Colorectal cancer is a digestive tract malignancy with clear molecular stratification and complex metastatic pathways, and is one of the most common malignancies worldwide. Alfa Cytology is a global leader in cancer research. With our extensive experience and advanced platforms, our talented scientists provide one-stop solutions for colorectal cancer animal model development, efficacy evaluation, cecal/colonic orthotopic model validation, liver metastasis research, primary induction models, tumor immunology testing, target expression validation, pathology testing, molecular mechanism testing, and PK/PD, based on client candidate drugs, molecular subtyping, treatment stage, cell line characteristics, intestinal organ microenvironment, liver metastasis requirement, immune system dependence, and R&D stages. We also provide zebrafish experimental services and cell-based experimental services, covering diverse research needs from in vitro to in vivo and from high-throughput screening to mechanism validation.
Colorectal cancer is a malignant tumor originating from colonic or rectal mucosal epithelium and is one of the most common digestive tract malignancies worldwide. Colorectal cancer is characterized by clear molecular stratification, well-defined metastatic pathways, and markedly different immune responses. Clinically, colorectal cancer is commonly managed based on MSI/MSS status, KRAS/BRAF/EGFR stratification, and tumor stage. MSI-H/dMMR colorectal cancer responds well to immune checkpoint inhibitors; MSS/KRAS background colorectal cancer generally has weaker immune response and relies more on chemotherapy, targeted agents, and combination strategies; BRAF V600E and KRAS G12C are important stratification markers in current targeted drug development. Liver metastasis is the most common distant metastatic route in colorectal cancer and a key factor affecting prognosis. The colorectal cancer immune microenvironment, tumor-infiltrating lymphocytes, MDSCs, macrophages, and cytokine networks play important roles in treatment response and resistance. AOM/DSS-induced models and CT26/MC38 syngeneic models are important platforms for inflammation-related carcinogenesis and immunotherapy research.
Fig.1 The three major molecular pathways of colorectal cancer. (Schmitt, M., & Greten, F. R., 2021)
In recent years, there have been advancements in the field of CRC therapy, leading to the emergence of new and promising approaches. Some of these emerging therapeutic approaches include:
| Types | Targets | Therapeutics | NCT | Phase |
| Checkpoint Inhibitors | PD-1 | PD-1 Antibody | NCT04833387 | Phase II |
| Non-coding RNA-Based Therapy | GSTP | NBF-006 | NCT03819387 | Phase I |
| Cell Therapy | Tumor Infiltrating Lymphocytes | / | NCT01174121 | Phase II |
| Cell Therapy | Anti-CEA CAR-T | / | NCT05240950 | Phase I |
Alfa Cytology has established a comprehensive solution platform for colorectal cancer animal experimental research, built around MSI-H/dMMR stratification, MSS/KRAS pathway, BRAF V600E, EGFR dependence, intestinal orthotopic microenvironment, liver metastasis, immunotherapy, humanized immunotherapy, local relapse, and minimal residual disease scenarios. Leveraging this integrated platform, Alfa Cytology provides end-to-end services covering the full colorectal cancer research workflow.
Colorectal cancer drug development requires model selection based on MSI/MSS status, RAS/BRAF/EGFR stratification, liver metastasis risk, immune background, and administration route. Alfa Cytology provides integrated animal study solutions, from cell line selection to model validation, for chemotherapy, small molecules, KRAS inhibitors, BRAF/EGFR combination, EGFR antibodies, ADCs, bispecifics, TCEs, CAR-T/NK, immune checkpoint inhibitors, STING, local delivery, and postoperative relapse programs.
Candidate Screening
Early screening typically requires rapid assessment of whether a candidate demonstrates in vivo antitumor signals. Alfa Cytology conducts TGI, RTV, PK/PD, and target evaluations using molecularly matched subcutaneous CDX models, providing data to support dose selection, dosing frequency, and candidate prioritization.
