A2780 / A2780-luc Orthotopic Mouse Model Service for Ovarian Cancer

The A2780 / A2780-luc orthotopic mouse model establishes a chemotherapy-naive, TP53 wild-type human ovarian endometrioid carcinoma — established before any patient treatment and parent to the most-cited isogenic resistance pairs in ovarian cancer — into the peritoneal cavity or ovarian site of immunodeficient mice, where intraperitoneal growth, peritoneal carcinomatosis, and ascites recapitulate the clinical spread pattern of the disease. Alfa Cytology delivers this resistance-research archetype with authenticated banking, subcutaneous and intraperitoneal configurations, matched A2780cis/A2780ADR resistant-derivative cohorts, and benchmark arms anchored to the published staged-xenograft cisplatin log-cell-kill record, so your platinum strategies, resistance-reversal agents, and intraperitoneal delivery approaches are tested against the line pair the ovarian literature was built on.

Overview of A2780 / A2780-luc Orthotopic Mouse Model for Ovarian Cancer

A2780 was established by Behrens and colleagues, published in Cancer Research in 1987, from tumor tissue of a patient with ovarian endometrioid adenocarcinoma who had received no prior chemotherapy — a chemotherapy-naive origin that makes the line a clean substrate for studying acquired, rather than pre-existing, drug resistance. The cells are epithelial, growing as a monolayer with suspension growth in spinner cultures, with TP53 wild-type status and documented STR authentication across curators (ECACC 93112519; BCRJ 0031). Its scientific architecture is its paired derivative platform: chronic exposure produced A2780cis (cisplatin-resistant, TP53 wild-type) and A2780ADR (doxorubicin/adriamycin-resistant, ~18-fold resistance with cross-resistance to platinum agents), while higher cisplatin pressure generated A2780-CP20 — which acquired a heterozygous TP53 V172F mutation alongside 11-fold cisplatin resistance, creating a matched series spanning wild-type-sensitivity, transporter-mediated resistance, and p53-mutant resistance in a single isogenic family.

Fig 1. Intraperitoneal A2780-luc xenograft model in nude mice treated with Ad-VT, Ad-T, Ad-VP3, Ad-MOCK or control, showing whole-body bioluminescence at week 2 and week 6 with quantified mean photons and tumor volume curves demonstrating that Ad-VT suppressed A2780-luc tumor growth by ~80% at week 6 (P<0.001 versus control) and conferred significant survival benefit (Kaplan-Meier, P<0.05). (Cui, Yingli, et al., 2024)

In vivo, the staged xenograft record is foundational. Rose and colleagues demonstrated in 1990 that A2780 and A2780/cDDP grow reproducibly as subcutaneous tumors in athymic mice with quantified, reproducible responses to intravenous cisplatin — a mean maximum log cell kill of 2.5 in sensitive A2780 versus 0.5 in the resistant subline — and used the pair to discriminate platinum analogs, which were active against A2780 but inactive against A2780/cDDP. Decades later, the pair still anchors combination pharmacology: APR-246 (eprenetapopt) combined with cisplatin produced 56% growth inhibition against aggressively growing A2780-CP20 xenografts (versus 21% and 32% for single agents), with caspase-3 activation confirming mechanism. Intraperitoneally, A2780 models peritoneal carcinomatosis — work showing that Rab25 expression converts A2780 to intraperitoneal growth in immunocompromised mice directly validated the IP configuration as the orthotopic route — and the A2780-luc derivative enables quantitative whole-body bioluminescence in vivo for carcinomatosis kinetics, with monoclonal quality control. For platinum benchmarking, resistance-mechanism dissection, and IP-delivery evaluation, no ovarian pair offers more inherited experimental infrastructure.

Cell Line Information: A2780 / A2780-luc

A2780 (ECACC 93112519; BCRJ 0031; Cellosaurus CVCL_0134) grows in vitro as an adherent epithelial monolayer — with mixed adherent/suspension properties reported — in RPMI-1640 modified with 2 mM L-glutamine, 1 mM sodium pyruvate, and 4.5 g/L glucose plus 10% fetal bovine serum. The line is documented with a full STR profile, biosafety level 1, and female origin. The A2780-luc derivative adds firefly luciferase for quantitative imaging in vivo, with monoclonal selection of high-signal clones in vitro recommended for uniform bioluminescence.

Our Services

Isogenic pairs only earn the name when both arms arrive identically prepared — and A2780's resistance family is only as valuable as the handling discipline behind each derivative. Alfa Cytology runs A2780 programs with STR-authenticated parental and A2780cis/A2780ADR/CP20 banking, TP53 status verified per batch, monoclonal luciferase quality control, benchmark arms anchored to the published log-cell-kill record, and IP-configured monitoring — abdominal girth, ascites scoring, and quantitative bioluminescence in vivo — so sensitivity, resistance, and reversal claims all land on the same isogenic scale.

