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C-33A Xenograft Model Service for Cervical Cancer

Fig 1.C-33A xenograft model for Cervical Cancer preclinical research.

The C-33A Xenograft Model Service for Cervical Cancer provides a robust, HPV-negative preclinical platform for evaluating therapeutic candidates against cervical squamous cell carcinoma. At Alfa Cytology, we specialize in delivering validated, reproducible C-33A xenograft models tailored to your discovery pipeline---from tumor establishment and in-life monitoring to comprehensive endpoint analysis---enabling data-driven decisions in oncology drug development.

Overview of C-33A Xenograft Model for Cervical Cancer

The C-33A cell line was originally established from a cervical biopsy of a 66-year-old patient and represents one of the few well-characterized HPV-negative cervical squamous carcinoma models available for preclinical research. Unlike the majority of cervical cancer cell lines that harbor high-risk human papillomavirus (HPV) DNA, C-33A is definitively negative for both HPV DNA and RNA, making it an indispensable tool for investigating non-viral pathways of cervical carcinogenesis. The line carries a documented TP53 point mutation at codon 273 (Arg->Cys substitution), resulting in elevated mutant p53 protein expression, and exhibits a pseudodiploid karyotype with modal chromosome number of 46. These genetic features render C-33A particularly relevant for studying p53-mutant, HPV-independent tumor biology and for evaluating therapies targeting alternative oncogenic drivers.

In vivo, C-33A demonstrates consistent tumorigenicity in immunodeficient mice, forming undifferentiated carcinomas upon subcutaneous or orthotopic implantation. The resulting xenografts recapitulate key histopathological features of human cervical squamous cell carcinoma, including epithelial morphology and aggressive growth kinetics. Researchers leverage this model to assess tumor growth inhibition, conduct pharmacokinetic/pharmacodynamic studies, and explore combination regimens. The HPV-negative status of C-33A also positions it as a critical comparator in studies evaluating HPV-targeted immunotherapies, ensuring that observed anti-tumor effects are not confounded by viral oncogene dependency.

Fig 2. Reference figures for C-33A cell-related literature.Figure 1. Effect of miR-218-5p, -124-3p, and -23b-3p overexpression on proliferation in CaSki and C-33A cells. (Romero-Lopez, M J, et al., 2024)

Cell Line Information: C-33A

C-33A is a human cervical squamous cell carcinoma cell line with well-defined genetic and phenotypic characteristics. Below is a comprehensive summary of its key attributes:

Feature Specification
Cell Line Name C-33A (also: C33A, C-33-A, C33)
Organism Homo sapiens (Human)
Tissue of Origin Cervix
Disease Cervical Squamous Cell Carcinoma
Age at Collection 66 years
Gender Female
Ethnicity Caucasian / White
Cell Type Epithelial
Morphology Adherent monolayer; epithelial morphology
Growth Mode Adherent
Biosafety Level BSL-1
HPV Status Negative (no detectable HPV DNA or RNA)
TP53 Status Point mutation at codon 273 (Arg->Cys); elevated mutant p53 expression
pRB Status Present but abnormal in size
Karyotype Pseudodiploid; modal chromosome number 46 (~70% of cells); occasional polyploid subpopulations; 7 consistent marker chromosomes
Tumorigenicity Yes; forms undifferentiated carcinoma in nude mice
Culture Conditions 37 degrees C, 5% CO2; standard epithelial cell culture media (e.g., MEM or DMEM with 10% FBS)
Applications Preclinical xenograft studies, drug screening, HPV-negative cervical cancer mechanism research, combination therapy evaluation
Special Features One of the few readily available HPV-negative cervical carcinoma cell lines; serves as stringent negative control in HPV studies
Contamination Screening Tested negative for HIV-1, HBV, HCV, Syphilis, Mycoplasma, Fungi, Yeast, and Bacteria

Our Services

Alfa Cytology offers end-to-end C-33A xenograft model services designed to accelerate your preclinical oncology programs. Our integrated platform encompasses tumor cell authentication, model establishment, in-life monitoring with calibrated caliper and imaging readouts, and comprehensive histopathological endpoint analysis---ensuring that every study generates publication-quality data with rigorous statistical support. Whether you require a standard subcutaneous xenograft or an orthotopic cervical implantation, our team delivers customized study designs aligned with your compound's mechanism of action and regulatory milestones.

Workflow of C-33A Xenograft Model Construction

Construction of the C-33A xenograft model follows a standardized, quality-controlled workflow that ensures reproducible tumor growth and reliable pharmacological readouts. Each stage is executed under strict pathogen-free conditions with documented batch records.

