MDA-MB-361 Xenograft Model Overview

The MDA-MB-361 xenograft model is derived from a human breast adenocarcinoma and represents a luminal B, HER2-positive subtype. It was established from a metastatic pleural effusion of a patient with advanced breast cancer. Unlike many other HER2-amplified cell lines, MDA-MB-361 co-expresses estrogen receptor (ER), allowing for unique exploration of hormone receptor and HER2 co-targeting strategies. The model exhibits moderate proliferative capacity in vivo and demonstrates distinct pharmacologic behavior depending on endocrine signaling status.

As a model of dual receptor positivity (ER+/HER2+), MDA-MB-361 is well suited for investigating crosstalk between the estrogen and HER2 pathways, elucidating resistance mechanisms to both anti-estrogens and HER2-targeted agents, and optimizing sequential versus combinatorial therapeutic strategies. It is commonly used in translational breast cancer research that focuses on tumor heterogeneity and treatment stratification.

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Biological and Molecular Characteristics

MDA-MB-361 cells exhibit amplification and overexpression of the HER2 (ERBB2) oncogene, alongside functional estrogen receptor expression. This dual receptor status mimics the luminal B breast cancer subtype and allows for estrogen-dependent growth in some contexts. The cell line is also characterized by partial progesterone receptor (PR) expression and retains functional responsiveness to estrogen and anti-estrogen compounds such as tamoxifen or fulvestrant.

The model harbors a wild-type BRCA1/2 background, distinguishing it from BRCA-deficient HER2 models. It possesses moderate expression of PI3K/AKT signaling components and is known to acquire resistance to HER2-directed therapies through ER upregulation and compensatory survival signaling.

Characteristic	MDA-MB-361 Profile
Tumor Type	Human breast adenocarcinoma
Receptor Status	ER+, PR±, HER2+
Molecular Subtype	Luminal B, HER2-enriched
Hormone Dependency	Estrogen-responsive
HER2 Amplification	Present (ERBB2 overexpression)
PI3K/AKT Signaling	Moderately active
BRCA1/2 Status	Wild-type
Proliferation Rate	Moderate (doubling time ~48 hrs)
Endocrine Therapy Sensitivity	Tamoxifen, fulvestrant (context-dependent)
Resistance Potential	ER upregulation, downstream escape

This receptor co-expression landscape enables the MDA-MB-361 model to serve as a valuable system for testing dual pathway inhibitors and identifying predictive biomarkers of response and resistance.

In Vivo Model Development and Tumorigenicity

MDA-MB-361 xenografts are established by subcutaneous injection of 5–10 × 10⁶ cells, often with estrogen supplementation in ovariectomized immunodeficient mice (e.g., athymic nude or NSG strains) to promote tumor establishment and maintain ER signaling. Without estrogen pellets, tumor take rates may be reduced due to hormone dependence, though HER2 signaling can sustain moderate growth independently.

Tumors typically become palpable within 12–16 days and reach experimental endpoint volumes (800–1,200 mm³) in 4–6 weeks. Growth rates are moderate and allow sufficient time for multi-cycle therapeutic evaluations. Orthotopic implantation into the mammary fat pad is also feasible and may more accurately reproduce the hormone-receptor interaction within the breast microenvironment.

This model is amenable to genetic labeling (e.g., luciferase or GFP) for non-invasive imaging and long-term tracking. It is suitable for evaluating agents targeting HER2, ER, and PI3K/AKT pathways both alone and in combination.

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Histopathology and Immunohistochemical Profile

MDA-MB-361 xenografts are moderately cellular, displaying glandular or solid patterns with variably pleomorphic nuclei, moderate mitotic activity, and minimal necrosis. The tumors exhibit features of ductal differentiation with fibrotic septa and occasional cystic structures. The tumor-stroma interface is typically well defined and displays minimal infiltration.

Immunohistochemical analysis reveals strong HER2 membrane staining (3+), nuclear ER expression in 60–80% of tumor cells, and variable PR staining. Ki-67 staining indices range from 30–50%, consistent with a moderately proliferative tumor. Phospho-AKT and phospho-ERK are detectable in the cytoplasm, while downstream markers such as mTOR and S6 kinase are moderately expressed.

This IHC profile supports the dual receptor-driven phenotype and confirms suitability for evaluating endocrine and HER2-directed pharmacodynamics.

Preclinical Applications and Drug Response

The MDA-MB-361 xenograft model is ideal for preclinical studies examining the interplay between HER2 and ER signaling pathways. It has been widely used to evaluate HER2-targeted monoclonal antibodies (trastuzumab, pertuzumab), tyrosine kinase inhibitors (lapatinib, neratinib), and antibody-drug conjugates (T-DM1). In parallel, the model supports studies involving selective estrogen receptor modulators (SERMs), degraders (SERDs), and aromatase inhibitors when used with exogenous estrogen support.

Combination therapy studies using anti-HER2 and anti-ER agents are frequently conducted in this model to explore resistance mechanisms such as ER reactivation, HER2 receptor heterodimerization, and downstream survival signaling via the PI3K/AKT/mTOR axis. The model is also applicable for investigating treatment sequences and understanding receptor plasticity under chronic therapeutic pressure.

Due to its receptor co-expression, MDA-MB-361 supports evaluation of predictive biomarkers for dual-targeted therapy and is used to identify patients who may benefit from tailored treatment regimens in the HER2+/ER+ population.

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To utilize the MDA-MB-361 xenograft model in studies of HER2/ER co-targeting, resistance mechanisms, or biomarker discovery in luminal B breast cancer, please submit a quote request below. Services include subcutaneous or orthotopic implantation, hormone supplementation protocols, and advanced pharmacodynamic profiling.

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