-
Mimic chemotherapy resistance, early oncogenesis, genomic maintenance and failure in cancer, instability in cancer and unregulated growth seen in tumors.
[81,82,83,84,85]
Table 3. Shared features between the human and hamster gastrointestinal tracts.
Table 3. Shared features between the human and hamster gastrointestinal tracts.
FeatureHamsterHuman
Major microbiota phylaFirmicutes, Bacteroidetes 
(Firmicutes dominant)		Firmicutes, Bacteroidetes (more balanced)
Main fermentation siteCecumColon
Stomach structureCompartmentalized
(nonglandular + glandular)		Simple glandular
CecumLarge, functionalRudimentary
Shared bacterial generaYes (e.g., Ruminococcus, Lactobacillus)Yes
Table 4. Comparative advantages of the hamster model over the mouse model in cancer research.
Table 4. Comparative advantages of the hamster model over the mouse model in cancer research.
FeatureHamster Model Advantage
Immune competencePermits study of intact immune responses to tumors and therapies [123].
Viral permissivenessSupports human AdV/VV replication, unlike mice [123].
Pathological fidelityPancreatic/oral carcinogenesis closely mimics human genetics and histology [18,59,121]
Therapeutic windowLarger body size allows repeated sampling and imaging [18].
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Singer, M.; Imagawa, D.K.; Alexander, M.; Abi-Jaoudeh, N. The Golden Hamster: A Valuable Model for Designing Cancer Therapies. Therapeutics 2025, 2, 10. https://doi.org/10.3390/therapeutics2030010

AMA Style

Singer M, Imagawa DK, Alexander M, Abi-Jaoudeh N. The Golden Hamster: A Valuable Model for Designing Cancer Therapies. Therapeutics. 2025; 2(3):10. https://doi.org/10.3390/therapeutics2030010

Chicago/Turabian Style

Singer, Mahmoud, David K. Imagawa, Michael Alexander, and Nadine Abi-Jaoudeh. 2025. "The Golden Hamster: A Valuable Model for Designing Cancer Therapies" Therapeutics 2, no. 3: 10. https://doi.org/10.3390/therapeutics2030010

APA Style

Singer, M., Imagawa, D. K., Alexander, M., & Abi-Jaoudeh, N. (2025). The Golden Hamster: A Valuable Model for Designing Cancer Therapies. Therapeutics, 2(3), 10. https://doi.org/10.3390/therapeutics2030010

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