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ID8 Syngeneic Model Service for Ovarian Cancer

Fig 1: ID8 Syngeneic Model for Ovarian Cancer preclinical research.

The ID8 syngeneic model of ovarian cancer implants spontaneously transformed C57BL/6 ovarian surface epithelial cells into the peritoneal cavity of immunocompetent hosts, where they reproduce the disease’s defining pattern of peritoneal carcinomatosis and hemorrhagic ascites. Alfa Cytology delivers the complete ID8 workflow—authenticated cell banking, intraperitoneal or intrabursal inoculation, bioluminescence- and ascites-aware monitoring, scheduled dosing and peritoneal- and survival-inclusive endpoint analysis—giving sponsors decision-ready preclinical datasets shaped to their program, strictly within a preclinical scope.

Overview of ID8 Syngeneic Model for Ovarian Cancer

ID8 began as an exercise in watching normal cells become malignant. Katherine Roby’s team cultured mouse ovarian surface epithelial cells from C57BL/6 mice through repeated passage until they spontaneously transformed, then cloned the population into a series of lines—IC5, ID3, ID8, ID9, IF5, IG10—reported in Carcinogenesis in 2000. The ID8 clone took: five million cells injected intraperitoneally into syngeneic mice killed with a mean latency of 114 ± 3 days, seeding the omentum, diaphragm and bowel serosa with tumor and filling the abdomen with hemorrhagic ascites. The model’s practical virtue is absolute reliability of take; its scientific caveat is equally well documented—ID8 carries no TP53 mutation, no BRCA1/2 loss, and none of the somatic copy-number chaos that defines human high-grade serous carcinoma, leaving it with low mutation burden and limited molecular representativeness. The field’s answer has been engineering: Walton’s CRISPR derivatives—ID8-Trp53−/− (faster growth, WT1 positivity, CCL2-driven myeloid suppression) and Trp53−/−Brca2−/− (with intraepithelial lymphoid aggregates) restore much of the high-grade phenotype while remaining fully syngeneic.

Fig 2: Reference figures for ID8 cell-related literature.Fig 1. In vivo characterization of the ID8-Defb29/Vegf-a syngeneic model in C57BL/6 mice: tumor growth curves and survival showing aggressive progression versus Vegf-only controls, with CD31 immunostaining and confocal microscopy revealing dendritic cell (CD11c) incorporation into tumor vasculature. (Conejo-Garcia, Jose R., et al., 2004)

Operationally, ID8 runs in three registers. The classic intraperitoneal format delivers five million cells in half a milliliter, with disease declaring over two to three months; luciferase-tagged versions accelerate and sharpen this—five million ID8-fLuc cells produce ascites around day sixty-five with a median survival of 63.5 days, ten million bring that to eight weeks, fifteen million to six—and, remarkably, repeated ascites drainage extended median survival from 63.5 to 73 days while also unmasking true tumor burden, since as little as fifteen milliliters of ascites dilutes D-luciferin and suppresses bioluminescent signal until drained. Intrabursal orthotopic injection (one million cells) supports organ-context studies with morbidity near day ninety, and an established port-site metastasis mimic—peritoneal tumors followed by abdominal-wall puncture—models surgical recurrence. The line has carried immunotherapy programs (checkpoint agents, CAR-T, vaccines, dendritic-cell transfer), chemotherapy combinations (carboplatin with FABP4 inhibition), and myeloid-biology work. Working caveats: the parental line’s slow latency makes the Trp53-deficient derivative the practical choice for most efficacy work; transduced lines grow faster than wild-type and their selection markers add immunogenicity; and ascites management—drainage, circumference and weight monitoring—must be built into every protocol.

Cell Line Information: ID8

Key characteristics of ID8 and its documented derivatives are summarized below.

Item Details
Cell line name ID8; derived from late-passage C57BL/6 mouse ovarian surface epithelial (MOSEC) cells spontaneously transformed in vitro; cloned series IC5/ID3/ID8/ID9/IF5/IG10 reported by Roby et al. (Carcinogenesis, 2000;21:585)
Species / strain background Mus musculus; syngeneic host: C57BL/6 (female mice most commonly used)
Molecular features Low mutation burden; no driver mutations — lacks TP53 (mutated in ~94% of human HGSC), BRCA1/2, NF1 and RB1 alterations; CRISPR derivatives restore HGSC features: ID8-Trp53−/− (faster growth, WT1 positive, CCL2-driven MDSC recruitment) and Trp53−/−Brca2−/− (intraepithelial lymphoid aggregates)
Disease phenotype Intraperitoneal inoculation → widespread peritoneal carcinomatosis (omentum, diaphragm, bowel serosa) with hemorrhagic ascites — recapitulating advanced-stage human disease
Growth kinetics Parental ID8 clone: 5 × 106 cells i.p. → mean survival 114 ± 3 days; sibling IG10 ~72 days; non-clonal late-passage MOSEC ascites in 22–48 days; ID8-fLuc grows faster in vivo than wild type
Luciferase formats 5 × 106 ID8-fLuc → ascites ~day 65, median survival 63.5 days (73 days with repeated drainage); 10 × 106 → 8 weeks; 15 × 106 → 6 weeks; luciferin dilution in ascites (up to 15 mL) underestimates tumor load until drainage
Orthotopic and surgical formats Intrabursal injection of 1 × 106 cells → moribund by ~day 90; ascites-derived re-injection (line 28-2) → day 60; port-site metastasis model: peritoneal tumors followed by abdominal-wall puncture, 83% take by 3–4 weeks
Culture conditions DMEM + 4% FBS + insulin/transferrin/selenium + penicillin/streptomycin + 2 mM glutamine (common practice) or MEM + 10% FBS (originator practice); use within 10–20 passages; 37 °C, 5% CO2
Research uses Immunotherapy testing (checkpoint agents, CAR-T, vaccines, dendritic-cell transfer — 2.5 × 106 i.p. gives untreated median survival ~79 days), chemotherapy combinations (carboplatin with FABP4 inhibition), myeloid-biology and TME studies, ascites biology, surgical port-site metastasis mimicry
Considerations Slow parental latency favors the Trp53-deficient derivative for routine efficacy work; transduced lines grow faster than wild type and selection markers add immunogenicity; luciferin-dilution artifact requires ascites-aware imaging; molecular non-representativeness of HGSC demands derivative-based designs when genotype matters
Representative applications Ovarian cancer immunotherapy screening, peritoneal dissemination biology, ascites and drainage research, DNA-repair-deficient (BRCA-context) therapy testing with derivatives, myeloid-targeting strategies, vaccine platforms