Clinical Relevance Studies
When programs advance to orthotopic intestinal microenvironment, liver metastasis, immunotherapy, MSS combination immunotherapy, local delivery, primary induction, or relapse/MRD stages, Alfa Cytology can further provide orthotopic models, liver metastasis models, syngeneic immunocompetent models, humanized immune models, or induced models to help clients generate evidence more aligned with clinical scenarios.
Colorectal Cancer Mechanism Research
For colorectal cancer studies, experimental design typically needs to address molecular stratification, intestinal microenvironment, liver metastasis, and immune microenvironment simultaneously. Alfa Cytology provides model development, dosing intervention, pathology testing, immunology testing, protein testing, and RNA testing services, covering MSI/dMMR, MSS/KRAS, BRAF V600E, EGFR dependence, liver metastasis, AOM/DSS inflammation-related carcinogenesis, TME remodeling, and relapse mechanisms.
In Vitro and In Vivo Layered Validation
Animal studies can evaluate whether a candidate inhibits tumor growth, local invasion, liver metastasis, or relapse; zebrafish platforms provide high-throughput in vivo screening covering tumor proliferation, intestinal colonization, liver metastatic invasion, angiogenesis, immune co-culture, and drug toxicity; cell-based experiments validate proliferation, apoptosis, migration and invasion, KRAS/BRAF/EGFR pathways, drug tolerance, target expression, and immune killing.
Molecular Mechanism Studies
Depending on program needs, we offer IHC, IF, flow cytometry, ELISA, Western blot, qPCR, RNA-seq, single-cell sequencing, TCR repertoire, ctDNA, target expression validation, immune profiling, liver tissue drug concentration, and PK/PD testing.
For clients with only a candidate drug, target direction, or preliminary mechanistic hypothesis, Alfa Cytology assists in structuring cell line selection, model pathways, group design, dosing regimens, detection endpoints, terminal sample collection, and data presentation, translating R&D questions into executable animal study protocols. Our capabilities support a broad spectrum of therapeutic modalities, including but not limited to:
| R&D Project | Cell Lines | Host System | Preferred Model | Key Endpoints |
| Early efficacy screening and dose exploration | HCT116, RKO, LoVo, DLD-1, SW480, SW620, HT29, DiFi, LIM1215, LS174T | BALB/c nude, NOD-SCID, NSG | Subcutaneous CDX | TGI, RTV, terminal tumor weight, body weight, Ki67, cleaved caspase-3, PK/PD. |
| MSI-H / dMMR efficacy and immune-related research | HCT116, RKO, LoVo | Immunodeficient mice or humanized system | MSI-H/dMMR CDX, escalation to syngeneic or humanized models for immunotherapy programs | TGI, MSI, TMB, DNA damage, PD-L1, ctDNA, immune cell infiltration. |
| MSS / KRAS pathway research | DLD-1, SW480, SW620 | BALB/c nude, NOD-SCID, NSG | MSS/KRAS CDX, orthotopic or liver metastasis model for confirmation | TGI, KRAS/MAPK pathway, pERK, pAKT, EMT, resistance markers, liver metastasis. |
| KRAS G12C programs | KRAS G12C-positive CRC cells or PDX | Project-dependent | KRAS G12C-stratified CDX, orthotopic/liver metastasis validation when needed | pERK, KRAS pathway inhibition, TGI, cetuximab combination effect, PK/PD. |
| BRAF V600E stratified therapy | RKO, HT29 | BALB/c nude, NOD-SCID, NSG | BRAF-stratified CDX, orthotopic or liver metastasis model for confirmation | TGI, pERK, pMEK, BRAF pathway, EGFR feedback, combination effect. |
