MFC Metastatic Tumor Model Service for Gastric Cancer

The MFC metastatic tumor model recreates the two routes that most often determine outcome in gastric cancer — hematogenous spread to the lung and peritoneal dissemination — using a murine forestomach carcinoma line engrafted in fully immunocompetent 615 hosts. Alfa Cytology delivers this model as a turnkey preclinical service: authenticated MFC and MFC-Luc/MFC-GFP cell banks, orthotopic gastric-wall or intraperitoneal inoculation under surgical SOPs, scheduled bioluminescent surveillance, and metastasis-focused endpoint analysis, all within IACUC-approved, preclinical-only workflows.

Overview of MFC Metastatic Tumor Model for Gastric Cancer

MFC (mouse forestomach carcinoma) occupies a special place in gastric cancer research: it is one of the very few mouse gastric carcinoma lines that grows reliably in immunocompetent hosts. The line was established in 1987 by Qian and colleagues from a forestomach squamous cell carcinoma that developed in a 615 inbred mouse treated with the gastric carcinogen N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), and it was characterized from the outset by spontaneous hematogenous metastasis. Grown in RPMI-1640 with 10% FBS, MFC cells adhere as an epithelial-like monolayer with a doubling time of roughly 18–25 hours, and they can also be induced into spheroid-like three-dimensional growth. Because tumor and host share the 615 genetic background, implanted MFC cells are never rejected: metastatic progression — from primary-site growth through vascular entry to lung colonization — proceeds in the presence of a complete immune system, which is precisely what makes the model valuable for immuno-oncology questions.

Fig 1. In vivo efficacy in the MFC-Luc intraperitoneal syngeneic model (615 mice, day 0 implantation, i.p. treatment on days 5/8/12/15, endpoint day 18): gross peritoneal tumors, tumor weight, longitudinal BLI at days 6/12/18, and immune profiling showing that GPR34i alone or with anti-PD-1 reduces metastatic burden and reshapes macrophage/T cell ratios (CD206+ macrophages, CD8+ and PD-1+ T cells, Gzmb+CD8/CD206 ratios). (Lv, Jialong, et al., 2026)

Two dissemination formats dominate the literature. In the orthotopic format, MFC cells are implanted into the gastric wall, where they form a primary tumor and subsequently shed cells into the circulation, giving rise to spontaneous lung metastases; this design captures the full metastatic cascade rather than bypassing it. In the intraperitoneal format — developed to mimic peritoneal carcinomatosis, the devastating complication that accounts for a large share of gastric cancer mortality — 1 × 10⁶ MFC or MFC-Luc cells are injected into the peritoneal cavity, producing quantifiable ascites and disseminated peritoneal nodules within about two to three weeks. Luciferase (MFC-Luc) and GFP (MFC-GFP) derivatives enable whole-body in vivo tracking of metastatic burden at the group level and, when paired with macrophage-depletion or checkpoint-blockade arms, allow the immune mechanisms behind metastatic outgrowth to be dissected directly at the metastatic site. One honest caveat accompanies the model’s strengths: the mouse forestomach is a squamous-lined structure without a direct human equivalent, so MFC is best regarded as an immunocompetent upper-gastric cancer platform rather than a perfect replica of human gastric adenocarcinoma histology.

Cell Line Information: MFC

MFC (Cellosaurus CVCL_5J48) was derived in China and is distributed through repositories such as CLS (300652), Hysigen (TCM-C744), and the Chinese cell bank KCB (KCB 92020YJ); reporter derivatives MFC-GFP (CVCL_BT06) and MFC-B5-GFP (CVCL_WI97) are cataloged as child lines. The parental tumor was induced by MNNG treatment in a 615 inbred mouse and diagnosed as forestomach carcinoma; the cell line retains epithelial-like adherent morphology, a ~18–25 h doubling time, and the capacity for both solid tumor formation and spheroid growth. Its defining biological property is spontaneous hematogenous metastatic capacity, which underpins its widespread use in syngeneic gastric cancer studies — including landmark work showing that radiotherapy primes the tumor microenvironment and potentiates anti-PD-1 therapy in this model. Key characteristics are listed below.

Our Services

Peritoneal spread and lung metastasis are the two failures that gastric cancer programs most urgently need to prevent, and few models address both within an intact immune system. Alfa Cytology has operationalized the MFC platform for exactly this purpose: qualified 615-host colonies, characterized MFC/MFC-Luc/MFC-GFP banks, standardized gastric-wall and intraperitoneal procedures, and imaging-plus-histology endpoints that quantify metastatic burden rather than merely observing it — all delivered within strictly preclinical, IACUC-approved frameworks.

