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ACHN / ACHN-luc Orthotopic Mouse Model Service for Renal Cancer

Fig 1: ACHN / ACHN-luc Orthotopic Mouse Model for Renal Cancer preclinical research.

The ACHN / ACHN-luc orthotopic mouse model for renal cancer is a human xenograft platform in which metastasis-derived ACHN renal adenocarcinoma cells are implanted into the kidney of immunodeficient mice, recreating organ-confined tumor growth within the native renal microenvironment together with spontaneous spread to the lung. Alfa Cytology provides this model as a fully managed preclinical capability — spanning authenticated ACHN / ACHN-luc expansion and luciferase-stable banking, precision intrarenal implantation, scheduled in vivo bioluminescence tracking of primary tumors and pulmonary lesions, and comprehensive necropsy histopathology — all configured to each sponsor’s agent, regimen, and endpoint plan.

Overview of ACHN / ACHN-luc Orthotopic Mouse Model for Renal Cancer

ACHN is among the oldest and most extensively characterized human renal cancer cell lines still in use, with a derivation history that makes it intrinsically a model of metastatic disease. The line was established in November 1979 from the malignant pleural effusion of a 22-year-old donor with widely metastatic renal cell adenocarcinoma (confirmed at autopsy), after the cells were seeded directly into culture and carried for 150 days before first passage into nude mice. Its histotype has been debated: early xenograft tumors were described as poorly differentiated clear cell carcinoma, whereas genomic and cytogenetic analyses — including a c-MET polymorphism characteristic of papillary renal cancer, gains of chromosomes 7 and 17, and 9p loss — point toward papillary features, while expression profiling shows clear cell-like behavior in the MYC pathway. Critically for experimental interpretation, ACHN carries no VHL mutation, consistent with its non-clear-cell character. The line is epithelial, G6PD type B, TP53 wild-type with detectable p53 protein, expresses carbonic anhydrase IX, and is growth-inhibited by human interferons — a property documented in both the original cells and cells recovered from mouse tumors.

Fig 2: Reference figures for ACHN / ACHN-luc cell-related literature.Fig 1. In vivo BLI of 786-O-luc and ACHN-luc tumor burden (Empty vs SMOC2-overexpressing) at day 7, day 14 and endpoint, with total body luminescence quantification and ex vivo lung imaging. (Feng, Daniel, et al., 2022)

When grafted into its organ of origin, ACHN reproduces the behavior that made it famous: subcutaneous inoculation into nude mice yields locally invasive tumors within about four weeks (with 100% take at 1 × 107 cells, appearing within 21 days), and intrarenal implantation converts this local invasiveness into a metastatic cascade that reaches the lung — the dominant clinical site of renal cancer dissemination. The ACHN-luc derivative, stably expressing firefly luciferase, quantifies every stage of that cascade non-invasively: primary renal tumor take and growth are followed by in vivo bioluminescence after luciferin administration, pulmonary metastatic seeding is flagged early by thoracic signal, and ex vivo organ imaging at necropsy confirms the metastatic map. Because the model has validated responsiveness to anti-angiogenic and targeted agents — including sunitinib in a left-ventricular bone metastasis setting, and the angiogenesis inhibitor TNP-470, which abolished lung metastasis from subcutaneous tumors — the ACHN / ACHN-luc orthotopic system supports angiogenesis research, VEGF/mTOR-pathway agent evaluation, interferon-response studies, and metastasis-biology work in a single, well-documented platform.

Cell Line Information: ACHN / ACHN-luc

The table below consolidates the key biological, cultural, and modeling characteristics of the ACHN parental line and its luciferase-labeled derivative ACHN-luc. Both are human-derived and require immunodeficient hosts for in vivo propagation.

Parameter Details
Cell line designation ACHN (parental line); ACHN-luc (luciferase-labeled derivative)
Species / donor Human (Homo sapiens), male; isolated from a 22-year-old Caucasian donor with widely metastatic renal cell adenocarcinoma (autopsy confirmed)
Origin Established in November 1979 (deposited by T.F. Hogan) from a malignant pleural effusion; cells were seeded directly into Eagle’s MEM with 10% FBS, maintained for 150 days in flasks, then inoculated subcutaneously into nude mice, forming locally invasive tumors within four weeks
Depository / catalogue ATCC CRL-1611; Cellosaurus CVCL_1067
Tumor type Renal cell adenocarcinoma; histotype debated — early xenografts described as poorly differentiated clear cell, while genomic features (c-MET polymorphism, chromosome 7 and 17 gains, 9p loss) support papillary characteristics
Molecular features No VHL mutation (consistent with non-clear-cell histology); TP53 wild-type with high p53 protein expression; NF2 mutation reported; carbonic anhydrase IX (CAIX) positive; G6PD isoenzyme type B
Cytogenetics Complex karyotype with gains of chromosomes 7 and 17 and loss of 9p
Growth properties Adherent epithelial cells forming cobblestone-shaped monolayers; comparatively moderate proliferative rate; anchorage-independent growth in soft agar
Recommended culture conditions Eagle’s Minimum Essential Medium (EMEM) supplemented with 10% fetal bovine serum at 37 °C in a humidified 5% CO₂ atmosphere (ATCC guidelines)
Interferon responsiveness Growth-inhibited by human interferons and interferon inducers — demonstrated in the original line and in cells recovered from nude-mouse tumors; useful for cytokine and interferon-based therapy studies
Reporter labeling (ACHN-luc) Stable firefly luciferase expression introduced by lentiviral transduction; supports in vitro reporter assays and non-invasive in vivo bioluminescence imaging
Standard orthotopic inoculum Published renal orthograft practice implants in the range of 1–5 × 106 cells in 20–30 μL of serum-free medium mixed 1:1 with Matrigel into the subcapsular space or parenchyma of the left kidney (subcutaneous reference dosing is 1 × 107 cells, at which 100% of nude mice develop tumors within 21 days)
Host strains Athymic nude (BALB/c-nu/nu), SCID, and NSG mice
Metastatic behavior Locally invasive xenografts with spontaneous spread to the lung from both subcutaneous and intrarenal sites; skeletal metastases reproducible via left ventricular (intracardiac) injection, a setting in which sunitinib treatment prevents tumor growth
Key research applications Angiogenesis and microvessel-density studies; VEGF- and mTOR-pathway targeted therapy evaluation; interferon and cytokine signaling research; epithelial-to-mesenchymal transition and metastasis mechanism work; combination regimen and sequential therapy testing in renal cancer

