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C1498 Syngeneic Model Service for Leukemia

Fig 1: C1498 Syngeneic Model for Leukemia preclinical research.

The C1498 syngeneic model service for leukemia is an immune-competent C57BL/6 platform in which the spontaneously arising murine acute myeloid leukemia line C1498 is infused systemically to recapitulate disseminated AML — with bone marrow, splenic, hepatic, and extramedullary infiltration — under a fully intact immune system. Alfa Cytology delivers this model as a complete preclinical capability — covering authenticated C1498 / reporter-enabled C1498 (luciferase, GFP, mCherry) expansion and banking, tail-vein or subcutaneous inoculation, scheduled bioluminescence and flow-cytometric burden tracking across organs, and full leukemic histopathology with immune-microenvironment profiling — all configured around each sponsor’s agent, combination strategy, and survival or burden endpoint.

Overview of C1498 Syngeneic Model for Leukemia

C1498 is one of the oldest continuously used cancer lines in existence — a murine leukemia that arose spontaneously in a female C57BL/6J mouse and was first described by Law in the 1940s, originally classified as a granulocytic leukemia and now designated by ATCC as a murine acute myeloid leukemia resembling the acute myelomonocytic subtype. The line is atypical in instructive ways: surface-marker analyses confirm a predominantly myeloid lineage of monoblasts and myeloblasts, yet it expresses molecules associated with natural killer T-cell populations, a quirk that has made it a recurring subject of immunophenotypic studies. Its defining experimental virtue is its behavior in vivo: infused intravenously into syngeneic C57BL/6 mice, C1498 cells circulate, seed, and expand with extraordinary aggression — peripheral blood, bone marrow, spleen, liver, lung, lymph nodes, ovaries, kidney, skin, and even the central nervous system become infiltrated, hepatosplenomegaly develops, and untreated animals succumb with a median survival of roughly two to three weeks, with bioluminescence-measured tumor doubling times as short as 1.3 days.

Fig 2: Reference figures for C1498 cell-related literature.Fig 1. Efficacy of RIG-I agonist immunotherapy in the C1498-GFP syngeneic AML model — treatment schedule, organ-resolved quantification of GFP-positive leukemia cells (bone marrow, liver, lung, ovary, spleen) showing marked reduction after ppp-RNA, and survival curves with significantly prolonged survival. (Ruzicka, Michael, et al., 2019)

The model’s immunology has been mapped with unusual thoroughness, much of it through the landmark Blood study of 2009. C1498 expresses PD-L1 in the host environment, PD-1-deficient mice survive significantly longer than wild-type after challenge, and anti-PD-L1 treatment improves survival — yet checkpoint monotherapy produces only modest delays, which is precisely why the model has become a preferred setting for combination-therapy research mirroring the clinical reality of AML immunotherapy. Reporter engineering has multiplied its utility: GFP-labeled C1498 enabled the first time-resolved tracking of leukemic burden in blood, marrow, liver, and spleen; dual luciferase-mCherry versions permit whole-body imaging plus single-cell flow quantification of tissue burden; the C1498.SIY variant presents a defined Kb-restricted model antigen monitorable by tetramers; and congenic CD45.1/CD45.2 configurations allow host-versus-leukemia cells to be distinguished without labeling. The line responds to hypomethylating agents such as 5-azacytidine — restoring immune transcripts, suppressing burden, and modeling relapse — and has been benchmarked against artesunate, acid ceramidase inhibitors, isatin analogs combined with cytarabine, and venetoclax-based regimens, cementing C1498 as the default immune-competent AML system for drug, vaccine, and cell-therapy programs.

Cell Line Information: C1498

The table below consolidates the key biological, cultural, and modeling characteristics of the C1498 line and its reporter-engineered derivatives.

