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BR-luc Orthotopic Mouse Model Service for Ovarian Cancer

Fig 1: BR-luc Orthotopic Mouse Model for Ovarian Cancer preclinical research.

The BR-luc orthotopic mouse model of ovarian cancer engrafts a defined-genetics murine high-grade serous ovarian carcinoma — carrying alterations in p53, Brca1, myc, and Akt — into the ovarian bursa of immunocompetent FVB mice, where 100% tumor penetrance, predictable latency, omental spread, and ascites unfold under full immune surveillance and are tracked quantitatively by luciferase bioluminescence. Alfa Cytology delivers this platform as an integrated preclinical service: BR-luc cell stewardship, ovarian intrabursal or intraperitoneal engraftment, scheduled whole-body imaging, checkpoint, PARP-inhibitor, and epigenetic-drug dosing, and endpoints spanning tumor burden, ascites, immune-infiltrate profiling, and histopathology.

Overview of BR-luc Orthotopic Mouse Model for Ovarian Cancer

BR-luc originates from the Orsulic laboratory’s effort to build mouse ovarian cancer lines with defined initiating genetic alterations — the key limitation of earlier syngeneic systems, whose spontaneous or chemically induced tumors carried unknown genomes. Starting from mouse ovarian surface epithelial cells, the team introduced combinations of lesions found in human high-grade serous ovarian carcinoma: p53 loss, Brca1 loss, c-myc activation, and myristoylated Akt. The resulting BR line and its luciferase-tagged derivative BR-luc carry a murine tumor genome that is genetically legible — every alteration is known and intentional — and the cells are transplanted into FVB hosts in which the immune system remains fully intact. Tumors form with 100% penetrance at predictable latency, recapitulate the histology of human serous papillary carcinoma, and spread through the peritoneal cavity in the same pattern as the human disease, with the omentum accumulating the bulk of tumor burden and ascites developing as disease advances.

Fig 2: Reference figures for BR-luc cell-related literature.Fig 1. Female FVB mice (6–8 weeks old) were inoculated with 1 × 10⁶ syngeneic BR-Luc murine ovarian cancer cells. Tumor growth was confirmed via IVIS Spectrum CT on day 6 post-inoculation; subsequently, the mice were randomized and treated with intraperitoneal injections of INHBA shRNA. At the study endpoint, tumor burden was quantified using IVIS, and tumors were harvested for analysis. (Hu, Ye, et al., 2024)

What makes BR-luc a favorite tool of immuno-oncologists is the combination of a defined genome with a live immune system. Luciferase signal appears within days of intrabursal implantation — images taken ten days after orthotopic injection already show growing disease — while an HA epitope tag on the same cells permits immunohistochemical identification of tumor cells admixed with host stroma and immune infiltrates. The platform has produced influential therapeutic findings: CXCL12/CXCR4 axis blockade selectively depleted intratumoral FoxP3+ regulatory T cells and unleashed T-cell-mediated antitumor immunity; the hypomethylating agent decitabine potentiated anti-CTLA-4 therapy by driving naive T-cell differentiation into effector cells and prolonging cytotoxic lymphocyte responses; and the model’s BRCA1-deficient background makes it a natural substrate for PARP-inhibitor and DNA-damage-response programs. Intraperitoneal injection of about 5×106 BR-luc cells produces disseminated peritoneal disease with ascites within roughly five weeks, giving sponsors a rapidly deployable dissemination arm alongside the surgically orthotopic intrabursal route.

Cell Line Information: BR-luc

BR-luc is a defined-genetics murine ovarian cancer line engineered to model human high-grade serous ovarian carcinoma, distinguished by its luciferase-HA dual tagging and its behavior in fully immunocompetent syngeneic hosts. Core attributes follow.

