SNU-16 Xenograft Model Service for Gastric Cancer

The SNU-16 xenograft model offers a robust preclinical platform for evaluating novel therapeutic strategies against gastric adenocarcinoma, leveraging a well-characterized cell line with distinct molecular drivers including FGFR2 and MET amplification. At Alfa Cytology, we specialize in constructing validated SNU-16 xenograft models with rigorous quality control and customizable study designs to accelerate your preclinical drug development pipeline.
Overview of SNU-16 Xenograft Model for Gastric Cancer
The SNU-16 cell line was established in 1987 by J. Park and colleagues from ascites-derived tumor cells of a 33-year-old female patient with poorly differentiated gastric carcinoma prior to chemotherapy. As a suspension-growing epithelial cell line, SNU-16 exhibits pronounced chromosomal instability and aneuploidy, characteristic of the chromosomal instability (CIN) molecular subtype of gastric cancer. The model is particularly notable for its amplification and overexpression of both c-MET and fibroblast growth factor receptor 2 (FGFR2), alongside homozygous TP53 mutation (p.Tyr205Phe) and heterozygous MSH6 frameshift mutation, making it an excellent representative of aggressive, genomically complex gastric malignancies.
In xenograft applications, SNU-16 demonstrates robust tumorigenicity across multiple immunodeficient mouse strains including M-NSG, CB-17 SCID, and Balb/c nude mice, with consistent subcutaneous tumor formation and measurable growth kinetics. Researchers have extensively utilized this model to evaluate FGFR-targeted inhibitors (e.g., AZD4547, E7090), MET inhibitors, and combination regimens with conventional chemotherapeutics, as well as to investigate resistance mechanisms to HER2-directed therapies. The SNU-16 xenograft thus serves as a critical bridge between in vitro findings and in vivo therapeutic efficacy, offering a reproducible system for pharmacokinetic, pharmacodynamic, and biomarker studies in gastric cancer drug development.
Figure 1. PC delayed tumor growth in an SNU-16-derived xenograft mouse model without toxicity. (Lee, Sunyi, et al., 2022)
Cell Line Information: SNU-16
The following table summarizes the essential characteristics and molecular profile of the SNU-16 cell line:
| Attribute |
Details |
| Cell Line Name |
SNU-16 (Synonyms: SNU16, NCI-SNU-16) |
| Cellosaurus Accession |
CVCL_0076 |
| ATCC Catalog Number |
CRL-5974 |
| Species |
Homo sapiens (Human) |
| Tissue of Origin |
Stomach (Gastric) |
| Disease |
Gastric adenocarcinoma, poorly differentiated |
| Metastatic Site |
Ascites |
| Patient Demographics |
33-year-old female, East Asian (Korean) |
| Year Established |
1987 |
| Establishment Details |
Established by J. Park et al. from ascites prior to chemotherapy |
| Morphology |
Epithelial; grows in suspension as multicellular aggregates |
| Growth Properties |
Suspension; doubling time approximately 27 hours |
| Culture Medium |
RPMI 1640 supplemented with 10% FBS, 25 mM HEPES |
| Biosafety Level |
BSL-1 |
| Tumorigenicity |
Yes; colony forming efficiency ~10% in semisolid medium |
| Surface Antigens |
Blood Type A, Rh+; CEA+; TAG 72+ |
| Oncogenes |
myc+, erb-B2 (HER2)+ |
| Key Amplifications |
c-MET amplification; FGFR2 amplification |
| TP53 Status |
Homozygous mutation p.Tyr205Phe (c.614A>T) |
| MSH6 Status |
Heterozygous frameshift p.Lys1358fs*2 (c.4065_4066insTTGA) |
| RHOA Mutations |
Heterozygous p.Arg5Trp and p.Phe39Leu |
| Fusion Gene |
CD44-SLC1A2 |
| Molecular Subtype |
Chromosomal Instability (CIN) per TCGA classification |
| STR Profile |
Amelogenin: X; CSF1PO: 12; D13S317: 8,12; D16S539: 11,13; D5S818: 10,13; D7S820: 12; THO1: 6,9 |
| Mycoplasma Status |
Negative |
| Quality Control |
Authenticated via STR profiling; batch CoA provided |
Our Services
Alfa Cytology leverages the SNU-16 cell line's well-documented molecular landscape and proven tumorigenic profile to deliver reproducible, high-quality xenograft models tailored to your preclinical study objectives. Our experienced team ensures stringent cell line authentication, controlled inoculation procedures, and comprehensive endpoint analyses to generate reliable data for your therapeutic development programs.
Workflow of SNU-16 Xenograft Model Construction
The construction of the SNU-16 xenograft model follows a standardized, multi-phase workflow designed to ensure consistent tumor engraftment, measurable growth kinetics, and reliable therapeutic response assessment. Each phase incorporates stringent quality control measures to maintain model integrity throughout the study duration.
