Cutaneous squamous cell carcinoma (CSCC), also referred to as squamous-cell skin cancer or squamous-cell carcinoma of the skin, is a prevalent form of skin cancer originating from the squamous cells located in the outermost layer of the skin. Our company is deeply dedicated to offering state-of-the-art services in drug and therapy development specifically tailored for CSCC.
Overview of Cutaneous Squamous Cell Carcinoma
Cutaneous squamous cell carcinoma (CSCC) is a malignant tumor originating from the squamous cells of the skin. These cells, located in the outermost layer of the skin, are crucial for its protection and regeneration. CSCC typically manifests in sun-exposed areas such as the face, ears, lips, and back of the hands. It can also develop in previously damaged or scarred regions. The incidence of CSCC in situ is approximately 72 cases per 100,000 person-years in women and 68 cases per 100,000 person-years in men.
Molecular Basis of Cutaneous Squamous Cell Carcinoma
The development and progression of CSCC involve complex molecular mechanisms. UV radiation-induced DNA damage leads to the accumulation of mutations in key genes involved in cell cycle regulation, DNA repair, and tumor suppression. These mutations contribute to the dysregulation of cellular processes, leading to uncontrolled growth and invasion of CSCC cells.
Genomic studies have identified recurrent mutations in genes such as TP53, FAT1, NOTCH1, and HRAS in CSCC. These mutations disrupt critical signaling pathways involved in cell proliferation, differentiation, and apoptosis. Additionally, alterations in the expression of microRNAs and long non-coding RNAs have been associated with CSCC development.
Fig. 1 Overview of cutaneous squamous cell carcinoma. (Basurto-Lozada P.,
et al., 2021)
Targets of Cutaneous Squamous Cell Carcinoma Therapy
EGFR
Epidermal growth factor receptor (EGFR) is overexpressed in a significant number of CSCC cases, making it an attractive target for therapy.
MAPK Pathway
Activation of the MAPK pathway, primarily through mutations in the RAS and RAF genes, is observed in CSCC. Inhibiting this pathway can disrupt tumor growth and survival.
Hedgehog Signaling Pathway
Aberrant activation of the Hedgehog signaling pathway has been implicated in CSCC. Targeting this pathway can inhibit tumor growth and progression.
Therapies of Cutaneous Squamous Cell Carcinoma
- Targeted Therapy
Targeted therapies aim to selectively inhibit the molecular targets that drive CSCC growth and survival. For example, targeting the EGFR pathway with inhibitors such as cetuximab or panitumumab has shown promising results in trials for CSCC. These agents block the activation of EGFR, leading to reduced proliferation and survival of CSCC cells. Other targeted therapies under investigation include inhibitors of the MAPK pathway, Hedgehog pathway, and immune checkpoint proteins.
- Immunotherapy
Immunotherapy has revolutionized the therapeutics landscape for various cancers, including CSCC. One of the most promising immunotherapy strategies is the use of immune checkpoint inhibitors that target proteins such as PD-1 and PD-L1. These inhibitors, including cemiplimab, have shown remarkable efficacy in treating advanced CSCC. By blocking the interaction between PD-1 and PD-L1, immune checkpoint inhibitors unleash the immune system to attack CSCC cells.
Our Services
At our company, we are dedicated to providing comprehensive diagnostics and therapy development services for cutaneous squamous cell carcinoma (CSCC). Our expertise in the field of rare diseases and pharmaceutical research allows us to offer tailored solutions for CSCC.
Therapy Development Platforms
Animal Models of Cutaneous Squamous Cell Carcinoma
We conduct rigorous preclinical studies to evaluate the efficacy and safety of potential CSCC therapies. Our experts collaborate with leading research institutions to develop relevant animal models that recapitulate the characteristics of CSCC.
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Induction Model Development |
| Our company provides comprehensive induction model development services that allow researchers to simulate and study the initiation and promotion phases of CSCC. By employing established protocols such as the DMBA/TPA model, we can induce CSCC-like lesions in animal subjects. This model involves the application of the carcinogen dimethylbenz(a)anthracene (DMBA) followed by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), which mimics the stages of tumor formation in human skin. |
| Optional Carcinogens |
- dimethylbenz(a)anthracene (DMBA)
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- 12-O-tetradecanoylphorbol-13-acetate (TPA)
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| Genetic Engineering Model Development |
| Utilizing advanced techniques such as knockout mouse technology, we can selectively disable TP53 in animal models, thereby studying the impact of its loss on CSCC development. Studies have shown that TP53 loss contributes to malignant progression in CSCC. Our company's expertise in genetic engineering enables precise targeting of tumor-suppressor ablation to specific cell subsets, facilitating a comprehensive understanding of the pathways involved in CSCC initiation and progression. |
| Optional Species |
Mouse, Rat, Non-human primates, Others |
In addition, we also provide other customized animal models to meet diverse needs. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.
References
- Corchado-Cobos R., et al. "Cutaneous squamous cell carcinoma: from biology to therapy." International journal of molecular sciences 21.8 (2020): 2956.
- Combalia A., and Carrera C., "Squamous cell carcinoma: an update on diagnosis and treatment." Dermatology Practical & Conceptual 10.3 (2020).
All of our services and products are intended for preclinical research use
only and cannot be used to diagnose, treat or manage patients.
