Basal-cell carcinoma

Basal-cell carcinoma (BCC), also known as basal-cell cancer, is the most common type of skin cancer. It often appears as a painless raised area of skin, which may be shiny with small blood vessels running over it. It may also present as a raised area with ulceration. Basal-cell cancer grows slowly and can damage the tissue around it, but it is unlikely to spread to distant areas or result in death. Risk factors include exposure to ultraviolet light, having lighter skin, radiation therapy, long-term exposure to arsenic and poor immune-system function. Exposure to UV light during childhood is particularly harmful. Tanning beds have become another common source of ultraviolet radiation. Diagnosis often depends on skin examination, confirmed by tissue biopsy. It remains unclear whether sunscreen affects the risk of basal-cell cancer. Treatment is typically by surgical removal. This can be by simple excision if the cancer is small; otherwise, Mohs surgery is generally recommended. Other options include electrodesiccation and curettage, cryosurgery, topical chemotherapy, photodynamic therapy, laser surgery or the use of imiquimod, a topical immune-activating medication. In the rare cases in which distant spread has occurred, chemotherapy or targeted therapy may be used. Basal-cell cancer accounts for at least 32% of all cancers globally. Of skin cancers other than melanoma, about 80% are basal-cell cancers. In the United States, about 35% of white males and 25% of white females are affected by BCC at some point in their lives. Basal-cell carcinoma is named after the basal cells that form the lowest layer of the epidermis. It is thought to develop from the folliculo–sebaceous–apocrine germinative cells called trichoblasts (of note, trichoblastic carcinoma is a term sometimes used to refer to a rare type of aggressive skin cancer that may resemble a benign trichoblastoma, and can also closely resemble basal cell carcinoma). Individuals with a basal-cell carcinoma typically present with a shiny, pearly skin nodule.

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Elucidating the role of lymphatic vessels within the tumor microenvironment of breast cancer

Ingrid Maria van Mier

Breast cancer is the most common cancer in women worldwide, with an estimated 1.7 million newly diagnosed cases in 2012. Despite the many clinical manifestations, metastatic disease is the main cause of death, and is responsible for 90% of all breast cancer-related deaths. Aggressive carcinomas of the breast preferentially spread via the lymphogenous route, and often co-opt and actively remodel the lymphatic vasculature in order to invade and metastasize to their draining lymph nodes (LNs) and, ultimately, to distant organs. Indeed, expression of vascular endothelial growth factor (VEGF)-C, the principal lymphangiogenic growth factor, by the tumor or recruited ancillary cells has been shown to correlate both with LN and distant metastasis, and shorter overall survival (OS), and LN status represents an important prognostic factor for patients diagnosed with breast cancer. Although traditionally considered as passive conduits that solely mediate tumor cell escape, more recent research aimed at discerning the interactions between the developing tumor and its associated lymphatic vessels has revealed that the lymphatic vasculature actively promotes lymphogenous metastasis of invasive tumor cells. Likewise, collaborative interactions between tumor cells and a multitude of other tissue-resident and recruited ancillary cells, which together constitute the tumor microenvironment, not only coercively contribute to tumor growth, progression and metastasis, but also suggest that interactions among primed stromal cells themselves may be important in the process of metastatic dissemination as well. Notably, expansion of tumor-associated lymphatic vessels in the tumor periphery leads to increased lymphatic drainage from the tumor to the tumor-draining LN, and interstitial flow-induced mechanical changes may alter tensional homeostasis within the tumor through stimulation of local fibroblasts that remodel and stiffen the extracellular matrix (ECM). Furthermore, VEGF-C-induced remodeling of the tumor-associated lymphatic vasculature has been shown to directly suppress the anti-tumor immune response, thereby promoting tolerance to the nascent tumor. Thus, to explore whether tumor-associated lymphatic vessels promote tumor metastasis not only via interactions with the incipient tumor, but also through cross-talk with the surrounding stromal cells, the different components of the tumor microenvironment, specifically tensional homeostasis and anti-tumor immunity, were evaluated upon modulation of lymphatic vessel growth in various experimental models of breast cancer. Accordingly, inhibition of VEGFR-3-mediated signaling upon administration of an antagonistic antibody in a genetically engineered preclinical mouse model specifically reduced the number of lymphatic endothelial cells (LECs) in the tumor, whereas conversely, orthotopic inoculation of a stable murine breast cancer cell line with enhanced expression of VEGF-C induced an expansion of the lymphatic endothelium. Although either experimental approach affected either regional or distant metastatic dissemination of the primary tumor to LN or the lungs, respectively, these effects did not seem to be mediated by interactions of the tumor-associated lymphatic vasculature with the tumor microenvironment in these particular experimental models.

EPFL2017

Mathematical modeling of the re-epithelialization of a 3 dimensional (3d) human skin equivalent

Raphaelle Luisier

Re-epithelialization is the dominant mode of healing in partial thickness wounds. In order to develop better strategies to monitor such wound healing, 3D HSE models and mathematical models have long been utilized to improve our understanding of epidermis formation and re-epithelialization. Using both approaches we endeavoured to generate two mathematical models of epidermis formation and one mathematical model of wound closure based on in vitro studies of epithelialization of 3D HSE models and re-epithlialization of wounded HSE models. We used immunohistochemistry to evaluate keratinocyte proliferation, differentiation and migration. The mathematical models investigated first the role of nutrient concentration (simple model of epidermis formation) and the concurrent roles of ATP, nutrient and calcium concentrations (improved model) in epidermis formation and homeostasis, to eventually lead to a two-dimensional model of wound closure. The 3D HSE model presented similar histology and immunohistochemistry as that of native skin after 11 days of culture. A complete differentiated epidermis filled the wound by day 14 after injury. Finally the contribution of basal cell proliferation in the neoepithelium has been demonstrated during wound closure. The improved mathematical model of epidermis formation produced reasonable representations with a complex cell layer dynamic, while the initial mathematical model presented the potential role of nutrient concentration in determining epidermis thickness. The model of wound closure further illustrated the critical role of nutrient concentration in the process of re-epithelialisation. The major drawback of existing wound closure models is that they neglect the differentiation and stratification; the models developed in this project innovatively integrates by both the second dimension and differentiation, and could consequently bring more insights into the regulation of epidermis homeostasis and wound repair

2009

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Basal-cell carcinoma

Cutaneous squamous-cell carcinoma

Cutaneous squamous-cell carcinoma (cSCC), or squamous-cell carcinoma of the skin, also known as squamous-cell skin cancer, is, with basal-cell carcinoma and melanoma, one of the three principal types of skin cancer. cSCC typically presents as a hard lump with a scaly top layer, but it may instead form an ulcer. Onset often occurs over a period of months. Cutaneous squamous-cell carcinoma is more likely to spread to distant areas than basal cell cancer.

Actinic keratosis

Actinic keratosis (AK), sometimes called solar keratosis or senile keratosis, is a pre-cancerous area of thick, scaly, or crusty skin. Actinic keratosis is a disorder (-osis) of epidermal keratinocytes that is induced by ultraviolet (UV) light exposure (actin-). These growths are more common in fair-skinned people and those who are frequently in the sun. They are believed to form when skin gets damaged by UV radiation from the sun or indoor tanning beds, usually over the course of decades.

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