| Model Type | Model Name/Description | Characteristics | Applications | Key Findings | References |
|---|---|---|---|---|---|
| Human MEC cell lines | **UM-HMC-1, UM-HMC-3A, UM-HMC-3B** | Established human salivary MEC cell lines used for CSC and signaling studies; support flow cytometry, sphere assays, gene silencing, drug treatment, and xenografting; used in both subcutaneous and orthotopic murine models (pqac-00000014) | Cancer stem cell biology, p53/MDM2 pathway studies, self-renewal assays, therapeutic testing, xenograft generation | p53 activation reduced stemness and self-renewal, drove differentiation, and prevented CSC-mediated recurrence in preclinical models; these lines are core experimental tools for MEC biology (pqac-00000014) | (pqac-00000014) |
| Human MEC cell lines / xenograft source | **MEC-derived xenograft-compatible cell lines carrying CRTC1-MAML2** | Used in inducible knockdown experiments and as source of established MEC xenografts; fusion-positive context enabled functional validation of the fusion as a driver (pqac-00000008) | Functional validation of oncogenic drivers, target dependency studies, in vivo therapeutic testing | Doxycycline-induced **CRTC1-MAML2** knockdown blocked growth of established MEC xenografts, demonstrating fusion dependency and validating the fusion as a therapeutic target (pqac-00000008) | (pqac-00000008) |
| Cell line-based CSC models | **ALDH-high/CD44-positive MEC CSC fractions derived from UM-HMC lines** | Subpopulation model of tumor-initiating/stem-like MEC cells; assessed with sphere assays and cell-fate analyses; linked to recurrence biology (pqac-00000014) | Study of self-renewal, plasticity, recurrence mechanisms, CSC-targeted therapy | Supports the concept that CSCs drive progression/recurrence in MEC and that p53 activation can suppress CSC properties without necessarily inducing apoptosis (pqac-00000014) | (pqac-00000014) |
| Patient-derived xenograft (PDX) | **Salivary MEC PDX models** | Generated from surgically resected human salivary gland carcinomas; in Aizawa et al., one series of MEC PDXs was successfully established; retained histologic features, transcription profiles, genomic variants, and fusion genes of original tumors (pqac-00000009) | Preclinical drug testing, translational modeling, preservation of patient tumor heterogeneity, study of molecular mechanisms | MEC PDXs recapitulated the original tumors and provide a resource for novel therapeutic strategy development (pqac-00000009) | (pqac-00000009) |
| Orthotopic xenograft | **Orthotopic murine MEC models** | In vivo implantation models using MEC cells/organoids into anatomically relevant sites; used to evaluate tumorigenicity, growth, and recurrence after surgery (pqac-00000014, pqac-00000009) | Tumor growth, recurrence modeling, validation of therapeutic interventions in a microenvironment closer to native salivary tissue | Orthotopic models were used to demonstrate recurrence-preventing effects of p53 activation and to confirm tumorigenicity of organoid-derived models (pqac-00000014, pqac-00000009) | (pqac-00000014, pqac-00000009) |
| Subcutaneous xenograft | **Subcutaneous MEC xenografts** | Standard in vivo transplantation model using MEC cell lines; enables longitudinal tumor growth measurements and therapeutic response evaluation (pqac-00000014, pqac-00000008) | Drug efficacy studies, tumor maintenance dependency, recurrence biology | Used in both p53-activation studies and CRTC1-MAML2 knockdown studies to show reduced tumor growth and therapeutic vulnerability (pqac-00000014, pqac-00000008) | (pqac-00000014, pqac-00000008) |
| Genetically engineered mouse model (GEMM) | **Conditional CRTC1-MAML2 transgenic mouse** | Cre-inducible mouse engineered to express **CRTC1-MAML2**; produced salivary gland tumors with **100% penetrance** that resembled histologic and molecular characteristics of human MEC (pqac-00000008) | Mechanistic dissection of tumor initiation, oncogenic driver validation, testing combination targeted therapy | Provided direct evidence that **CRTC1-MAML2 is a major oncogenic driver** of MEC; revealed cooperating dysregulation of the **p16-CDK4/6-RB** pathway and supported combined **palbociclib + erlotinib** therapy in vitro/in vivo (pqac-00000008) | (pqac-00000008) |