  1. Cell Authentication and Quality Control: C-33A cells are authenticated via STR profiling and confirmed HPV-negative status prior to expansion. Mycoplasma and sterility testing are performed to ensure contamination-free cultures suitable for in vivo use.
  2. In Vitro Expansion and Harvest: Cells are expanded under standard culture conditions (37 degrees C, 5% CO2) to the required biomass. At 70--90% confluence, cells are harvested using trypsin-EDTA, washed, and resuspended in serum-free medium or PBS at a defined concentration.
  3. Cell Viability Verification: Post-harvest cell viability is assessed by trypan blue exclusion, with only preparations exceeding 95% viability approved for implantation to maximize tumor take rates.
  4. Matrigel or Scaffold Preparation (Optional): For enhanced engraftment, C-33A cells may be mixed with a defined ratio of basement membrane matrix immediately prior to injection, providing an extracellular scaffold that supports early tumor vascularization.
  5. Animal Preparation and Implantation: Immunodeficient mice (commonly NOD/SCID or nude mice, 6--8 weeks old) are acclimated and randomized. C-33A cells are implanted subcutaneously into the flank (1x10^6 to 5x10^6 cells per site) or orthotopically into the cervix, depending on study objectives.
  6. Tumor Monitoring and Randomization: Tumors are monitored by palpation and electronic caliper measurement twice weekly. Once tumors reach a mean volume of 80--150 mm^3, animals are randomized into treatment and vehicle-control cohorts to minimize inter-group variability.
  7. Dosing and In-Life Assessment: Test articles are administered according to the study protocol (route, schedule, and formulation). Body weight and tumor dimensions are recorded at defined intervals; clinical signs are monitored daily to evaluate treatment tolerability.
  8. Endpoint Analysis and Sample Collection: At study termination, tumors are excised, weighed, and photographed. Tissues are fixed in formalin for H&E and IHC analysis, or snap-frozen for molecular profiling (Western blot, qPCR, proteomics) to elucidate mechanism of action.

Fig 3. Workflow for the establishment of C-33A cell line-derived xenograft (CDX) models.Figure 2. C-33A xenograft model construction workflow.

Case Study-C-33A Xenograft Model Development

In a representative preclinical engagement, Alfa Cytology established subcutaneous C-33A xenografts in immunodeficient mice and evaluated a novel therapeutic candidate targeting the PI3K/AKT signaling axis. Tumors were successfully engrafted with a take rate exceeding 90%, reaching evaluable volumes within 14--18 days post-implantation. Dosing commenced once tumors achieved the target volume threshold, with treatment administered over a 21-day cycle. Preliminary data indicated dose-dependent tumor growth inhibition compared to vehicle controls, with no significant body weight loss observed in treated cohorts. Comprehensive endpoint analysis---including tumor weight, H&E histology, and biomarker expression profiling---was completed to support mechanism-of-action claims. Full datasets are available upon formal inquiry.

Fig 4. Case Study-C-33A Xenograft Model Development.

Why Choose Alfa Cytology?

Alfa Cytology combines scientific rigor with operational flexibility to deliver xenograft models that meet the highest preclinical standards. Our C-33A service is built on validated protocols, transparent reporting, and a commitment to advancing your oncology pipeline.

  • Validated HPV-negative C-33A cell stocks with full STR authentication and sterility clearance.
  • Customizable study designs encompassing subcutaneous, orthotopic, and metastatic model configurations.
  • Real-time tumor monitoring via electronic caliper and optional non-invasive imaging (bioluminescence or MRI).
  • Comprehensive endpoint packages including histopathology, immunohistochemistry, and molecular profiling.
  • Dedicated project management with weekly progress updates and raw data transparency.
  • Competitive timelines with tumor establishment typically achieved within 2--3 weeks post-implantation.

Contact Us

Ready to advance your cervical cancer therapeutic program with a validated C-33A xenograft model? Contact us today to discuss your study requirements, receive a tailored proposal, and access our preclinical oncology expertise. Please reach out to us today via our inquiry form or email to learn more about our C-33A Xenograft Model services.

Reference

  1. Romero-Lopez, Manuel Joaquin, et al. "miR-218-5p, miR-124-3p and miR-23b-3p act synergistically to modulate the expression of NACC1, proliferation, and apoptosis in C-33A and CaSki cells." Non-coding RNA Research 9.3 (2024): 720-731.

For research use only. Not intended for any clinical use.

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