| EGFR-dependent / RAS wild-type programs | DiFi, LIM1215, RAS WT background models | BALB/c nude, NOD-SCID, NSG | EGFR-dependent CDX, orthotopic validation when needed | TGI, pEGFR, pERK, cetuximab response, EGFR expression, resistance bypass. |
| Mucinous / luminal secretion and liver metastasis | LS174T, LS174T-luc | BALB/c nude, NOD-SCID, NSG | LS174T CDX, orthotopic or liver metastasis model for deeper evaluation | Mucin secretion, orthotopic burden, liver metastasis, luminal phenotype, histopathology. |
| Cecal/colonic orthotopic microenvironment | HCT116-luc, HT29-luc, LS174T-luc, SW620-luc, CT26-luc, MC38-luc | BALB/c nude, NOD-SCID, NSG; BALB/c, C57BL/6 immunocompetent mice | Human or syngeneic orthotopic model | Orthotopic tumor burden, intestinal wall invasion, BLI/IVIS, colonoscopy/ultrasound, survival. |
| Experimental liver metastasis | CT26-luc, MC38-luc, HCT116, HT29, LS174T | BALB/c, C57BL/6 immunocompetent mice; BALB/c nude, NSG | Intrasplenic or portal vein injection model | Liver metastatic nodule count, liver weight, BLI/IVIS, MRI/CT, liver pathology, survival. |
| Orthotopic spontaneous liver metastasis | CT26-luc, MC38-luc, HCT116-luc, HT29-luc, LS174T-luc | BALB/c, C57BL/6 immunocompetent mice; BALB/c nude, NSG | Cecal/colonic orthotopic model with long-term observation | Orthotopic burden, liver metastasis, peritoneal dissemination, relapse, survival. |
| Inflammation-related carcinogenesis / precancerous lesions | AOM/DSS induced model | C57BL/6 or other strains, project-dependent | AOM/DSS primary induction model | Tumor number, tumor burden, inflammation, intestinal barrier, adenoma-carcinoma transformation, immune microenvironment. |
| Immunotherapy and TME remodeling | CT26 / CT26-luc + BALB/c; MC38 / MC38-luc + C57BL/6; CMT-93 | BALB/c, C57BL/6 immunocompetent mice | Syngeneic immunocompetent model, orthotopic or liver metastasis preferred | TGI/BLI, survival, CD8/Treg, MDSC, macrophages, PD-L1, cytokines, TCR repertoire. |
| TCE / CAR-T/NK / human immune-dependent therapies | HCT116, RKO, DLD-1, HT29, DiFi, LS174T and other target-positive models | huPBMC or huHSC-reconstituted NSG/NOG mice | Humanized immune model | hCD45, hCD3, hCD8, hNK, T cell activation, cytokines, xGvHD/CRS risk. |
| Post-surgical recurrence / MRD / anti-metastatic maintenance | CT26-luc, MC38-luc, HCT116-luc, HT29-luc | Immunodeficient or immunocompetent mice (e.g., BALB/c, C57BL/6, BALB/c nude, NSG) | Orthotopic model with local resection followed by recurrence or liver metastasis follow-up | Time to recurrence, liver recurrence, peritoneal recurrence, MRD clearance, survival, ctDNA. |
For colorectal cancer programs focused on MSI/MSS stratification and liver metastasis evaluation, we configure TGI, RTV, terminal tumor weight, BLI, colonoscopy, ultrasound, survival, liver metastatic nodules, peritoneal dissemination, MSI, TMB, ctDNA, KRAS/BRAF/EGFR, pERK, and liver tissue exposure, covering orthotopic intestinal evaluation, liver metastasis monitoring, and molecular stratification.
Multimodal In Vivo Imaging
Pathology and IHC/IF Staining
TME Microenvironment and Immune Profiling
Alfa Cytology's colorectal cancer cell line panel covers MSI/MSS stratification, RAS/BRAF/EGFR molecular background, liver metastasis, intestinal orthotopic microenvironment, and immuno-oncology, enabling cell line selection and matching based on molecular stratification, metastatic pattern, target expression, and immune system requirements.
