ETS2 is crucial in squamous cell carcinoma development and could be a therapeutic target.
28 citations
,
February 2007 in “Cancer Research” Blocking certain proteins in mouse skin can reduce and shrink skin tumors.
99 citations
,
February 2000 in “PubMed” Overexpressing PKCepsilon in mice reduces papillomas but increases carcinomas.
135 citations
,
January 1996 in “Journal of Investigative Dermatology”
August 2013 in “Nature Reviews Drug Discovery” New cancer treatments show promise in reducing tumor growth and improving skin regeneration in mice.
May 2025 in “Journal of the ASEAN Federation of Endocrine Societies” VHL disease can cause early paragangliomas, needing lifelong monitoring.
638 citations
,
October 1997 in “Nature” 157 citations
,
October 2002 in “Journal of Cutaneous Pathology” p63 may influence skin cancer development and cell differentiation.
64 citations
,
March 2004 in “Journal of Clinical Investigation” Targeting ornithine decarboxylase can help prevent skin cancer.
24 citations
,
April 2017 in “Oncology Reports” The hair keratin gene KRT81 is found in both normal and breast cancer cells and helps them invade surrounding tissues.
ETS2 drives cancer progression in squamous cell carcinoma and is linked to poor patient outcomes.
3 citations
,
January 2005 in “Photochemistry and Photobiology” Protein kinase C epsilon may promote skin cancer development after UV exposure by affecting nearby cells.
17 citations
,
September 2019 in “Journal of Cell Biology” Hair follicle regeneration may slow tumor growth.
21 citations
,
August 2007 in “Experimental Dermatology” Overexpression of hurpin in mice leads to abnormal skin and higher skin cancer risk.
4 citations
,
February 2022 in “International Journal of Dermatology” Porocarcinoma generally has low rates of recurrence, spread to lymph nodes, and death.
5 citations
,
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.
January 2019 in “Publisher” Human basal cell carcinomas and squamous cell carcinomas have unique gene expression patterns not fully mirrored in mouse models.
1 citations
,
September 2011 in “Journal of Dermatology” A woman with a new PTCH gene mutation has both Gorlin syndrome and severe hair loss.
70 citations
,
August 2006 in “Cancer Research” AP-1 controls tumor cell type by affecting key signaling pathways.
65 citations
,
March 2004 in “Journal of Clinical Investigation” Inhibiting ornithine decarboxylase may help prevent certain skin cancers.
5 citations
,
September 2010 in “Cancer Prevention Research” The research suggests new treatments for skin cancer could target specific cell growth pathways.
8 citations
,
August 2014 in “Biochemical and Biophysical Research Communications” ODC overexpression in hair cells increases tumor growth by reducing Notch signaling.
5 citations
,
September 2018 in “Journal of Investigative Dermatology” Keratinocyte cytokines and genetic variations influence the development of moles and skin pigmentation.
145 citations
,
May 2008 in “Cancer Science” Cancer cells often have more copies of TERT and TERC genes, which helps them grow and could affect patient outcomes.
12 citations
,
April 2014 in “Molecular Medicine Reports” Targeting specific miRNAs may help treat hair follicle issues caused by hydrogen peroxide.
28 citations
,
January 2005 in “Photochemistry and Photobiology” Protein kinase C epsilon may increase skin cancer risk by affecting nearby cells.
25 citations
,
July 1994 in “Journal of Cell Science” Immortalized rat dermal papilla cells can still induce hair growth.
1 citations
,
March 2003 in “Journal of Investigative Dermatology” Early sunburn treatment with certain inhibitors may reduce skin cancer risk.
11 citations
,
March 2021 in “Molecular Carcinogenesis” Twist1 is crucial for UVB-induced skin cancer development.
July 2022 in “Journal of Investigative Dermatology” A specific mutation in Kras causes abnormal tissue changes by making a cell signal continuously active, which disrupts normal cell coordination.