Our Services

Operating the ACHN / ACHN-luc orthotopic model demands disciplined surgical technique and quantitative imaging discipline, and Alfa Cytology brings both: validated cell banks, subcapsular implantation into the left kidney with consistent take rates, weekly in vivo bioluminescence schedules, and metastasis-focused endpoint pathology — all delivered as one accountable preclinical program.

Workflow of ACHN / ACHN-luc Orthotopic Mouse Model Construction

Construction follows established intrarenal xenograft methodology: luciferase-labeled ACHN cells are expanded under authenticated conditions, formulated in a Matrigel-supported suspension, surgically implanted beneath the renal capsule or into the renal parenchyma of immunodeficient mice, and followed by serial imaging with metastasis-oriented endpoint analysis. The workflow comprises the following stages.

  1. Cell authentication and banking: ACHN or ACHN-luc cells are verified by STR profiling, confirmed mycoplasma-free, and expanded into low-passage working banks under standardized EMEM culture conditions.
  2. Cell harvest and formulation: Healthy cultures are trypsinized, washed, counted and viability-checked, then resuspended at the study-specified dose in the range of 1–5 × 106 cells in 20–30 μL of serum-free medium mixed 1:1 with cold Matrigel and kept on ice until implantation.
  3. Anesthesia and renal exposure: Male immunodeficient mice are anesthetized with isoflurane; a left flank incision opens the retroperitoneal space and gently exteriorizes the left kidney through a warm saline-moistened window.
  4. Intrarenal implantation: The cell suspension is slowly injected beneath the renal capsule or into the parenchyma of the left kidney; the needle is held briefly after injection so the Matrigel partially sets, limiting reflux and ensuring uniform tumor take.
  5. Closure and perioperative care: The kidney is returned to the retroperitoneum, muscle and skin layers are sutured, and animals receive analgesia with close post-operative monitoring until fully recovered.
  6. Engraftment confirmation and serial imaging: Luciferin is administered intraperitoneally and bioluminescence is acquired to confirm renal tumor take and normalize group allocation; imaging repeats on a weekly cadence to track primary growth and flag emerging thoracic metastatic signal.
  7. Intervention and endpoint analysis: Experimental arms — VEGF-pathway tyrosine kinase inhibitors, mTOR inhibitors, anti-angiogenic agents, interferon-based regimens, and combinations — proceed per study design; endpoints integrate imaging with tumor-bearing kidney weight, ex vivo lung bioluminescence and surface lesion counts, and histopathology (H&E with CD31, Ki67, and marker-specific immunohistochemistry).

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

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

Alfa Cytology has conducted preclinical programs on the ACHN / ACHN-luc orthotopic platform covering targeted-therapy evaluation, anti-angiogenesis research, and metastasis-biology investigation. In these studies, intrarenally implanted ACHN-luc tumors were longitudinally quantified by in vivo bioluminescence, with pulmonary metastatic burden assessed by ex vivo organ imaging and histopathological confirmation at endpoint. Program-specific datasets are available upon request.

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

Why Choose Alfa Cytology?

Alfa Cytology pairs seasoned renal-xenograft expertise with unified surgical, imaging, and pathology teams, so every ACHN / ACHN-luc orthotopic study is executed with reproducible technique and reporting that sponsors can stand behind.

  • Demonstrated experience with intrarenal orthografts and metastasis-forward renal cancer study designs.
  • A single integrated team managing cell banking, kidney implantation surgery, in vivo imaging, and endpoint pathology under one quality framework.
  • Quantitative longitudinal bioluminescence readouts covering primary renal growth and early pulmonary metastatic emergence.
  • Flexible regimens spanning VEGF, mTOR, anti-angiogenic, and interferon-based intervention arms.
  • Clear milestone reporting and rapid scientific feedback throughout the engagement.

Contact Us

If your renal cancer program needs a rigorously controlled orthotopic platform with bioluminescent metastasis tracking, Alfa Cytology is ready to help. Reach out to us to discuss your agent, study design, and endpoint requirements, or contact us today for a customized proposal and quotation for the ACHN / ACHN-luc orthotopic mouse model service.

Reference

  1. Feng, Daniel, et al. "SMOC2 promotes an epithelial-mesenchymal transition and a pro-metastatic phenotype in epithelial cells of renal cell carcinoma origin." Cell death & disease 13.7 (2022): 639.

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

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