Our Services

With in vivo oncology specialists guiding each stage and bioluminescence imaging, ascites management and flow-cytometry capabilities in-house, Alfa Cytology molds every ID8 engagement around the sponsor’s question—selecting parental or Trp53-deficient cells, scheduling intraperitoneal or intrabursal inoculation, and pairing dosing with ascites-aware imaging, peritoneal nodule counts and survival readouts for clean, decision-grade preclinical data.

Workflow of ID8 Syngeneic Model Construction

Construction of the ID8 syngeneic model is an inoculation workflow whose quality rests on low-passage cells, strain-matched recipients, ascites-aware monitoring and disciplined welfare scoring. A standard engagement proceeds as follows:

  1. Source and qualify cells: ID8 or derivative stocks are cleared by mycoplasma PCR and identity-verified, kept within 10–20 passages, with genotype documented (parental versus Trp53−/− or combined knockouts); luciferase expression is titrated in vitro where imaging readouts are required.
  2. Prepare recipients: female C57BL/6 mice (typically 6–8 weeks old) complete acclimation and health screening and are individually marked before inoculation.
  3. Prepare the inoculum: log-phase cells are harvested, washed, counted and resuspended in PBS (5 × 106 cells in 500 µL for the standard intraperitoneal format; 1 × 106 for intrabursal injection; spheroids from ultra-low-attachment plates as an alternative).
  4. Inoculate: cells or spheroids are delivered into the peritoneal cavity through a fine needle, or beneath the ovarian bursa for the orthotopic format, with consistent technique for reproducible dissemination patterns.
  5. Assign groups: animals are randomized by body weight at inoculation, or by bioluminescence signal at the one-to-two-week staging scan where imaging designs call for burden-balanced groups.
  6. Dose and follow: test articles are administered on schedule; body weight and abdominal circumference are recorded every 48 hours; weekly bioluminescence imaging tracks dissemination with the luciferin-dilution caveat in mind, and ascites is drained when clinically indicated (documented to extend median survival).
  7. Terminate and analyze: ascites volume is measured; peritoneal nodules on the omentum, diaphragm and bowel serosa are counted; tumors are weighed and processed for histopathology; tumor-infiltrating lymphocytes and ascitic immune cells are profiled by flow cytometry; survival curves complete the dataset.

Fig 3: Workflow for the establishment of ID8 Syngeneic Models.Fig 2. ID8 Syngeneic Model construction workflow.

Case Study-ID8 Syngeneic Model Development

Alfa Cytology keeps an active file of preclinical case studies on the ID8 platform: establishment-phase optimization of inoculum and derivative selection, in vivo dissemination tracking by bioluminescence with ascites-drainage management, immunotherapy- and chemotherapy-based intervention studies, and systematic endpoint analyses covering ascites volume, peritoneal nodule counts and survival. Representative imaging series, survival curves and endpoint summaries can be shared upon request and will be updated as new programs conclude.

Fig 4: Case Study-ID8 Syngeneic Model Development.

Why Choose Alfa Cytology?

A model whose readout is ascites and peritoneal seeding rather than a flank mass rewards specialized monitoring—which is where Alfa Cytology invests:

  • Derivative-flexible banking spanning parental ID8, Trp53−/− and combined-knockout lines with documented genotypes.
  • Ascites-aware bioluminescence imaging that treats drainage as both welfare and data recovery.
  • Intraperitoneal and intrabursal execution with spheroid-format options for dissemination studies.
  • Peritoneal carcinomatosis endpoint expertise: nodule mapping, ascites volumetrics and diaphragmatic disease scoring.
  • Low-passage discipline (<10–20) protecting the line’s reliability of take.
  • Compressed-course options through Trp53-deficient derivatives when timelines demand four-to-five-week studies.
  • One accountable project contact with milestone-by-milestone visibility.
  • A strictly preclinical scope—every study is planned, executed and reported as non-clinical research.

Contact Us

Interested in the ID8 syngeneic ovarian cancer model for your next preclinical program? Reach out to us with your agent, timeline and endpoint wish-list, and the Alfa Cytology team will respond with a customized plan covering model setup, dosing strategy and analysis workflow—contact us today and move your program forward with confidence.

Reference

  1. Conejo-Garcia, Jose R., et al. "Tumor-infiltrating dendritic cell precursors recruited by a β-defensin contribute to vasculogenesis under the influence of Vegf-A." Nature medicine 10.9 (2004): 950-958.

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

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