Carcinome basocellulaire

Résumé

Le carcinome basocellulaire (CBC, ou BCC pour l'anglais basal cell carcinoma ou basal cell cancer) est un cancer de la peau dont l'évolution est très favorable sous traitement. Le carcinome basocellulaire concerne les cellules basales de l'épiderme. Les autres cancers de la peau sont le carcinome spinocellulaire (qui concerne les kératinocytes), le mélanome malin (mélanocytes) et certains sarcomes. Le carcinome basocellulaire touche particulièrement les personnes à la peau claire (blonds ou roux), et il est corrélé à l'exposition au soleil et aux rayonnements ultraviolets. En effet, ceux-ci causent des mutations génétiques qui peuvent favoriser l'apparition de ce cancer. De plus, une forte exposition au soleil en jeunesse augmente le risque de développer un CBC au cours de la vie adulte. Il s'agit du plus fréquent des cancers : près de la moitié des cancers aux États-Unis, plusieurs milliers de nouveaux cas chaque année dans le monde. Son incidence semble s'accroître. Le carcinome basocellulaire peut prendre plusieurs formes. L'aspect pathognomonique (signant à coup sûr le diagnostic) est la perle translucide. Le carcinome plan cicatriciel : sous forme de petite papule translucide au début puis s'étale progressivement et prend l'aspect d'une plaque à centre cicatriciel blanchâtre Le carcinome basocellulaire ulcéreux : forme creusant l'épaisseur de la peau (ulcération), avec ou sans bordure nette, pouvant atteindre les structures anatomiques sous-jacentes et les endommager. Le carcinome basocellulaire nodulaire : forme des petits nodules saillants, globuleux, de teinte cireuse. Le carcinome basocellulaire bourgeonnant et végétant : de couleur rouge foncé, saignant volontiers, a différencier du carcinome spinocellulaire. Le carcinome basocellulaire pagétoïde : se présente comme une nappe rosée recouverte de squames. Le carcinome basocellulaire érythémateux : forme une plaque rouge avec des bords perlés. Le carcinome basocellulaire sclérodermiforme ou morphéiforme : se présente sous la forme d'une plaque blanchâtre.

Source officielle

https://fr.wikipedia.org/wiki/Carcinome_basocellulaire

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Personnes associées (4)

Unités associées (2)

Concepts associés (35)

Cours associés (6)

Séances de cours associées (40)

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

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

Raphaelle Luisier

2009

EPFL2017