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Colorectal Cancer (CRC)

Colorectal cancer (CRC) is a significant global health concern, accounting for a substantial number of cancer-related deaths. By combining our expertise in rare disease therapy development and animal model generation, our company is committed to advancing the field of colorectal cancer research and providing high-quality rectal cancer drug and therapy development services.

Overview of Colorectal Cancer (CRC)

Colorectal cancer, also known as colon cancer, bowel cancer, or rectal cancer, is a malignant tumor that develops in the colon or rectum. The colon and rectum are part of the large intestine and play vital roles in digestion and waste elimination. The incidence of CRC is about 35.7/100 000. CRC typically originates from the inner lining of the colon or rectum, and if left untreated, it can invade surrounding tissues and metastasize to other organs.

Pathogenesis of Colorectal Cancer (CRC)

  • One crucial aspect of CRC pathogenesis is the presence of microsatellite instability (MSI). MSI occurs due to defects in DNA mismatch repair genes, leading to the accumulation of mutations in repetitive DNA sequences. This phenomenon can be used as a diagnostic marker for CRC.
  • Aberrant DNA methylation known as CpG island methylator phenotype (CIMP) plays a role in CRC pathogenesis. CIMP involves DNA hypermethylation at promoter CpG islands, leading to the silencing of tumor-suppressor genes.
Fig.1 Colorectal adenoma-carcinoma sequence.Fig.1 Colorectal adenoma-carcinoma sequence. (Nguyen Ha Thi, et al., 2018)

Targeted Therapy Development of Colorectal Cancer (CRC)

Epidermal Growth Factor Receptor (EGFR)

Epidermal growth factor receptor signaling plays a critical role in promoting cell growth and survival. Targeting EGFR with monoclonal antibodies, such as cetuximab and panitumumab, has shown efficacy in selected CRC patients.

Vascular Endothelial Growth Factor (VEGF)

Angiogenesis, the formation of new blood vessels, is crucial for tumor growth and metastasis. Inhibiting VEGF, either with monoclonal antibodies like bevacizumab or small molecule inhibitors like regorafenib, has demonstrated benefits in advanced CRC.

BRAF and KRAS

Mutations in the BRAF and KRAS genes are commonly found in CRC and can impact therapeutics response. BRAF mutations are associated with poor prognosis, while KRAS mutations are associated with resistance to certain therapies. Targeted therapies against these mutations are being actively researched.

Immune Checkpoint Inhibitors

Immunotherapy, specifically immune checkpoint inhibitors such as pembrolizumab and nivolumab, have shown promising results in CRC patients with high microsatellite instability (MSI-H) or mismatch repair deficiency (dMMR). These inhibitors unleash the body's immune system to attack cancer cells.

Fig.2 Pathways offering potential sites for CRC targeted therapy.Fig.2 Pathways offering potential sites for CRC targeted therapy. (Xie Yuan-Hong, et al., 2020)

Our Services

With a comprehensive understanding of the pathogenesis of colorectal cancer, the identification of key targets, and the application of various therapy modalities, we are inching closer to the development of personalized and precise therapies for colorectal cancer. Our company is committed to CRC diagnostics and therapy development services, providing one-stop solutions to global pharmaceutical companies.

Therapy Development Platforms

Animal Models of Colorectal Cancer (CRC)

Our company offers comprehensive animal model development services, including the generation of genetically engineered mouse models (GEMMs) with specific CRC-associated mutations, patient-derived xenograft (PDX) models, and chemically induced models. These models enable us to test the efficacy and safety of potential therapies, optimize therapeutic regimens, and accelerate the development of personalized therapeutics approaches.

Chemical Induction Models
At our company, we offer comprehensive chemical induction model development services for CRC research. For instance, the azoxymethane (AOM) and dextran sulfate sodium (DSS) model is a widely used chemical induction model for CRC. AOM, a DNA-damaging agent, is administered to initiate tumor formation, while DSS, an inflammatory agent, promotes tumor growth and progression. 
Optional Models
  • 3,2′-Dimethyl-4-Aminobiphenyl (DMAB) Induced Models
  • N-Methyl-N-Nitrosourea (MNU) Induced Models
  • N-Methyl-N-Nitrosoguanidine (MNNG) Induced Models
  • 1,2-Dimethylhydrazine (DMH) Induced Models
  • Azoxymethane (AOM) Induced Models
  • Dextran-Sodium Sulfate Model (DSS) Induced Models
  • 2-Amino-1-Methyl-6-Phenylimidazo (4,5-b) Pyridine (PhIP) Induced Models
  • Adenomatous Polyposis Mouse Models (APC) Induced Models
Genetically Engineered Models
By manipulating specific genes associated with CRC development and progression, we can create models that faithfully recapitulate human disease. One such model is the Adenomatous Polyposis Mouse Model (APC), which involves the mutation of the APC gene, a key regulator of cellular processes. The APCMin mouse model, a widely studied variant, develops adenomas resembling human colorectal cancer. 
Xenograft and Syngeneic Models
Xenograft and syngeneic models involve the transplantation of human tumor cells or grafts into animals, enabling the study of tumor development, progression, and response to treatments. At our company, we offer comprehensive xenograft and syngeneic model development services for CRC research.
Optional Species Mice, Rats, Others

In addition to the aforementioned model development services, our company also offers a range of other custom model development services for CRC research. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.

References

  • Nguyen, Ha Thi, and Hong‑Quan Duong. "The molecular characteristics of colorectal cancer: Implications for diagnosis and therapy." Oncology letters 16.1 (2018): 9-18.
  • Xie, Yuan-Hong, Ying-Xuan Chen, and Jing-Yuan Fang. "Comprehensive review of targeted therapy for colorectal cancer." Signal transduction and targeted therapy 5.1 (2020): 22.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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