Cutaneous squamous cell carcinoma

Que, Syril Keena T.; Zwald, Fiona O.; Schmults, Chrysalyne D.

doi:10.1016/j.jaad.2017.08.059

Cited by 523 publications

(286 citation statements)

References 62 publications

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“…Cutaneous squamous cell carcinoma (CSCC), a malignant tumor, is most effectively known for arising in keratinocytes (40). Currently, CSCC is widely considered as one of the most common skin cancers, secondary only to basal-cell carcinoma and represents between 20%-50% of all known skin cancers worldwide (10,16,41). Although most CSCC lesions can be successfully removed with surgical excision, there are subsets of lesions that metastasize, leading to both a severe morbidity and mortality rate.…”

Section: Introductionmentioning

confidence: 99%

Specific knockdown of HOXB7 inhibits cutaneous squamous cell carcinoma cell migration and invasion while inducing apoptosis via the Wnt/β-catenin signaling pathway

Gao

Chen

2018

American Journal of Physiology-Cell Physiology

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Metastatic cutaneous squamous cell carcinoma (CSCC) is a major cause of death associated with non-melanoma skin cancer. The involvement of homeobox B7 (HOXB7) in cancers has been reported. Thus, the current study intends to explore the effect of HOXB7 on CSCC and its relationship with the Wnt/β-catenin signaling pathway. Initially, microarray-based gene expression profiling of CSCC was performed and HOXB7 was identified as an upregulated gene based on the microarray data of GSE2068. Following this, the experimental results indicated that HOXB7 and β-catenin formed a composite, demonstrating that endogenous HOXB7 binds to β-catenin. Subsequently, CSCC cells were treated with siRNA against HOXB7 or inhibitor of Wnt/β-catenin signaling pathway (IWR-1) in order to analyze any underlying regulatory mechanism of HOXB7 on the CSCC cells. Tumor growth involving xenografts in nude mice was also observed so as to explore whether or not HOXB7 could regulate subcutaneous tumor growth through in vivo culturing. In order to investigate the potential effects of HOXB7 on the Wnt/β-catenin signaling pathway, we determined the expression of HOXB7 and downstream genes of the Wnt/β-catenin signaling pathway. Notably, siRNA-mediated knockdown of HOXB7 inhibited the activation of the Wnt/β-catenin signaling pathway, thereby impeding the progression of cell viability, migration, and invasion as well as of the tumor growth, while contrarily facilitating cell apoptosis. Taken together, silencing of the HOXB7 has the mechanism of inactivating the Wnt/β-catenin signaling pathway, thereby accelerating cell apoptosis and suppressing cell migration and invasion in CSCC, which could provide a candidate target for the CSCC treatment.

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Section: Introductionmentioning

confidence: 99%

Specific knockdown of HOXB7 inhibits cutaneous squamous cell carcinoma cell migration and invasion while inducing apoptosis via the Wnt/β-catenin signaling pathway

Gao

Chen

2018

American Journal of Physiology-Cell Physiology

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“…With respect to the former, older age, male sex, fair skin, immunosuppression, and a previous history of actinic keratosis (AK) are of known importance. Chronic sun exposure is the most important and well-known environmental factor associated with CSCC [9][10][11][12][13][14]. Solid-organ transplant recipients, who have a human papillomavirus infection or chronic lymphocytic leukemia, have a higher risk of developing CSCC than the general population [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Cutaneous Squamous Cell Carcinoma: From Biology to Therapy

Corchado-Cobos

García-Sancha

González-Sarmiento

et al. 2020

IJMS

110

111

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Cutaneous squamous cell carcinoma (CSCC) is the second most frequent cancer in humans and its incidence continues to rise. Although CSCC usually display a benign clinical behavior, it can be both locally invasive and metastatic. The signaling pathways involved in CSCC development have given rise to targetable molecules in recent decades. In addition, the high mutational burden and increased risk of CSCC in patients under immunosuppression were part of the rationale for developing the immunotherapy for CSCC that has changed the therapeutic landscape. This review focuses on the molecular basis of CSCC and the current biology-based approaches of targeted therapies and immune checkpoint inhibitors. Another purpose of this review is to explore the landscape of drugs that may induce or contribute to the development of CSCC. Beginning with the pathogenetic basis of these drug-induced CSCCs, we move on to consider potential therapeutic opportunities for overcoming this adverse effect.

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“…Each sample was analyzed and registered the following histopathologic features using hematoxylin‐eosin stained slides: maximum diameter, tumor thickness (dichotomized as ≤6 mm or >6 mm; none lower than 2 mm), anatomic level (Clark's level), histopathologic degree of differentiation classified as well differentiated, moderately differentiated, and poorly differentiated, presence of desmoplasia, perineural or perivascular invasion, and the presence and number of tumor budding. Tumor budding is defined as the presence of either isolated single cells or small cell clusters (≤4) scattered in the stroma ahead of the invasive tumor front.…”

Section: Methodsmentioning

confidence: 99%

“…Cutaneous squamous cell carcinoma (cSCC) is the second most common malignancy of the skin after basal cell carcinomas, with an estimated annual incidence of 700 000 cases in the United States . There are high geographic and racial variations in the incidence of cSCC, ranging in Europa from 5‐9 to 68‐96 per 100 000 inhabitants to 291‐499 per 100 000 in Australia …”

Section: Introductionmentioning

confidence: 99%

Correlation of focal adhesion kinase expression with nodal metastasis in patients with head and neck cutaneous squamous cell carcinoma

et al. 2018

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Background Focal adhesion kinase (FAK) and cortactin overexpression is frequently detected in a variety of cancers, and has been associated with poor clinical outcome. However, there are no data in cutaneous squamous cell carcinoma (cSCC). Objective To investigate the relationship of FAK and cortactin expression with the clinicopathologic features and the impact on the prognosis of cSCC patients. Methods FAK and cortactin expression was analyzed by immunohistochemistry on paraffin‐embedded tissue samples from 100 patients with cSCC, and correlated with the clinical data. Results FAK overexpression was a significant risk factor for nodal metastasis with crude and adjusted ratios (HRs) of 2.04, (95% CI [1.08‐3.86], [P = 0.029]) and 2.23 (95% CI [1.01‐4.91], [P = 0.047]), respectively. Cortactin expression was not a significant risk factor for nodal metastasis. Conclusion These findings demonstrate that FAK overexpression is an independent predictor of nodal metastasis that might be helpful for risk stratification and management of patients with cSCC.

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Cutaneous squamous cell carcinoma

Cited by 523 publications

References 62 publications

Specific knockdown of HOXB7 inhibits cutaneous squamous cell carcinoma cell migration and invasion while inducing apoptosis via the Wnt/β-catenin signaling pathway

Specific knockdown of HOXB7 inhibits cutaneous squamous cell carcinoma cell migration and invasion while inducing apoptosis via the Wnt/β-catenin signaling pathway

Cutaneous Squamous Cell Carcinoma: From Biology to Therapy

Correlation of focal adhesion kinase expression with nodal metastasis in patients with head and neck cutaneous squamous cell carcinoma

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