Parameter Details
Cell line designation C1498 (parental line); reporter derivatives include C1498-GFP, C1498-Luc, C1498-Luc-mCherry, C1498-Luc-GFP, and the C1498.SIY model-antigen variant
Species / genetic background Mouse (Mus musculus), C57BL/6J inbred background; syngeneic in C57BL/6 hosts, with congenic B6.SJL (CD45.1) configurations available for host-versus-leukemia discrimination
Origin Arose spontaneously in a female C57BL/6J mouse; first described in the 1940s (Law, Journal of the National Cancer Institute, 1944) as a granulocytic leukemia; now classified by ATCC as murine acute myeloid leukemia (acute myelomonocytic-type)
Depository / catalogue ATCC TIB-49; Cellosaurus CVCL_3494
Tumor type Murine acute myeloid leukemia; predominantly monoblast/myeloblast morphology with CD45 positivity
Immunophenotype Myeloid-lineage surface markers with an atypical signature expressing molecules associated with natural killer T-cell populations; PD-L1 expressed in vivo; Ly6a/Sca-1 expression level modulates aggressiveness in vivo
Growth properties Suspension-adapted leukemia cells proliferating rapidly in standard culture; exceptionally aggressive dissemination in vivo
Recommended culture conditions RPMI-1640 (or equivalent complete medium) supplemented with 10% fetal bovine serum at 37 °C in a humidified 5% CO₂ atmosphere; reporter lines maintained under the appropriate selectable marker
Standard inoculum and routes Systemic model: 0.5–2 × 106 cells intravenously via tail vein in C57BL/6 mice; subcutaneous flank challenge forms solid tumors and prolongs survival relative to systemic dosing, enabling adaptive-immunity-dependent study designs
Dissemination pattern Intravenous infusion seeds bone marrow, peripheral blood, spleen, liver, lung, lymph nodes, ovaries, kidney, skin, and central nervous system; macroscopic masses commonly arise in ovaries, liver, and spine; hepatosplenomegaly is a hallmark
Disease kinetics Bioluminescence-measured tumor doubling time as short as 1.3 days; median survival approximately 15 days after 1 × 106 C1498-GFP cells (Zhang et al., Blood 2009) to approximately 23 days in luciferase-mCherry configurations; disease progresses without body-weight loss, so humane endpoints rely on hindlimb paralysis and ascites-related abdominal distention
Documented in vivo responses PD-1-deficient mice survive significantly longer than wild-type (median ≈14 → ≈21.5 days); anti-PD-L1 improves survival while anti-PD-1/PD-L1 monotherapy delays progression only modestly (approximately 3–5 days), motivating combination designs; responsive to hypomethylating agents (5-azacytidine restores immune-related transcripts and extends survival with subsequent relapse), artesunate, acid ceramidase inhibition (LCL204), and the isatin analog KS99 combined with cytarabine
Host strains C57BL/6 or C57BL/6J immunocompetent mice (syngeneic); B6.SJL (CD45.1) congenic hosts for unlabeled discrimination of leukemia cells; PD-1-knockout and other knockout variants for mechanism studies
Key research applications AML immunotherapy and checkpoint combination evaluation; hypomethylating-agent and epigenetic-therapy responsiveness and relapse modeling; drug-benchmarking (venetoclax-based, antimalarial-derived, and metabolic inhibitors); vaccine and cell-therapy programs using defined antigens (C1498.SIY) or congenic tracking; dissemination and organ-infiltration biology; dietary, microbiome, and tumor-microenvironment interaction studies

Our Services

A disseminated leukemia model lives or dies on the quality of its burden tracking, and Alfa Cytology runs C1498 accordingly: authenticated banks of the parental and reporter lines, validated tail-vein inoculation with engraftment verification, weekly in vivo bioluminescence with single-cell flow confirmation of organ burden, and survival-grade documentation with the model’s characteristic humane endpoints — all under one accountable preclinical program.

Workflow of C1498 Syngeneic Model Construction

Construction follows the published systemic-infusion methodology: C1498 cells (parental or reporter-labeled) are expanded under authenticated conditions, formulated as a defined intravenous dose, infused into C57BL/6 mice, verified for engraftment by imaging or flow cytometry, treated, and followed for burden and survival. The workflow comprises the following stages.

