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This study suggests that erlotinib exacerbates inflammation in a mouse model of skin disease and that IL-1 inhibition could mitigate skin-related side effects of EGFR inhibitors.

In this study, researchers found that disrupting EGFR signaling in mice led to increased inflammation and hair follicle damage but that inhibiting the JAK-STAT1 pathway could restore hair growth and skin function.

This study found that KRT6A expression increases after epidermal barrier disruption, worsening skin inflammation in disease conditions, and suggests that targeting KRT6A could offer a new treatment approach for inflammatory skin diseases linked to epidermal dysfunction.

This study shows that NIPP1 deficiency in mouse epidermis leads to hyperproliferation, hair loss, and chronic skin inflammation, which can be partially alleviated by dexamethasone treatment.

This study found that AP-2α and AP-2β transcription factors are crucial for maintaining adult skin homeostasis, with their inactivation in keratinocytes leading to impaired differentiation, hair abnormalities, and inflammation, highlighting their key regulatory roles.

Blocking EGFR in mice causes hair loss and skin changes.

This study identified gene expression patterns in a mouse model that may influence tumor susceptibility and tissue functions related to inflammation and cell proliferation, highlighting Lgr5 and the vitamin D receptor as key regulators.

This study reports that Iressa, an anti-cancer agent, commonly causes acneiform eruptions and xerosis as cutaneous side effects, similar to other agents targeting epidermal growth factor receptors.

This study found that interleukin-1 directly induces the expression of keratin 6 in keratinocytes, which is a marker of activation and involved in inflammatory skin responses.

This study demonstrated that epidermal neural crest stem cells and bone marrow-derived stem cells migrated toward inflammatory brain lesions in rats and were successfully tracked using noninvasive MRI.

In this study, epidermal Notch activation increased jagged 1 expression, leading to skin changes like thickening and blistering, with these effects inhibited when jagged 1 was absent.

This study found that conditional knockout of N-WASP in keratinocytes of mice led to skin barrier defects, increased immune cell infiltration, and hyperproliferation of keratinocytes, indicating its crucial role in skin homeostasis.

This study found that actively targeted AN2728-loaded nanocarriers reduced inflammation and improved skin condition in a mouse model of psoriasiform inflammation compared to free drug and non-targeted nanoparticles.

This study observed that transgenic mice expressing keratin K10 under bovine K6beta control developed severe oral abnormalities, suggesting keratin composition changes can affect the physiology of epithelial cells, especially in the oral mucosa.

This review discusses the early phases of melanomagenesis and the factors influencing melanoma cell variability and reports no new clinical results.

This study describes a case of erlotinib-induced alopecia, unresponsive to traditional corticosteroid treatments, that was successfully managed with doxycycline, suggesting a novel approach for EGFR inhibitor-associated alopecia.

This review discusses how ionizing radiation causes skin damage by inducing cellular senescence in keratinocytes, which secrete inflammatory mediators, recruiting immune cells and exacerbating inflammation, impacting the skin barrier function and healing.

In this study using tamoxifen-inducible claudin-1 knockout mice, researchers observed that tight junction barrier leakage induced stratum corneum barrier defects and skin inflammation, suggesting a possible cycle of barrier damage and inflammation in atopic dermatitis.

In this case report, a 67-year-old woman with Netherton syndrome experienced significant improvement in skin inflammation, pruritus, and hair growth after treatment with dupilumab, suggesting potential benefits for addressing both cutaneous and hair manifestations of the condition.

This case study documented that a 67-year-old woman with Netherton syndrome experienced significant improvements in skin inflammation, pruritus, and hair growth after treatment with dupilumab, addressing symptoms of the syndrome and showing promising results for resolving "bamboo" hair.

This case study reported that in a 67-year-old woman with Netherton syndrome, treatment with dupilumab improved skin inflammation and pruritus and was associated with significant improvements in hair growth and structure, including the resolution of "bamboo" hair.

This study highlights that ZNF750, a zinc-finger transcription factor, is crucial for epidermal differentiation and barrier formation in skin by activating genes involved in lipid processing and stratum corneum development, and links ZNF750 sequence variations to skin inflammatory diseases like psoriasis.

This review highlights that iron deficiency is a significant yet often overlooked contributor to the development of immune-mediated inflammatory skin diseases, suggesting that iron dysregulation may drive inflammation and metabolic imbalances in conditions like psoriasis and atopic dermatitis.

This study found that mice exposed to low humidity showed altered epidermal gene expression, which was modulated by topical emollient application; this suggests emollients may help manage dry skin in low-humidity environments by affecting specific gene pathways.

In this animal study, researchers found that the simultaneous deletion of ERBB2 and ERBB3 in mice results in impaired skin differentiation, inflammation, and sebaceous gland alteration, leading to skin lesions, while highlighting potential side effects in cancer therapies targeting these receptors.

This study found that in atrophic acne scars, inflammation infiltrates the pilosebaceous unit over time, affecting resident stem cells and hindering the normal regeneration of the epidermis and adnexal structures, leading to scarring.

In this study, researchers found that AP-2α and AP-2β are critical for maintaining epidermal homeostasis in adult skin, with their combined loss leading to severe skin and hair abnormalities and early skin inflammation due to impaired keratinocyte differentiation.

This study reported that in mouse models, deletion of EGFR resulted in stem cell hyper-proliferation followed by apoptosis, leading to scarring alopecia, and implicated EGFR's role in maintaining hair follicle quiescence and immune privilege during inflammation.

In this study, researchers found that the loss of SETDB1 in epidermal keratinocytes led to altered chromatin states, increased ERV expression, and activation of immune responses, while inhibiting these effects with certain antiviral drugs reduced skin inflammation and hair loss in a mouse model.

This study implicates EGFR as a critical regulator of immune privilege and stem cell quiescence in hair follicles, suggesting a link between EGFR inhibition and inflammation-driven hair loss during cancer therapy.