Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Focal adhesion kinase is a protein-tyrosine kinase that is found in cellular contact sites and is phosphorylated in response to cell attachment. It is possible that the immunohistochemical detection of this enzyme might be increased in keratinocytes involved in an acantholytic process. Normal skin, pemphigus vulgaris and foliaceus, Darier's disease, Hailey--Hailey disease, warty dyskeratoma, Grover's disease and spongiotic dermatitis were assayed for the immunohistochemical expression of focal adhesion kinase. Focal adhesion kinase was not observed in normal epidermis. This antigen was observed in keratinocytes adjacent to acantholytic spaces and in acantholytic cells in pemphigus vulgaris and foliaceus. Focal adhesion kinase was not detected in keratinocytes involved in focal acantholytic dyskeratoses such as Darier's disease, Grover's disease and warty dyskeratoma but was weakly detected in Hailey--Hailey disease. One consequence of immunologically mediated acantholysis is the upregulation of focal adhesion kinase possibly as a component of biochemical pathways that reconstruct the process of adhesion or respond to the process of acantholysis.
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PMID:Focal adhesion kinase is expressed in acantholytic keratinocytes associated with pemphigus vulgaris and pemphigus foliaceus. 891 52

Hyperkeratotic skin adverse events are a group of toxic effects, characterized by the disruption of epidermal homeostasis and interaction with keratinocyte proliferation/differentiation or keratinocyte survival, and frequently reported with systemic anticancer treatments. These types of reactions include hand-foot skin reaction or palmoplantar keratoderma, induced psoriasis, keratosis pilaris-like or pityriasis rubra pilaris-like rashes, Grover's disease, and contact hyperkeratosis. Cutaneous squamoproliferative lesions are also described because of the presence of abnormal keratinocyte proliferation. They are usually observed with tyrosine kinase inhibitors but have also been described in association with cytotoxic chemotherapeutic agents. Their pathogenesis is related mainly to the disruption of epidermal homeostasis and interaction with keratinocyte proliferation/differentiation or keratinocyte survival caused by anticancer treatment. Early recognition and adequate management are critical to prevent exacerbation of the lesions, to limit treatment interruption, and to minimize impairment of quality of life. This review summarizes the current knowledge concerning the presentation, pathogenesis, and management of secondary hyperkeratotic reactions to anticancer therapies. It also includes hyperkeratotic reactions that have been more recently described with newly approved targeted therapies or immune checkpoint inhibitors, such as keratosis pilaris-like exanthema with second-generation BCR-ABL inhibitors, lamellar ichthyosis-like lesions with ponatinib, pityriasis rubra pilaris with the newly approved selective phosphoinositide 3 kinase inhibitor idelalisib, or psoriasis with anti-programmed death-1 and programmed death ligand-1.
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PMID:Hyperkeratotic Skin Adverse Events Induced by Anticancer Treatments: A Comprehensive Review. 3198 Oct 81