Our spatial transcriptomic results from thousands of spots across multiple KS tumors indicated a correlation between high levels of STC1 and decreased expression of macrophage markers. Together, these analyses offer potential mechanisms by which KSHV infection may remodel skin tissue, inhibit immune responses against KSHV infection, and confer resistance to anticancer therapies.
Our findings show that the manipulation of UV-induced Tregs prevents early cSCC establishment. Thus, strategies aimed at modulating Treg function or abundance in the skin may represent a feasible therapeutic avenue for the prevention of cSCC tumor emergence in patients.
2 days ago
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TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains 2) • CD4 (CD4 Molecule) • FOXP3 (Forkhead Box P3)
Building on this foundation, the potential clinical value of immune checkpoint inhibitors (cemiplimab, pembrolizumab) in treating advanced cSCC is summarized based on data from relevant clinical trials. This review is distinguished from general tumor immunotherapy reviews by offering dedicated references for cSCC precision immunotherapy. In addition, priority is emphasized for future investigations into combination therapy regimens and the development of personalized tumor vaccines.
Metastatic BFH remains a rare but clinically significant condition. Early recognition, accurate histopathological diagnosis, and multimodal therapies are crucial for effective management.
3 days ago
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CD163 (CD163 Molecule) • VIM (Vimentin) • CD68 (CD68 Molecule)
This review consolidates existing evidence and suggests that mixed cancer syndromes, especially LFS, LS, and HBOC but also pathogenic ATM and CHEK2 variants may predispose individuals to skin cancers, warranting tailored screening and preventive measures. On the basis of emerging evidence, we recommend dermatologic evaluation and individualized UV protection strategies for patients with reviewed hereditary cancer syndromes to reduce skin cancer risk and enhance early detection.
The ferroptosis inducer erastin also inhibits melanoma growth. Combining the ATAD2 inhibitor BAY-850 with the MEK inhibitor trametinib potently suppresses melanoma growth. Our study identifies ATAD2 as a key driver of melanoma and provides a rationale for targeting ATAD2 in conjunction with the MAPK pathway to treat melanoma.
Immunosuppression with calcineurin inhibitor (CNI) plus azathioprine (AZA) was independently associated with increased skin cancer risk (odds ratio [OR] 9.41, p = 0.044), especially for SCC (OR 6.6, p = 0.027)...Skin cancer is a relevant long-term complication after HTx, particularly SCC in patients receiving AZA. Our findings support limiting AZA use and reinforce the importance of structured dermatologic surveillance and early mammalian target of rapamycin conversion strategies to improve long-term outcomes.
Consequently, ZDHHC13 activity suppresses tumor growth and metastasis in immunocompetent mice. Our study highlights the therapeutic potential of targeting the ZDHHC13-E-cadherin axis and its downstream metabolic and immune-modulatory mechanisms, offering additional strategies to inhibit melanoma progression and metastasis.
About 40% of cutaneous melanomas carry BRAF mutations-more common in younger patients-and these are linked to more aggressive behaviour and a higher risk of brain metastasis. Over the past decade, targeted therapies (TT) using BRAF and MEK inhibitors (BRAFi, MEKi), along with immune checkpoint inhibitors (ICI), have significantly improved response rates and survival in metastatic melanoma.
This case highlights the importance of considering MF in patients presenting with tissue eosinophilia or Langerhans cell infiltration, even when initial biopsies lack definitive features.