Item Description
Cell line name BR-luc (BR-Luc); derived from the BR line of the Orsulic laboratory murine ovarian cancer series
Species / background Mouse; syngeneic FVB hosts (immunocompetent)
Cell of origin Mouse ovarian surface epithelial cells, transformed ex vivo with defined genetic alterations
Defined genetic alterations Combination of p53 loss, Brca1 loss, c-myc activation, and myristoylated Akt — mirroring genetic features of human high-grade serous ovarian carcinoma
Molecular rationale BRCA1-deficient background provides a native substrate for PARP-inhibitor and DNA-damage-response programs
Reporter system Stably expressed firefly luciferase for whole-animal bioluminescence imaging, plus an HA epitope tag for immunohistochemical detection of tumor cells within host stroma
Model fidelity 100% tumor penetrance with predictable latency; recapitulates human serous histology and peritoneal metastatic spread
Engraftment routes Orthotopic intrabursal injection into the ovarian bursa (surgical); intraperitoneal injection (about 5×106 cells) for disseminated peritoneal disease with omental predominance and ascites (~5 weeks)
Imaging kinetics Luciferase signal detectable within days of implantation (ten-day post-orthotopic images documented); intraperitoneal D-luciferin before IVIS-class imaging
Disease pattern Peritoneal carcinomatosis with omental tumor bulk and ascites, matching human ovarian cancer dissemination
Culture conditions Standard complete medium with 10% fetal bovine serum and antibiotics per laboratory SOP; 37 °C, 5% CO2
Companion models Sibling lines of the Orsulic series with alternative defined alteration sets (e.g., T and TBR lines), supporting genotype-comparison designs
Immune profiling Host infiltrates profiled across CD4+ and CD8+ T cells, B cells, NK cells, CD4+ FoxP3+ regulatory T cells, tumor-associated macrophages, and MDSCs
Published therapeutic findings CXCL12/CXCR4 blockade selectively reduces intratumoral FoxP3+ Tregs and enhances T-cell antitumor immunity; decitabine potentiates anti-CTLA-4 efficacy via effector T-cell differentiation; response to standard and targeted therapies documented
Key applications Checkpoint-inhibitor and epigenetic-drug combinations, PARP and DDR programs in a BRCA1-deficient context, Treg/MDSC-targeting agents, chemokine-axis therapeutics, peritoneal-dissemination biology, immune microenvironment dynamics

Our Services

BR-luc asks everything of an execution team at once: microsurgical intrabursal precision, immunocompetent-animal husbandry, imaging cadences matched to a fast-emerging signal, and immune-infiltrate analytics at endpoint. Alfa Cytology runs all four as one program. BR-luc stocks are stewarded with verified luciferase output and HA-tag integrity, implantation follows the published ovarian-bursa technique with ten-day signal verification, intraperitoneal dissemination arms deploy 5×106 cell challenges with weekly imaging, and dosing arms span checkpoint antibodies, PARP inhibitors, hypomethylating agents, and chemokine-axis blockers. Terminal workups quantify tumor burden, ascites, and a full immune-infiltrate panel. From first image to final flow-cytometry report, Alfa Cytology keeps the BR-luc orthotopic workflow under single-point accountability.

Workflow of BR-luc Orthotopic Mouse Model Construction

The BR-luc orthotopic workflow pairs defined-genetics tumor biology with a genuinely intact immune system, and its construction reflects both halves of that identity: surgical placement in the ovarian bursa (or rapid intraperitoneal dissemination), imaging from day ten, and immune-aware endpoints throughout.