MSI-H / dMMR Representative Cell Lines
MSS / KRAS Pathway Representative Cell Lines
BRAF, EGFR-Dependent, and Mucinous Representative Cell Lines
Syngeneic Immunocompetent Representative Lines
Target and Drug Type Selection-Related Cell Lines
Alfa Cytology provides end-to-end colon cancer animal model development services, spanning model design, cell line selection, model construction, dosing intervention, efficacy evaluation, pathology, immunology, molecular mechanism testing, and PK/PD analysis. The models below represent our core capabilities across MSI-H/dMMR stratification, MSS/KRAS pathway, BRAF V600E, EGFR dependence, intestinal orthotopic microenvironment, liver metastasis, immunotherapy, humanized immunotherapy, local relapse, and minimal residual disease research. Each model can be customized to match your program's molecular stratification, treatment stage, cell line characteristics, intestinal organ microenvironment, liver metastasis requirement, immune system dependence, and R&D stage, from early screening to clinical relevance validation.
Subcutaneous Xenograft Model (CDX)
Subcutaneous CDX models typically involve inoculating human colorectal cancer cells subcutaneously into immunodeficient mice, followed by randomization and dosing once tumors reach a predetermined volume. Commonly used hosts include BALB/c nude, NOD-SCID, and NSG mice. Commonly used cell lines include HCT116, RKO, LoVo, DLD-1, SW480, SW620, HT29, DiFi, LIM1215, and LS174T.
Model characteristics
HCT116, RKO, and LoVo are suitable for MSI-H/dMMR background small molecules, cytotoxic agents, PARP combinations, ADCs, and immune-related mechanism early screening. DLD-1, SW480, and SW620 are suitable for MSS/KRAS, chemotherapy combinations, small molecule inhibitors, resistance, and invasion/metastasis background early screening. RKO and HT29 are suitable for BRAF V600E and MAPK pathway programs; DiFi and LIM1215 are suitable for EGFR-dependent programs; LS174T is suitable for mucinous type and liver metastasis direction. This model has high standardization and good reproducibility, suitable for early screening and PK/PD research; its limitations are the lack of intestinal orthotopic microenvironment, intestinal wall invasion, luminal factors, local lymphatic drainage, and liver metastasis cascade.
Modeling and dosing timelines
Conventional inoculation typically reaches enrollment volume within 1–3 weeks, with randomization commonly performed at tumor volumes of approximately 80–150 mm³. The conventional treatment period is 2–4 weeks. For resistance, withdrawal rechallenge, long-term maintenance, or combination therapy, this can be extended to 4–8 weeks. Small molecules can be dosed daily or every other day; chemotherapy can be dosed cyclically; antibodies, ADCs, and bispecifics require dosing intervals based on half-life, target expression, and tolerance.
Detection endpoints
Recommended positive controls
5-FU at 20–50 mg/kg IP, 1–3 times weekly; oxaliplatin at 5–10 mg/kg IP or IV, once weekly; irinotecan at 20–50 mg/kg IP, 1–2 times weekly; capecitabine can be designed with an oral cyclic dosing approach. Cetuximab as an EGFR-dependent/RAS wild-type reference. BRAF V600E can reference encorafenib combined with cetuximab and mFOLFOX6; KRAS G12C can reference adagrasib combined with cetuximab; fruquintinib as a later-line therapy reference.
Cecal/Colonic Orthotopic Model
Human orthotopic models commonly use HCT116-luc, HT29-luc, LS174T-luc, or SW620-luc, inoculating cells or small tumor fragments into the cecal or colonic wall. CT26-luc, MC38-luc, and CMT-93 can be used for cecal/colonic orthotopic models in immunocompetent backgrounds.
Model characteristics
Human orthotopic models are suitable for studying intestinal organ microenvironment, local invasion, postoperative relapse, and spontaneous liver metastasis. CT26 is suitable for rapid immune validation in BALB/c background, and MC38 is suitable for immunotherapy and mechanism research in C57BL/6 background. This model has complex surgery, lower throughput, and greater inter-batch variability, and is not suitable as a first-round rapid ranking platform for multiple candidates.
