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http://dx.doi.org/10.1007/s00403-025-04071-8 | DOI Listing |
Arch Dermatol Res
March 2025
Department of Pathology, Kocaeli University Faculty of Medicine, Kocaeli, Türkiye.
To gain insight into biological mechanisms that cause resistance to DNA damage, we performed parallel pooled genetic CRISPR-Cas9 screening for survival in high risk HNSCC subtypes. Surprisingly, and in addition to ATM, DNAPK, and NFKB signaling, JAK1 was identified as a driver of tumor cell radiosensitivity. Knockout of JAK1 in HNSCC increases cell survival by enhancing the DNA damage-induced G2 arrest, and both knockout and JAK1 inhibition with abrocitinib prevent subsequent formation of radiation-induced micronuclei.
View Article and Find Full Text PDFAm J Cancer Res
January 2025
Department of Biomedicine, University Hospital Basel and University of Basel Basel, Switzerland.
Mastocytosis is characterized by an abnormal accumulation of mast cells (MC) in various organs. In most patients, the disease is driven by the D816V mutation, leading to activation of the KIT receptor and subsequent downstream signaling, including the JAK/STAT pathway. In recent years, KIT-targeting tyrosine kinase inhibitors (TKI) have emerged for the treatment of systemic mastocytosis; however, the overall response rate is often not sufficient.
View Article and Find Full Text PDFSAGE Open Med Case Rep
February 2025
Division of Dermatology, Department of Medicine, The Ottawa Hospital, Ottawa, ON, Canada.
Lichen planus is a chronic inflammatory disorder, with vulvar variants often resistant to multiple treatments. The primary therapeutic goals for vulvar lichen planus are to prevent scarring and the development of squamous cell carcinoma. Management also involves treating associated symptoms such as pruritus and pain.
View Article and Find Full Text PDFIndian Dermatol Online J
October 2024
Department of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
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