16 citations
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December 2006 in “International Journal of Dermatology” A woman died from cancer that spread from a long-standing cyst on her abdomen.
Deleting Smad4 and PTEN genes in mice causes rapid, invasive forestomach cancer.
Deleting Smad4 and PTEN genes in mice causes rapid, invasive stomach cancer.
August 2022 in “JAAD case reports” A woman with a long-term skin condition developed a serious skin cancer that led to her death.
36 citations
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January 2019 in “Nature communications” High lactate dehydrogenase activity is not necessary for the growth of squamous cell carcinoma.
14 citations
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August 2010 in “Journal of Investigative Dermatology” HPV does not cause aggressive cancer in RDEB patients.
5 citations
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July 2022 in “Orphanet journal of rare diseases” RSPO1 mutations in certain patients lead to skin cells that don't develop properly and are more likely to become invasive, increasing the risk of skin cancer.
October 2023 in “bioRxiv (Cold Spring Harbor Laboratory)” Blocking both main energy pathways can stop hair follicle stem cell-induced skin cancer growth.
76 citations
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June 2018 in “EMBO Reports” YAP and TAZ proteins are necessary for the development of two types of skin cancer.
48 citations
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April 2021 in “Pharmaceuticals” Liposomal curcumin improves skin cancer treatment effectiveness while sparing normal cells.
31 citations
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October 2019 in “Genes & Diseases” Basal cell carcinomas and squamous cell carcinomas have different gene activity patterns, suggesting unique treatment approaches.
2 citations
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June 2003 in “American Journal of Dermatopathology” A unique case of skin cancer showed unusual calcification, possibly linked to calcium-binding proteins.
174 citations
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November 2016 in “Cell stem cell” Different types of skin cells have unique genetic markers that affect how likely they are to spread cancer.
100 citations
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May 2006 in “American Journal Of Pathology” Matriptase is crucial for skin barrier, hair growth, and may contribute to skin cancer.
76 citations
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February 2007 in “Cancer Research” Protein Kinase Cε increases skin sensitivity to UV damage and skin cancer risk.
65 citations
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March 2004 in “Journal of Clinical Investigation” Inhibiting ornithine decarboxylase may help prevent certain skin cancers.
64 citations
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March 2004 in “Journal of Clinical Investigation” Targeting ornithine decarboxylase can help prevent skin cancer.
35 citations
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January 2006 in “Cancer Research” Mice with extra PKCδ resist chemical-induced skin cancer but not UV-induced.
34 citations
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August 2018 in “Cancer research” Fixing DNA errors is crucial to prevent skin cancer.
28 citations
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January 2005 in “Photochemistry and Photobiology” Protein kinase C epsilon may increase skin cancer risk by affecting nearby cells.
10 citations
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January 2013 in “Journal of skin cancer” PKC ε increases hair follicle stem cell turnover and may raise skin cancer risk.
8 citations
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April 2016 in “Experimental Dermatology” The type of tumor suppressor affects the form of skin cancer from hair follicle stem cells.
3 citations
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November 2011 in “Small GTPases” Researchers found that hair follicle stem cells can become squamous cell carcinoma due to Ras activation, which could lead to new treatments.
3 citations
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May 2018 in “European Journal of Dermatology” Photodynamic therapy may not work for erythroplasia of Queyrat and could lead to invasive squamous cell carcinoma.
3 citations
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January 2005 in “Photochemistry and Photobiology” Protein kinase C epsilon may promote skin cancer development after UV exposure by affecting nearby cells.
January 1990 in “The Nishinihon Journal of Dermatology” Follicular structures help differentiate keratoacanthoma from squamous cell carcinoma.
Ribonucleotide excision repair is crucial to prevent skin cancer.
Ribonucleotide excision repair is crucial to prevent skin cancer.
January 2019 in “Publisher” Human basal cell carcinomas and squamous cell carcinomas have unique gene expression patterns not fully mirrored in mouse models.
April 2018 in “Journal of Investigative Dermatology” CREB, a protein that can promote cancer traits, is controlled by β-catenin in skin cancer cells.