- Cell Line Preparation and Authentication: SNU-16 cells are revived from cryopreserved stocks and cultured in RPMI 1640 medium with 10% FBS under standard conditions (37 degrees C, 5% CO2). Prior to inoculation, cells undergo STR authentication to confirm identity and mycoplasma testing to ensure purity. Only low-passage cells in logarithmic growth phase are selected for implantation to maximize viability and tumorigenic potential.
- Recipient Mouse Selection and Conditioning: Immunodeficient mice (commonly M-NSG, CB-17 SCID, or Balb/c nude) are acclimatized for 5-7 days under pathogen-free conditions. Mice are randomized by body weight and assigned to treatment groups based on the study design. Baseline body weights and clinical observations are recorded prior to tumor cell inoculation.
- Tumor Cell Inoculation: SNU-16 cells are harvested, washed, and resuspended in a serum-free medium such as PBS or Matrigel-containing buffer at a concentration typically ranging from 1x10^6 to 5x10^6 cells per 100-200 uL. The cell suspension is injected subcutaneously into the flank of each mouse using a sterile syringe. Tumor formation is monitored by palpation beginning 3-5 days post-inoculation.
- Tumor Growth Monitoring and Randomization: Once tumors reach a palpable volume (typically 50-100 mm3), mice are randomized into vehicle control and treatment cohorts. Tumor dimensions are measured twice weekly using calipers, and volumes are calculated via the modified ellipsoid formula (length x width^2 x 0.5). Body weights are recorded concurrently to monitor general health and treatment-related toxicity.
- Therapeutic Intervention and Endpoint Assessment: Test compounds are administered according to the predefined dosing regimen (route, frequency, and duration). Tumor growth inhibition (TGI) is calculated by comparing treatment group tumor volumes to vehicle controls. At study termination, tumors are excised, weighed, and processed for histopathology, immunohistochemistry, or molecular analyses as specified in the study protocol.
- Data Compilation and Reporting: All raw data including tumor growth curves, body weight trajectories, survival metrics, and histopathological findings are compiled into a comprehensive study report. Statistical analyses are performed using appropriate methods, and results are presented with clear interpretation to support downstream decision-making in drug development.
Figure 2. SNU-16 xenograft model construction workflow.
Case Study-SNU-16 Xenograft Model Development
In a representative preclinical engagement, SNU-16 cells were successfully engrafted into immunodeficient mice to evaluate the efficacy of a novel targeted therapeutic agent. Tumors established consistently within the expected latency period and exhibited growth kinetics suitable for pharmacological intervention. Treatment cohorts demonstrated dose-dependent tumor growth inhibition compared to vehicle controls, with acceptable tolerability profiles as indicated by stable body weights throughout the study duration. Histopathological examination of excised tumors confirmed viable human gastric carcinoma tissue with characteristic morphological features. Additional biomarker analyses provided mechanistic insights into target engagement and pathway modulation. These results illustrate the utility of the SNU-16 xenograft model in generating actionable preclinical data to support candidate selection and IND-enabling studies. Specific quantitative data and treatment modalities can be customized and adjusted according to client requirements and compound properties.

Why Choose Alfa Cytology?
Alfa Cytology delivers comprehensive, client-centric preclinical services built on scientific rigor and operational excellence. Our SNU-16 xenograft model service is designed to provide reliable, reproducible data that advances your therapeutic candidates efficiently.
- Validated cell line sourcing with full STR authentication and mycoplasma testing to ensure model integrity from inception.
- Proven tumorigenicity across multiple immunodeficient strains with optimized inoculation protocols for rapid, consistent tumor establishment.
- Flexible study designs accommodating monotherapy, combination therapy, dose-response, and biomarker-driven endpoints.
- Comprehensive in-life monitoring including tumor caliper measurements, body weight tracking, and clinical observation by trained personnel.
- Integrated endpoint analysis encompassing tumor excision, histopathology, immunohistochemistry, and molecular profiling under one service roof.
- Dedicated project management with regular progress updates and transparent communication to align deliverables with your timeline.
- Competitive turnaround times and cost-effective pricing structures tailored to biotech and pharmaceutical client needs.
Contact Us
Ready to advance your gastric cancer therapeutic program with a validated SNU-16 xenograft model? Contact us today to discuss your study requirements, receive a customized proposal, and partner with Alfa Cytology for reliable preclinical data. Reach out to our scientific team to explore how our expertise can accelerate your drug development pipeline. Please reach out to us today via our inquiry form or email to learn more about our SNU-16 Xenograft Model services.
Reference
- Lee, Sunyi, et al. "Policosanol suppresses tumor progression in a gastric cancer xenograft model." Toxicological Research 38.4 (2022): 567-575.
For research use only. Not intended for any clinical use.