Modeling and dosing timelines
Orthotopic models typically form monitorable burden within 1–3 weeks after modeling. The conventional treatment period is 2–6 weeks. If studying spontaneous liver metastasis, postoperative relapse, or long-term maintenance therapy, follow-up should be extended. Treatment can begin after BLI/IVIS confirmation of orthotopic tumors, or after orthotopic tumor burden reaches a predetermined level, followed by surgical treatment or local therapy.
Detection endpoints
Recommended positive controls
5-FU, oxaliplatin, and irinotecan can serve as orthotopic model chemotherapy references. EGFR-dependent/RAS wild-type orthotopic programs can set cetuximab-related references. Syngeneic orthotopic models can set anti-PD-1, anti-PD-L1, anti-CTLA-4, or STING-related references.
Experimental Liver Metastasis Model
Experimental liver metastasis models typically use intrasplenic injection, portal vein injection, or splenectomy combined with tumor cell injection to preferentially form metastases in the liver. Commonly used models include CT26-luc, MC38-luc, HCT116, HT29, and LS174T.
Model characteristics
Suitable for liver colonization, liver-targeted delivery, anti-adhesion, anti-microenvironment remodeling, and advanced liver metastasis research. This model has a relatively high success rate and shorter cycle, but mainly addresses the liver colonization process.
Detection endpoints
Liver metastatic nodule count, liver weight, BLI/IVIS, MRI/CT, liver tissue HE, Ki67, apoptosis, immune infiltration, and survival.
Recommended positive controls
5-FU, oxaliplatin, irinotecan, and fruquintinib can be set as systemic therapy references based on program; EGFR or BRAF stratified programs should set corresponding combination references based on molecular background.
Orthotopic Spontaneous Liver Metastasis Model
Orthotopic spontaneous liver metastasis models first establish cecal/colonic orthotopic tumors, then observe liver dissemination. Liver relapse and peritoneal relapse can continue to be followed after primary lesion resection. Commonly used models include CT26-luc, MC38-luc, HCT116-luc, HT29-luc, and LS174T-luc.
Model characteristics
Suitable for primary lesion to liver metastasis full-process, postoperative relapse, anti-metastasis maintenance, and long-term therapy research. This model is closer to the clinical process but has longer cycles and greater variability, with higher requirements for surgical consistency, in vivo imaging, and long-term follow-up.
Detection endpoints
Orthotopic tumor burden, liver metastatic nodule count, peritoneal dissemination, liver weight, BLI/IVIS, survival, liver tissue pathology, and metastasis-related markers.
Recommended positive controls
5-FU, oxaliplatin, or irinotecan can be split based on FOLFOX/FOLFIRI framework. EGFR-dependent, BRAF V600E, or KRAS G12C programs can set targeted agent combination maintenance references based on molecular background. Syngeneic orthotopic relapse models can set anti-PD-1, anti-CTLA-4, or immune combination strategies.
AOM/DSS Primary Induction Model
The AOM/DSS model typically uses azoxymethane to induce mutations, followed by DSS to promote intestinal inflammation and carcinogenesis, forming an inflammation-related colorectal cancer model. The experimental cycle is typically 8–14 weeks or longer, depending on DSS cycle number, animal strain, sex, housing conditions, and research objectives.
Model characteristics
Suitable for inflammation-related carcinogenesis, premalignant lesions, long-term intervention, and chemoprevention research, as well as studying the "inflammation-adenoma-carcinogenesis" continuum, intestinal immune microenvironment, and long-term preventive intervention. This model has long cycles and low throughput, and is not suitable as a rapid ranking model for multiple candidates.
Detection endpoints
Body weight, hematochezia, disease activity index, colon length, tumor count, tumor burden, inflammation score, adenoma-carcinoma ratio, Ki67, inflammatory cytokines, intestinal barrier, and immune cell infiltration.
Recommended positive controls
Prevention and anti-inflammatory directions can set 5-ASA, NSAID, or anti-inflammatory mechanism references; anti-tumor directions can add 5-FU or other candidate drugs based on program.