Workflow of A2780 / A2780-luc Orthotopic Mouse Model Construction

A2780 construction spans two validated philosophies: staged subcutaneous benchmarking for quantified platinum evaluation, and intraperitoneal delivery for carcinomatosis realism. The workflow below covers both configurations from authenticated preparation through ascites-aware endpoints.

1. Cell Expansion and Quality Control: A2780 or A2780-luc cells (or matched A2780cis/A2780ADR/CP20 derivatives) are expanded in vitro in modified RPMI-1640 + 10% FBS to the logarithmic phase; batches are confirmed mycoplasma-negative, STR-authenticated, and verified for TP53 status and derivative identity, with monoclonal luciferase populations confirmed for tagged lines.
2. Host Selection and Acclimatization: BALB/c nude, NOD-SCID, NSG, or CD-1 nude female mice, 5–7 weeks of age, are acclimatized under SPF conditions and health-screened before assignment to study cohorts.
3. Configuration Selection and Inoculation: For staged benchmarking, 5 × 10⁶ cells are implanted subcutaneously into the flank; for orthotopic designs, cells are administered intraperitoneally in ~200–500 µL (peritoneal carcinomatosis with ascites), with ovarian/intrabursal implantation available for organ-site studies — implantation day recorded for the dosing calendar.
4. Engraftment Verification and Randomization: Subcutaneous arms are staged by caliper to predefined volumes (classically ~100–150 mm³); intraperitoneal cohorts are imaged by bioluminescence in vivo after D-luciferin, confirmed by peritoneal signal distribution, and randomized at defined flux or clinical thresholds.
5. Treatment Administration: Test agents are dosed on study-defined schedules — intravenous or intraperitoneal cisplatin and platinum analogs, doxorubicin, resistance-reversal agents such as APR-246-class compounds, or IP-delivery formats — with body weight, abdominal girth, and clinical condition recorded throughout.
6. Longitudinal Monitoring: Subcutaneous tumors are measured two to three times weekly; intraperitoneal cohorts are monitored weekly by bioluminescence quantification in vivo with abdominal girth and ascites scored on a defined scale, giving carcinomatosis studies quantified kinetics.
7. Survival Follow-Up: Animals are followed to humane endpoints — ascites burden, body condition, or tumor size — with Kaplan–Meier analysis across arms.
8. Endpoint Analysis and Reporting: At termination, subcutaneous tumors are excised and weighed, and peritoneal cavities are inspected with peritoneal nodules counted and ascites volume measured; tissues are processed for H&E and cleaved caspase-3 immunohistochemistry (per the published combination benchmark), platinum-DNA adduct or TP53 pathway staining where mechanistic attribution is required, ex vivo bioluminescence maps signal distribution, and tumor-growth, log-cell-kill, imaging, ascites, and survival data are compiled into the final report.

Fig 2. A2780 / A2780-luc orthotopic mouse model construction workflow.

Case Study-A2780 / A2780-luc Orthotopic Mouse Model Development

A2780 and its isogenic derivatives are the most cited ovarian resistance family in the xenograft literature — from the 1990 staged log-cell-kill characterization through modern TP53-rescue combination studies — and the platform has carried a broad range of Alfa Cytology client programs. Across these programs, readouts have combined staged tumor-growth and log-cell-kill quantification, intraperitoneal bioluminescence kinetics in vivo, and ascites-aware endpoints with matched sensitive-versus-resistant comparisons. Anonymized case summaries and representative deliverable formats are available on request.

Why Choose Alfa Cytology?

A2780's power is its isogenic architecture — and isogenic architecture demands that every arm be run identically. Alfa Cytology has built its ovarian service around that requirement.

• A chemotherapy-naive, TP53 wild-type parental archetype — the cleanest substrate for acquired-resistance research.
• A three-member isogenic family (A2780cis, A2780ADR, CP20) spanning transporter-mediated and TP53-mutant resistance.
• A foundational in vivo benchmark: quantified cisplatin log-cell-kill sensitivity versus resistance, reproducible across laboratories.
• Validated intraperitoneal carcinomatosis behavior with documented IP-growth conversion — the clinically faithful route.
• Staged xenograft discipline matched to the published platinum-analog evaluation format.
• Monoclonal, high-signal luciferase banks with quantitative peritoneal imaging in vivo.
• Ascites-aware endpoints: abdominal girth scoring, peritoneal nodule counts, and ascites volumetrics.

Contact Us

If your ovarian cancer program needs a chemotherapy-naive substrate with isogenic resistant arms and a forty-year xenograft pedigree, the A2780 / A2780-luc orthotopic model is the reference pair — and Alfa Cytology runs it with the staging and IP-configuration discipline the literature expects. Reach out to us to review derivative pairing, staged versus intraperitoneal designs, and benchmark arm options, and receive a customized study quotation today.

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