  1. Line stewardship and dual-tag verification: BR-luc stocks are expanded from master banks, mycoplasma-tested, and released only after confirming uniform luciferase expression by in vitro glow assay and intact HA-tag integrity for downstream immunohistochemistry.
  2. Inoculum preparation: Log-phase cultures are harvested, washed, counted, and resuspended in sterile PBS at the study dose (about 5×106 cells in 100-200 µL for intraperitoneal dissemination; 1-5×105 cells in 5-10 µL for intrabursal placement, calibrated during pilot runs).
  3. Recipient preparation: Female FVB mice are acclimatized, body-weight stratified, and anesthetized; intrabursal procedures proceed under aseptic surgical conditions with stereomicroscope visualization of the ovarian bursa.
  4. Route-specific engraftment: For the orthotopic arm, the cell suspension is microinjected into the space between the bursal membrane and the ovary with slow plunger pressure to avoid capsule rupture, then the reproductive tract is repositioned and the abdomen closed in layers; intraperitoneal arms receive the 5×106 cell challenge directly.
  5. Early verification imaging: Ten days after implantation, intraperitoneal D-luciferin and whole-body imaging verify engraftment and record baseline burden, confirming the model’s documented early-signal kinetics.
  6. Randomized treatment and serial monitoring: Cohorts are randomized by matched photon flux into checkpoint, PARP-inhibitor, epigenetic-drug, or chemokine-axis arms; weekly in vivo imaging tracks peritoneal spread, omental accumulation, and ascites onset, with body weight and abdominal girth scored throughout.
  7. Endpoint and immune-infiltrate analysis: At termination, primary ovarian tumors, omentum, peritoneal deposits, and ascites are collected; tumor nodules are counted and weighed; ex vivo imaging localizes deposits; HA-tag immunohistochemistry identifies tumor cells within stroma; and flow cytometry profiles CD4+, CD8+, B, NK, FoxP3+ Treg, macrophage, and MDSC compartments to connect tumor control with immune mechanism.

Fig 3: Workflow for the establishment of BR-luc Orthotopic Mouse Models.Fig 2. BR-luc orthotopic mouse model construction workflow.

Case Study-BR-luc Orthotopic Mouse Model Development

Alfa Cytology has implemented the BR-luc orthotopic platform in preclinical programs spanning checkpoint-inhibitor combinations, PARP and DNA-damage-response agents in a BRCA1-deficient context, and epigenetic-drug strategies. In these studies, early ten-day verification imaging confirmed clean engraftment before randomization, weekly bioluminescence resolved peritoneal spread and omental accumulation alongside ascites onset, and terminal analyses combined tumor and ascites metrics with HA-tag immunohistochemistry and a full immune-infiltrate flow-cytometry panel — connecting tumor control to Treg, macrophage, and MDSC dynamics. Where programs required them, intraperitoneal dissemination arms paralleled the surgical orthotopic cohorts. Study-specific designs and results are retained as sponsor-confidential deliverables, and representative outlines can be furnished upon request.

Fig 4: Case Study-BR-luc Orthotopic Mouse Model Development.

Why Choose Alfa Cytology?

BR-luc’s power comes from pairing a known genome with a live immune system — and that pairing demands a CRO fluent in both surgery and immunology. Alfa Cytology’s service delivers both halves. Sponsors benefit from:

  • Verified dual-tag integrity — uniform luciferase output plus intact HA epitope for stromal-context IHC.
  • Written ovarian-bursa microsurgical technique with ten-day imaging verification of engraftment.
  • Fully immunocompetent FVB hosts preserving T-cell, B-cell, NK, Treg, macrophage, and MDSC dynamics.
  • Defined-genetics BRCA1-deficient background natively suited to PARP and DDR programs.
  • Rapid intraperitoneal dissemination arm (5×106 cells, ascites at ~5 weeks) paralleling orthotopic cohorts.
  • Published-anchored combination designs spanning checkpoint, epigenetic, and chemokine-axis agents.
  • Terminal packages connecting tumor and ascites metrics to full immune-infiltrate profiling.

Contact Us

Need an immunocompetent, defined-genetics ovarian cancer model with imaging-grade peritoneal tracking and immune-infiltrate endpoints? Contact us to discuss engraftment route, dosing arms, and correlative panels for the BR-luc orthotopic platform. You can also reach out to Alfa Cytology for a customized proposal and quotation — our team will respond with a study design aligned to your therapeutic strategy.

Reference

  1. Hu, Ye, et al. "INHBA (+) cancer-associated fibroblasts generate an immunosuppressive tumor microenvironment in ovarian cancer." NPJ precision oncology 8.1 (2024): 35.

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

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