  1. Cell authentication and banking: C1498 or reporter derivatives are identity-verified, confirmed mycoplasma-negative, checked for reporter fidelity by flow cytometry, and expanded into low-passage working banks under selection where applicable.
  2. Cell harvest and formulation: Healthy log-phase cultures are counted and viability-checked, then resuspended at 0.5–2 × 106 cells in 100 μL of PBS per animal, with dose titration performed when a longer survival window is required.
  3. Anesthesia and intravenous infusion: C57BL/6 mice are anesthetized with isoflurane, and the cell suspension is infused via the lateral tail vein using a controlled, pre-warmed injection technique that avoids cell loss.
  4. Engraftment verification: Luciferase-arm animals are imaged within days of infusion to confirm systemic seeding and establish baseline burden; GFP/mCherry arms are verified by peripheral-blood flow cytometry on a study-defined schedule.
  5. Randomization and treatment administration: Animals are randomized by burden or study day; experimental arms — checkpoint inhibitors, hypomethylating agents, targeted and metabolic inhibitors, vaccines, and cell therapies alone or in combination — are dosed per study design with toxicity monitoring.
  6. Longitudinal burden and immune monitoring: Weekly in vivo bioluminescence tracks whole-body kinetics; periodic blood sampling quantifies circulating leukemia cells; tumor-infiltrating-lymphocyte and antigen-specific responses are profiled by multi-parametric flow cytometry, tetramer staining, and ELISPOT where antigen systems are in place.
  7. Endpoint and histopathological analysis: Endpoints integrate survival and burden kinetics with necropsy-based organ mapping, single-cell flow quantification of leukemia burden per tissue, and histopathology (H&E confirming myeloid-blast morphology with Ki67 and marker-specific immunohistochemistry), documented against the model’s ascites- and paralysis-based humane endpoints.

Fig 3: Workflow for the establishment of C1498 Syngeneic Models.Fig 2. C1498 Syngeneic Model construction workflow.

Case Study-C1498 Syngeneic Model Development

Alfa Cytology has conducted preclinical programs on the C1498 platform spanning checkpoint combination evaluation, epigenetic-therapy responsiveness and relapse monitoring, and dissemination-focused burden tracking. In these studies, systemically infused C1498 tumors were longitudinally quantified by in vivo bioluminescence and organ-level flow cytometry, treated per randomized regimens, and characterized at endpoint by histopathology and immune-microenvironment profiling. Study-level datasets are available upon request.

Fig 4: Case Study-C1498 Syngeneic Model Development.

Why Choose Alfa Cytology?

Alfa Cytology pairs leukemia-specific operational discipline with quantitative imaging and congenic-analytics capability, so every C1498 study is executed with the burden-tracking rigor a disseminated model demands.

  • Focused experience with systemic syngeneic leukemia models, including reporter, model-antigen (SIY), and CD45.1/45.2 congenic configurations.
  • A single coordinated team managing cell banking, tail-vein infusion, in vivo imaging, flow-cytometric organ burden quantification, and endpoint pathology under one quality framework.
  • Design fluency with checkpoint combinations, hypomethylating agents, and survival-based endpoints using the model’s characteristic humane criteria.
  • Endpoint panels pairing bioluminescence kinetics with single-tissue flow quantification and myeloid-blast histopathology.
  • Transparent milestone reporting and rapid scientific feedback throughout the engagement.

Contact Us

If your leukemia program needs an immune-competent, disseminated AML platform with quantitative burden tracking across organs, Alfa Cytology is ready to build the study around your regimen. Reach out to us with your study design and endpoint requirements, or contact us today for a customized proposal and quotation for the C1498 syngeneic model service.

Reference

  1. Ruzicka, Michael, et al. "RIG-I-based immunotherapy enhances survival in preclinical AML models and sensitizes AML cells to checkpoint blockade." Leukemia 34.4 (2019): 1017.

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

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