Syngeneic Subcutaneous Model
CT26, MC38, and CMT-93 can establish syngeneic subcutaneous models in matched strains. CT26 pairs with BALB/c, MC38 pairs with C57BL/6, and CMT-93 can serve as a supplementary resource. Randomization occurs when tumor volume reaches approximately 50–100 mm3, with a treatment period of typically 10–21 days.
Model characteristics
Suitable for immune checkpoint, STING, cytokines, radiotherapy combination, and early immune screening. Immunotherapy programs need to cover a sufficient immune response window.
Detection endpoints
Tumor volume, TGI, survival, body weight, flow cytometry immune profiling, CD8/Treg, MDSC, macrophages, PD-L1, cytokines, and IHC/IF.
Recommended positive controls
anti-PD-1, anti-PD-L1, anti-CTLA-4, STING agonists, radiotherapy combination, and cytokine strategies can be set according to program mechanism. Antibody doses typically start at 100–200 μg/mouse IP, twice weekly or once every 3 days, for 2–3 consecutive weeks.
Syngeneic Orthotopic and Liver Metastasis Model
CT26-luc or MC38-luc can be used for syngeneic cecal/colonic orthotopic models, or establish syngeneic liver metastasis models via intrasplenic or portal vein injection.
Model characteristics
Suitable for immunotherapy, local therapy, TME remodeling, postoperative relapse, and liver metastasis research. For colorectal cancer immunotherapy programs, syngeneic orthotopic or liver metastasis models have greater translational value than syngeneic subcutaneous models. Their limitation is that murine tumors differ from human colorectal cancer in targets, mutations, and heterogeneity.
Detection endpoints
Orthotopic burden, liver metastasis, survival, flow cytometry immune profiling, single-cell sequencing, TCR repertoire, cytokines, tumor tissue immunohistochemistry, and intrahepatic immune microenvironment.
Recommended positive controls
anti-PD-1, anti-PD-L1, anti-CTLA-4, STING agonists, radiotherapy combination, and cytokine strategies can be set according to program mechanism. Antibody doses typically start at 100–200 μg/mouse IP, twice weekly or once every 3 days, for 2–3 consecutive weeks.
huPBMC Model
The huPBMC model establishes a short-term human immune effector environment by infusing human peripheral blood mononuclear cells into immunodeficient mice, combined with human colorectal cancer cell lines. Recommended cells include HCT116, RKO, DLD-1, HT29, DiFi, and LS174T.
Model characteristics
Suitable for TCE, bispecific antibodies, CAR-T/NK, human cytokines, and ADCs or antibody programs highly dependent on human immune effects. This model has high cost, long cycles, significant donor variability, and carries xGvHD or cytokine release risk.
Detection endpoints
hCD45, hCD3, hCD4, hCD8, hNK, T cell activation, tumor infiltration, IFN-γ, TNF-α, IL-6, Granzyme B, tumor burden, body weight, CRS, and xGvHD risk markers.
Recommended positive controls
anti-human PD-1, anti-human PD-L1, or anti-human CTLA-4 can serve as mechanism references. TCE, CAR-T, or CAR-NK programs should include target-positive, low/negative, effector cell, and empty vector/irrelevant TCE controls. Cell therapy doses are often designed on the order of 106–107 cells/mouse.
huHSC Model
The huHSC model reconstructs a relatively long-term human immune system via human hematopoietic stem cells, suitable for complex combination therapy, human immune cell differentiation, sustained immune activation, and immune resistance research.
Model characteristics
Suitable for long-cycle TCE, CAR-T/NK, bispecifics, immune resistance, and complex TME mechanism validation. This model has high cost, long cycles, significant donor variability, and carries xGvHD or cytokine release risk; it is not recommended as a first-round screening platform.
Detection endpoints
Human immune reconstitution ratio, T/B/NK/myeloid cell spectrum, tumor infiltration, cytokines, human immune checkpoint expression, tumor burden, survival, and major organ pathology.