| Patient-derived organoid (PDO) | **MEC PDOs** | In Aizawa et al., one series of patient-derived MEC organoids was established from resected tumors; organoids maintained pathologic and genetic features of the source tumor and could be cryopreserved/recovered (pqac-00000009) | Ex vivo biology, personalized drug screening, preservation of subtype-specific fusion and expression features, organoid transplantation | MEC PDOs retained transcriptional profiles, genomic variants, and fusion genes, supporting organoid use as a clinically relevant preclinical platform (pqac-00000009) | (pqac-00000009) |
| PDX-derived organoid (PDXO) | **MEC PDXOs** | Organoids derived from established MEC PDXs; histologically and genetically similar to original tumors and paired PDXs (pqac-00000009) | Scalable ex vivo therapeutic testing, bridging in vivo and in vitro modeling, mechanistic studies | PDXOs preserved salient tumor traits and, together with PDXs/PDOs, form a linked platform for translational MEC research (pqac-00000009) | (pqac-00000009) |
| Organoid-transplanted animal model | **Orthotopic transplantation of MEC PDOs/PDXOs** | In vivo tumorigenicity assay using organoids implanted orthotopically; tests whether organoids can regenerate tumors resembling parent lesions (pqac-00000009) | Functional validation of organoids, tumorigenicity assessment, therapy testing in organoid-derived tumors | Orthotopic transplants from PDOs/PDXOs showed similar histological features as original MEC tumors, validating these models biologically (pqac-00000009) | (pqac-00000009) |
| Conditionally reprogrammed primary tumor cells | **CR models from primary tumor cells; proposed/used broadly for MEC-related research** | Feeder-cell plus ROCK-inhibitor system enabling rapid proliferation of primary epithelial tumor cells; review literature explicitly notes value for cancer biology, therapeutic target exploration, individualized drug screening, and improvement of patient-derived animal models; relevant to MEC cell growth applications (pqac-00000009) | Expansion of primary MEC cells, personalized testing, short-term translational assays, support for PDX development | CR systems are highlighted as a promising platform for studying tumor biology and drug response where classic models are limited; useful conceptually for rare tumors like MEC, though disease-specific standardization remains limited (pqac-00000009) | (pqac-00000009) |
| Molecularly defined preclinical combination-therapy model | **CRTC1-MAML2–driven MEC models treated with palbociclib + erlotinib** | Uses fusion-driven in vitro and in vivo MEC models, including xenografts and transgenic contexts, to interrogate pathway cooperation (pqac-00000008) | Precision-therapy development, pathway cotargeting, proof-of-concept preclinical intervention | Cotargeting **AREG/EGFR** signaling and **CDK4/6-RB** signaling produced enhanced antitumor responses, identifying a rational combination strategy for MEC (pqac-00000008) | (pqac-00000008) |
| Recurrence model | **Post-resection recurrence model in murine MEC** | Follow-up after tumor resection for up to 250 days in murine MEC models; specifically designed to study disease recurrence (pqac-00000014) | Recurrence prevention studies, CSC-targeted interventions, longitudinal efficacy assessment | Therapeutic p53 activation prevented CSC-mediated tumor recurrence in preclinical trials, providing a rare disease-relevant recurrence model for MEC (pqac-00000014) | (pqac-00000014) |
| Other reported MEC cell line | **YD-15 MEC cells** | Mentioned in unobtainable later literature as a mucoepidermoid carcinoma cell model with enhanced tumor formation after intradermal injection in nude mice; detailed primary evidence was not available in retrieved contexts, so characterization remains limited here | Potential xenograft/tumor formation studies | Evidence in the retrieved corpus is insufficient for detailed annotation; include as a named model of interest requiring direct source confirmation before database use | (pqac-00000014) |


*Table: This table summarizes experimental models used to study mucoepidermoid carcinoma, spanning cell lines, xenografts, organoids, and engineered mice. It highlights what each model captures biologically and how each has been used for mechanistic or therapeutic research.*