Myc-CaP Syngeneic Model Service for Prostate Cancer

The Myc-CaP syngeneic model is the c-myc-driven, androgen-receptor-positive immunocompetent platform for prostate cancer, engrafting a Hi-Myc transgenic-derived line that faithfully recapitulates the androgen-dependent-to-castration-resistant transition and forms mixed osteolytic-osteoblastic bone metastases in syngeneic FVB/NJ hosts. Alfa Cytology delivers this mechanistically rich model as a complete preclinical service — authenticated cell banking from the 2005 Cancer Research reference, subcutaneous and intraosseous formats, castration and enzalutamide-resistance arms, radiation-immunotherapy configurations, and full histopathology — giving sponsors the rare combination of androgen signaling, intact immunity, and metastatic competence in one system.

Overview of Myc-CaP Syngeneic Model for Prostate Cancer

Myc-CaP occupies a distinctive place in prostate cancer modeling: it is the cell-line embodiment of the Hi-Myc transgenic program, established in 2005 by Watson, Ellwood-Yen, and colleagues from a spontaneous tumor of a c-myc-overexpressing mouse, and it answers the two complaints that have long dogged the field — that xenografts lack immunity and are largely deaf to androgen signaling, and that most murine prostate lines are immunologically trivial. The line overexpresses wild-type androgen receptor, expresses AR splice variants in its FVB background (a feature the C57BL/6-backcrossed counterpart lacks), and is genuinely androgen dependent: subcutaneous tumors in intact FVB/NJ mice regress after medical or surgical castration, then uniformly progress within two months as castration-resistant disease that still requires AR transcription — the exact clinical arc from hormone sensitivity to CRPC, including the AR-V7-class splice-variant biology that explains how tumors escape while remaining AR-driven.

Fig 1. Intraosseous Myc-CaP model in syngeneic FVB mice: in vivo bioluminescence imaging of bone-localized tumors, survival to humane endpoint, μCT showing osteoblastic changes, and H&E/Masson's trichrome/TRAP histology—establishing an immune-competent, AR-positive prostate cancer bone metastasis platform. (Wang, Yu, et al., 2021)

The platform's metastatic and immunological dimensions are equally developed. Systemically, cells injected into the left cardiac ventricle form bone metastases in the majority of syngeneic hosts — confirmed by AR and EpCAM immunohistochemistry and tdTomato flow cytometry — while direct tibial intraosseous injection produces tumors grossly confined to bone with mixed osteolytic/osteoblastic morphology and increased bone volume, and hemi-spleen injection yields liver tumors. Immunologically, Myc-CaP is a "cold" tumor with rare T-cell infiltrates, yet it has generated some of the most instructive combination data in the field: PIM inhibition with PIM447 plus anti-PD-1 reduced tumor volume by roughly 80% versus 20% for either agent alone; a two-graft design in castrated hosts — one tumor irradiated with 20 Gy in two fractions, one shielded — dissected radiotherapy-plus-checkpoint abscopal effects; and the enzalutamide-resistant Myc-CaP MDVR derivative explained a clinical failure mode, showing suppressed interferon pathways, PD-L1 upregulation, and MDSC expansion that mirrors the IMbassador250 trial experience. Derivatives extend the design space further: Myc-CaP-Bo, selected through three rounds of in vivo bone homing with luciferase tracking for bone-lesion quantification, and a neuroendocrine derivative born of androgen-free culture, castrated-host passage, and enzalutamide selection. For sponsors working on hormonal-immunological crosstalk, metastatic prostate cancer, or resistance mechanisms, Myc-CaP offers a uniquely coherent system.

Cell Line Information: Myc-CaP Syngeneic Model

Myc-CaP (Watson et al., Cancer Res. 65:11565–11571, 2005) is the androgen-dependent, AR-positive murine prostate cancer line derived from a spontaneous Hi-Myc transgenic tumor, distributed within the prostate cancer research community. Derivatives including Myc-CaP MDVR, Myc-CaP-Bo, and reporter-labeled variants extend the platform. Core characteristics are compiled below.

Our Services

Engaging Alfa Cytology for the Myc-CaP syngeneic model places a mechanistically coherent prostate cancer system under one accountable team: authenticated, low-passage Myc-CaP banks are maintained with AR expression verified, syngeneic FVB/NJ hosts are sourced and acclimated, tumors are established subcutaneously for immunotherapy evaluation or intraosseously/intracardially for metastatic questions, and treatment arms — castration and enzalutamide-resistance schedules, checkpoint and PIM-inhibitor combinations, radiation-immunotherapy configurations, or radiopharmaceutical benchmarks — run through scheduled caliper, bioluminescence, and PET/CT monitoring to terminal bone and prostate histopathology, all under IACUC-compliant conditions and returned as an audit-ready data package.

