WM115 / WM115-luc Orthotopic Mouse Model Service for Melanoma

The WM115 / WM115-luc orthotopic mouse model of melanoma implants a slower-growing, primary-site BRAF V600D human melanoma into the skin, offering an indolent-growth counterpart to aggressive metastatic lines — with luciferase bioluminescence quantifying tumor expansion, nodal spread, and treatment response over extended observation windows. Alfa Cytology delivers this platform as an integrated preclinical service: authenticated CRL-1675 banking, luciferase line qualification, intradermal or flank engraftment in nude or NSG recipients, scheduled whole-body and ex vivo imaging, BRAF-pathway dosing, and endpoints spanning tumor metrics, metastatic survey, methylation-aware molecular analysis, and histopathology.

Overview of WM115 / WM115-luc Orthotopic Mouse Model for Melanoma

WM115 belongs to the WM melanoma series established at The Wistar Institute beginning in 1977 — a collection built by Meenhard Herlyn’s laboratory patient by patient, primary lesion by metastasis, and distributed so widely that its founder once estimated more than 800 pounds of WM-derived tumor had been grown in culture worldwide. WM115 itself was deposited with ATCC as CRL-1675, with documented STR identity, and carries a BRAF V600D mutation — an uncommon variant at codon 600 — alongside wild-type NRAS, distinguishing it from the V600E-dominant melanoma panel. Its most scientifically elegant property is relational: WM115’s metastatic counterpart, WM266-4 (ATCC CRL-1676), derives from the same patient, making the pair a living model of the primary-to-metastasis transition — the pairing exploited in genome-wide methylation sequencing studies that tracked epigenetic rewiring during metastatic progression, including the candidate driver EBF3.

Fig 1. Melanoma xenograft model in NSG mice established with 5×10⁵ eGFP-FFLuc-labeled WM115 cells, showing the s.c.-to-i.v. CAR-T treatment schema (day 0 inoculation, day 7 CAR-T) and 63-day longitudinal tumor bioluminescence kinetics where control tumors grew exponentially to 2×10¹⁰ total flux while 763.74(B) CD28 CAR-T (framework region–optimized) kept WM115 tumors suppressed near baseline, with h763.74#2/#5 variants partially controlling WM115 growth. (Landoni, Elisa, et al., 2021)

In behavior, WM115 reflects its primary-site origins: the cells are epithelial-like and adherent, double roughly every 36-48 hours, and grow more deliberately than their metastatic cousins — a tempo that demands longer observation windows but rewards them with biologically interpretable progression. The line is a melanoma staple for signaling studies of S100B-RSK complexes, estrogen-receptor-β pharmacology, and comparative oncology work. Orthotopically, WM115 and its luciferase derivatives are implanted intradermally or subcutaneously in immunodeficient mice, where bioluminescence imaging after D-luciferin administration turns slow growth into a quantitative longitudinal readout and flags nodal and visceral spread as it emerges. For sponsors, the WM115-luc orthotopic model fills a distinct niche: a BRAF-mutant, wild-type-NRAS, primary-site melanoma whose unhurried kinetics suit mechanism-of-action studies, combination-schedule exploration, epigenetic-drug programs, and any design where watching slow biology clearly matters more than racing fast biology.

Cell Line Information: WM115 / WM115-luc

WM115 is a primary-site melanoma line from the Wistar WM series, valued for its uncommon BRAF V600D allele and its patient-matched metastatic counterpart. Its luciferase derivative supports imaging-guided orthotopic studies. Core attributes follow.

Our Services

Slow-growing models punish impatient execution — missed imaging windows compound quietly, and small baseline imbalances linger for weeks. Alfa Cytology therefore runs WM115-luc with calendar-driven discipline: authenticated CRL-1675 stocks with documented STR identity, capped passages, reporter lots released only after uniform in vitro luminescence, and intradermal implantation followed by fixed-schedule imaging tuned to the model’s measured growth rate. Signal-matched randomization, optional paired-line designs with WM266-4, and methylation-aware molecular endpoints round out the offering. From first baseline scan through the final histopathology slide, Alfa Cytology keeps the WM115 / WM115-luc orthotopic workflow under single-point, week-by-week accountability.

