{"id":29640,"date":"2019-11-13T17:54:52","date_gmt":"2019-11-13T16:54:52","guid":{"rendered":"https:\/\/cancerprev.com\/?page_id=29640"},"modified":"2025-02-28T16:49:40","modified_gmt":"2025-02-28T15:49:40","slug":"dotto","status":"publish","type":"page","link":"https:\/\/cancerprev.com\/de\/dotto\/","title":{"rendered":""},"content":{"rendered":"

Laboratory of Skin Aging and Cancer Prevention <\/strong><\/p>\n\n\n\n

Head of laboratory : Gian-Paolo Dotto, M.D., Ph.D. <\/a><\/kbd><\/p>\n\n\n\n

Research Program Overview<\/strong><\/h2>\n\n\n
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Photo by Liv Bruce<\/a> on Unsplash<\/a><\/figcaption><\/figure><\/div>\n\n\n

Cancer risk is exponentially increasing with aging and aging-related diseases. Cumulative exposure to environmental agents are connected with increased cancer risk.  There are significant sex-related differences in aging that may contribute to sexual dimorphism in cancer susceptibility. <\/p>\n\n\n\n

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Aging has been connected with senescence of cells, which can function both as a fail safe mechanism against cancer development but also facilitate this process. The dual tumor-suppressing and -promoting function of cellular senescence depends on cell types and cell-cell interactions. <\/p>\n\n\n

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Cancers do not arise solely from a single deregulated group of cells but rather as a combined result of alterations in tissues and organs associated with the aging and cellular senescence processes in widespreading cancer fields. <\/p>\n\n\n\n

Within this context, our main research focuses on genetic and epigenetic determinants of field cancerisation<\/a><\/em><\/strong>, a very frequent condition consisting of multifocal and recurrent lesions at various stages of neoplastic progression connected with widespread aging-associated changes of surrounding tissues. <\/p>\n\n\n\n

We focus on field cancerization<\/em> of the skin, as a benchmark of major clinical significance. We are exploring genetic and epigenetic determinants of squamous cell carcinoma and melanoma development, with a specific focus on precursor lesions and their risk of malignant conversion. <\/p>\n\n\n\n

In this context, we are exploring genetic and epigenetic determinants of cancer variability across gender and race. This is a topic of great interest as there are significant differences in cancer susceptibility between individuals of different sex and race that cannot solely be attributed to socioeconomic and behavioural factors and instead, are the likely result of an interplay with biological factors.<\/p>\n\n\n

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Cloccchiatti el al., JCI 2014
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Field Cancerization\u00a0:\u00a0bad seed \/ bad soil hypothesis<\/strong>. Environmental insults, like UV irradiation or smoke, can target both epithelial and stromal compartments of organs such as skin, head\/neck, lung, bladder or breast, with ensuing genetic and\/or epigenetic changes. Establishment and spreading of \u201ccancer fields\u201d is the likely result of an interplay between epithelial and stromal alterations, with the latter playing an equally important and possibly primary role. The situation leading to multifocal and recurrent neoplastic lesions may be analogous to that of a bad plant difficult to eradicate.\u00a0\u00a0This may be due to roots deeply embedded in the terrain or the spreading of bad multiple seeds, growing in the presence of a permissive or favorable soil. An alternative possibility with important conceptual implications is that the main problem is the soil itself. A bad soil could corrupt properties of otherwise perfectly good plants or seeds. According to this view, unless the soil is corrected, various forms of prevention and intervention would be of little or no use.<\/em><\/p>\n\n\n\t\t\t\n\t\t\t\tshow less\n\t\t\t<\/a>\n\t\t<\/div>\n<\/div>\n\n\n

Recent Highlights<\/strong><\/h2>\n\n\n\n