Workflow of Myc-CaP Syngeneic Model Construction

Myc-CaP studies divide into the flank immunotherapy format — where androgen manipulation is the experimental lever — and the bone-metastasis formats, where intraosseous or intracardiac delivery defines the geometry. A standard program proceeds as follows.

1. Cell preparation and quality control: Myc-CaP cells are expanded at low passage, confirmed mycoplasma-free, and AR expression and splice-variant status spot-checked; for bone formats, luciferase- or tdTomato-labeled derivatives are signal-validated in vitro.
2. Host selection and acclimation: Male FVB/NJ mice, typically 8–12 weeks of age, are quarantined and acclimated in a specific-pathogen-free barrier facility, with cohorts designated as intact or pre-castrated per study arm.
3. Implantation: subcutaneous route. 10⁶ cells in 0.1 mL sterile PBS are injected into the flank; the site is compressed briefly, and tumors are established for immunotherapy, castration, or combination arms.
4. Implantation: intraosseous or intracardiac routes. For bone-metastasis studies, labeled cells are injected into the tibial marrow cavity (tumors grossly confined to bone) or into the left cardiac ventricle (disseminated bone metastases in the majority of animals, with mediastinal tumors noted); hemi-spleen injection serves liver-metastasis formats.
5. Randomization and androgen manipulation: Mice are randomized by tumor volume or imaging signal; castration or enzalutamide schedules are applied at defined thresholds, with the documented shrink-then-progress arc of the parental line and the MDVR resistance line providing benchmark comparators.
6. Treatment administration. Test articles: checkpoint inhibitors, PIM inhibitors, integrin antagonists, radiopharmaceuticals (²²⁵Ac/¹⁷⁷Lu-NM600 class), or radiation-immunotherapy regimens using the two-graft design — are dosed per protocol, with body weight recorded.
7. Longitudinal monitoring: Flank tumors are measured by caliper; bone-format cohorts undergo bioluminescence imaging after intraperitoneal D-luciferin injection and PET/CT where radiotracers are employed, with bone-volume and serum TRAcP-5b assessments for osteolytic-osteoblastic characterization.
8. Endpoint analysis and reporting: At termination, tumors, bones, and organs are resected; tissues undergo H&E with prostate and bone histology, immunohistochemistry (AR, EpCAM, CD8, CD4, FoxP3, F4/80, PD-L1, Ki-67 panels), micro-CT bone-volume analysis, and tumor-infiltrating-leukocyte flow cytometry, with all data consolidated into the final report.

Fig 2. Myc-CaP Syngeneic Model construction workflow.

Case Study-Myc-CaP Syngeneic Model

Alfa Cytology has applied the Myc-CaP syngeneic platform to preclinical programs spanning checkpoint and PIM-inhibitor combinations, castration-resistance and enzalutamide-resistance mechanisms, bone-metastasis evaluation using intraosseous and intracardiac formats, and radiation-immunotherapy configurations in prostate cancer. In these engagements, caliper and bioluminescence readouts tracked primary and bone tumor kinetics, androgen manipulation followed the documented regression-then-progression arc, and terminal bone and prostate histopathology with immune-marker panels and micro-CT analysis completed the pharmacological and immunological assessment. Study parameters — implantation format, androgen manipulation, treatment arms, and endpoint panels — are tailored to each program. Case materials can be shared under confidentiality agreements upon request.

Why Choose Alfa Cytology?

Myc-CaP rewards teams that understand its logic: an androgen-immunology axis that cuts both ways, a castration arc with a two-month clock, and bone formats with defined osteolytic-osteoblastic readouts. Alfa Cytology fields these capabilities in-house, making the Myc-CaP syngeneic model a dependable backbone for your prostate cancer program.

• Hi-Myc provenance with AR verification, from the 2005 Cancer Research reference line.
• Authentic androgen axis, deploying the castration shrink-then-progress arc natively.
• Documented metastatic geometry, including tibial, intracardiac, and hemi-spleen formats.
• Quantified combination benchmarks, including the PIM447 + anti-PD-1 precedent.
• Resistance derivative access, including Myc-CaP MDVR and Myc-CaP-Bo with luciferase tracking.
• Radiation-immunotherapy configurations, with the validated two-graft design.
• IACUC-compliant, documentation-rich operations delivering audit-ready records throughout the study.

Contact Us

If your prostate cancer program involves the androgen-immunity axis, castration resistance, or bone metastasis, contact us today to discuss Myc-CaP study design, implantation format, and endpoint strategy with our scientific team. Reach out for a confidential consultation and project quotation — Alfa Cytology looks forward to advancing your next preclinical study.

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