Workflow of WM115 / WM115-luc Orthotopic Mouse Model Construction

The WM115-luc orthotopic workflow is calibrated for deliberately slow biology: longer horizons, denser documentation, and imaging schedules matched to measured doubling times. The sequence below is the standard construction-to-analysis flow.

1. Authentication and reporter release: WM115 / WM115-luc stocks are expanded from authenticated master banks at capped passage, mycoplasma-tested, STR-verified, and released only after uniform firefly luciferase expression is confirmed by serial in vitro luminescence assay.
2. Inoculum preparation: Log-phase adherent cultures are trypsinized, washed, counted, and resuspended in sterile PBS at the study dose (commonly 1×10⁶ to 5×10⁶ cells in 20-100 µL, calibrated during pilot runs to the model’s growth tempo).
3. Recipient preparation: Nude or NSG mice are acclimatized, body-weight stratified, shaved, and anesthetized with the implantation site disinfected; where paired-line designs are used, WM266-4 cohorts are prepared in parallel.
4. Orthotopic intradermal implantation: The suspension is delivered intradermally into dorsal skin using a fine needle; flank cohorts are implanted in parallel where designed.
5. Baseline imaging and randomized allocation: Baseline bioluminescence after D-luciferin documents engraftment; cohorts are randomized with matched photon flux, and dosing begins once signals establish — schedules tuned to slower kinetics than aggressive-line models.
6. Longitudinal monitoring: On a fixed schedule matched to measured growth, in vivo whole-body imaging and caliper measurements track primary tumor signal, with focused imaging for nodal spread; body weight and clinical condition are scored throughout the extended observation window.
7. Endpoint analysis and molecular workup: At termination, primary tumors and lymph nodes are excised and weighed, lungs and viscera are imaged ex vivo and inspected, histopathology confirms melanoma involvement, and molecular analyses — including BRAF-pathway markers and, where designs require, DNA-methylation profiling — are performed on recovered tumor tissue.

Fig 2. WM115 / WM115-luc orthotopic mouse model construction workflow.

Case Study-WM115 / WM115-luc Orthotopic Mouse Model Development

Alfa Cytology has implemented the WM115 orthotopic platform in preclinical programs where slower growth kinetics serve the science — mechanism-of-action studies, combination-schedule exploration, and epigenetic-drug evaluation among them. In these studies, extended imaging calendars matched to the model’s measured doubling times captured clean progression curves, randomized arms started from matched photon flux, and terminal analyses combined tumor and node metrics with ex vivo organ imaging and histopathology. Where sponsors requested primary-to-metastasis context, paired-line arms with the WM266-4 counterpart were incorporated, and recovered tissue was profiled for pathway markers and DNA methylation. Study-specific parameters and outcomes are retained as sponsor-confidential deliverables, and representative outlines can be furnished upon request.

Why Choose Alfa Cytology?

Indolent biology is a design choice, not a compromise — but only when execution respects its tempo. Alfa Cytology’s WM115-luc service is organized around exactly that respect. Sponsors benefit from:

• Authenticated CRL-1675 stocks with STR-documented identity and capped passage before animal use.
• Reporter lines qualified for uniform luciferase expression before release into studies.
• Imaging calendars calibrated to the model’s measured 36-48-hour doubling kinetics.
• Intradermal orthotopic technique with signal-matched randomization for clean baselines.
• Optional paired-line designs with the patient-matched WM266-4 metastatic counterpart.
• Molecular endpoints spanning BRAF-pathway markers and DNA-methylation profiling.
• Single-point study accountability with week-by-week reporting across extended horizons.

Contact Us

Need a slower-growing, primary-site melanoma context for mechanism or schedule studies? Contact us to discuss engraftment, tempo-matched imaging calendars, and endpoint design for the WM115 / WM115-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 scientific goals.

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