Workflow of MFC Metastatic Tumor Model Construction

Building an MFC metastatic study is a coordinated effort across cell preparation, microsurgical delivery, and image-guided follow-up, with the intraperitoneal format adding ascites and nodule quantification to the usual metastasis endpoints. The sequence below is the standard operating flow; inoculation route, imaging cadence, and endpoint panels are configured for each project.

1. Cell line recovery and qualification: MFC cells are expanded from authenticated stocks in RPMI-1640 + 10% FBS; identity is verified, cultures are confirmed mycoplasma-free, and — for imaging cohorts — the MFC-Luc or MFC-GFP derivative is checked for stable reporter expression in vitro so that signal faithfully tracks viable cell number.
2. Inoculum preparation: Logarithmic-phase adherent cells are detached, gently dissociated, counted, and adjusted to the route-specific dose — for example 5 × 10⁵ cells for subcutaneous priming or 1 × 10⁶ cells in a small volume (50–100 µL) for intraperitoneal or gastric-wall delivery.
3. 615 host acclimatization and grouping: Syngeneic 615 inbred mice are acclimatized under SPF conditions and health-screened; animals are randomized by body weight, and pre-inoculation baseline bioluminescence is recorded where imaging will be used.
4. Route-specific tumor inoculation: For the orthotopic format, cells are injected into the sub-serosal plane of the gastric wall through a fine needle to form a localized primary tumor; for the peritoneal-carcinomatosis format, cells are delivered into the peritoneal cavity; experimental lung seeding can alternatively be achieved by tail-vein injection.
5. Metastatic progression monitoring: Tumor signal is imaged on a fixed schedule — for instance every 5 days for intraperitoneal MFC-Luc models — alongside body weight and abdominal circumference measurements that flag developing ascites, with clinical condition scored daily.
6. Treatment and interim imaging: Test articles such as checkpoint antibodies, kinase inhibitors, oncolytic or cellular therapies, or radio-immunotherapy combinations are dosed per schedule; interim imaging sessions capture individual metastatic trajectories and allow on-study randomization at matched burden.
7. Necropsy and metastasis scoring: At endpoint, the peritoneal cavity is inspected and lavaged where relevant; ascites volume is recorded, peritoneal and mesenteric nodules are counted, lungs are inflated and examined for surface metastases, and primary gastric tumors (if present) are weighed for completeness.
8. Histopathology, immune analysis, and reporting: Lung, peritoneum, and gastric tissues are fixed for H&E and IHC confirmation of metastatic foci; flow cytometry and cytokine profiling of peritoneal lavage or tumor tissue characterize the immune milieu; all data are analyzed and compiled into a structured final report.

Fig 2. MFC Metastatic Tumor Model construction workflow.

Case Study-MFC Metastatic Tumor Model Development

Alfa Cytology has implemented MFC-based metastatic models across preclinical gastric cancer programs, covering both the orthotopic gastric-wall format with spontaneous lung dissemination and the intraperitoneal format that mirrors peritoneal carcinomatosis. These engagements have yielded reproducible metastatic burdens, imaging-quantified responses to therapeutic interventions, and histologically confirmed lesion maps that informed sponsor decisions on candidate advancement and combination strategies. Study-specific configurations and representative findings can be discussed directly with our scientific team.

Why Choose Alfa Cytology?

An MFC metastatic study succeeds or fails on execution details — reporter stability, surgical placement, imaging discipline, and honest lesion accounting. Alfa Cytology controls each of these elements through standardized SOPs and experienced teams, so that the data you receive measure genuine antimetastatic activity.

• Immunocompetent 615 syngeneic hosts preserve the full tumor-immune interplay during metastatic progression.
• Established metastatic capacity: spontaneous hematogenous lung spread documented since the line’s original derivation.
• Two clinically relevant dissemination formats — orthotopic gastric wall and intraperitoneal carcinomatosis — plus tail-vein experimental seeding.
• Cataloged reporter derivatives (MFC-Luc, MFC-GFP) with pre-validated in vivo imaging performance.
• Quantitative peritoneal endpoints including ascites volume, nodule counts, and abdominal-circumference kinetics.
• Immune-rich readouts from peritoneal lavage and metastatic tissue suited to macrophage, checkpoint, and combination studies.
• IACUC-approved, preclinical-only operation with full traceability from cell bank to final report.

Contact Us

If your gastric cancer program needs a metastatic platform in which the immune system is fully present and measurable, the MFC model at Alfa Cytology deserves a close look. Reach out to us to align on inoculation format, imaging cadence, and endpoint panels for your compound. Contact us today and start building a preclinical metastasis study designed around your question.

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