Recommended positive controls
anti-human PD-1, anti-human PD-L1, or anti-human CTLA-4 can serve as mechanism references. TCE, CAR-T, or CAR-NK programs should include target-positive, low/negative, effector cell, and empty vector/irrelevant TCE controls. Cell therapy doses are often designed on the order of 106–107 cells/mouse.
Relapse and Minimal Residual Disease Model
Relapse and MRD models are typically based on CT26-luc, MC38-luc, HCT116-luc, or HT29-luc cecal/colonic orthotopic models, first establishing monitorable orthotopic tumor burden, followed by local resection, debulking, or short-course therapy. Liver relapse, peritoneal relapse, and local relapse are followed after primary lesion resection.
Model characteristics
Suitable for simulating postoperative minimal residual disease and metastatic relapse processes, with preoperative therapy, postoperative adjuvant therapy, perioperative combination therapy, or maintenance therapy setups. This model has strong clinical mapping but is technically complex with longer cycles and high requirements for postoperative care and local resection consistency; it is not suitable for early large-scale screening.
Modeling and dosing timelines
First establish orthotopic tumor burden and confirm the window by BLI/IVIS, colonoscopy, or local pathology. Local resection, debulking, or primary lesion control can be performed based on program. Postoperative observation continues for 2–8 weeks or longer, recording local relapse, liver metastasis, peritoneal dissemination, survival, and ctDNA.
Detection endpoints
Recommended positive controls
5-FU, oxaliplatin, or irinotecan can serve as postoperative adjuvant and perioperative therapy references. EGFR-dependent, BRAF V600E, or KRAS G12C programs can set targeted agent combination maintenance references based on molecular background. Syngeneic orthotopic relapse models can set anti-PD-1, anti-CTLA-4, or immune combination strategies.
By Molecular Stratification
By Drug Type
By Research Objective
By Route of Administration
By Development Pathway
Consensus Molecular Subtype (CMS) & Driver Modeling
Colorectal cancer exhibits marked heterogeneity governed by genomic instability (MSI-H vs. MSS) and Consensus Molecular Subtypes (CMS1–CMS4). Alfa Cytology designs tailored evaluation pathways based on core drivers (KRAS, BRAF, PIK3CA, APC/Wnt) and mismatch repair status, avoiding cross-subtype misinterpretation.
Stratified Cell Line & Syngeneic Directory
Model selection dictates therapeutic responsiveness to targeted agents and immunotherapies. Alfa Cytology helps clients match optimal systems, such as HCT116, HT-29, SW480, CT26, and MC38, based on MSI/MSS status, KRAS/BRAF mutations, and immunocompetence.
Orthotopic Cecal & Liver Metastasis Models
Flank subcutaneous models cannot replicate bowel wall microarchitecture, mesenteric lymphatic drainage, or hepatic tropism. Alfa Cytology helps clients generate clinical-correlative evidence through orthotopic cecal wall injection and portal vein/hemisplenic liver metastasis models.
Target Validation & Integrated PK/PD Workflows
Programs targeting EGFR, mutant KRAS, VEGF, or immune checkpoints in MSS disease require precise microenvironment profiling. Alfa Cytology configures target expression verification, liver metastatic burden quantification, and integrated PK/PD workflows to track deep tumor response.
Alfa Cytology is a global leader in colorectal cancer translational research, delivering integrated animal model solutions that span MSI/MSS and RAS/BRAF/EGFR stratification, orthotopic intestinal microenvironment, liver metastasis, immunotherapy, and relapse/MRD evaluation. If you are interested in our services, please don't hesitate to contact us to learn how we can accelerate your colorectal cancer drug development.
Reference
For research use only.
Alfa Cytology, a preclinical research solution provider, provides its clients with one-stop solutions to accelerate cancer therapeutics discovery and development.
Copyright © 2026 Alfa Cytology. All rights reserved.
