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keratoacanthoma/l tyrosine
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12 résultats
P53 oncoprotein expression and gene mutations in some keratoacanthomas.
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OBJECTIVE
To analyze the relationship of p53 oncoprotein overexpression in most keratoacanthomas (KAs) with gene mutations.
METHODS
Expression of p53 oncoprotein in immunohistochemical staining and its correlation to gene mutations in DNA extracted from KAs and tested in single-strand conformational
Treatment of multiple keratoacanthomas with erlotinib.
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An 82-year-old male presented with numerous pruritic erythematous nodules over his trunk and extremities. Histopathology was consistent with keratoacanthomas. Given the extent of his disease, medical therapy was recommended. Based on phosphorylated epidermal growth factor receptor expression in
Refractory aggressive keratoacanthoma centrifugum marginatum of the scalp controlled with the epidermal growth factor receptor inhibitor erlotinib.
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Keratoacanthomas are squamous cell neoplasms known to be abundant in epidermal growth factor receptors (EGFRs). Erlotinib (Tarceva(®); Roche) is a low molecular weight oral quinazoline compound that binds to the intracellular EGFR tyrosine kinase domain and inhibits receptor phosphorylation and
[Sorafenib-induced multiple eruptive keratoacanthomas].
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BACKGROUND
Sorafenib has been approved for use in the treatment of metastatic renal cell carcinoma. Cutaneous side-effects are common, including rash, hand-foot syndrome, alopecia, pruritus, dry skin and erythema. We report an original unexpected cutaneous effect: multiple keratoacanthomas. In the
Eruptive keratoacanthoma-type squamous cell carcinomas in patients taking sorafenib for the treatment of solid tumors.
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BACKGROUND
Protein kinases (PKs) are indispensable for most cellular processes, and deregulation of PKs can lead to activation of oncogenic and anti-apoptotic pathways and immune dysregulation.
OBJECTIVE
To report the development of keratoacanthoma (KA)-type squamous cell carcinomas (SCCs) in
XB130 deficiency enhances carcinogen-induced skin tumorigenesis.
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XB130 is an adaptor protein that functions as a mediator of multiple tyrosine kinases important for regulating cell proliferation, survival, migration and invasion. Formerly predicted as an oncogene, alterations of its expression are documented in various human cancers. However, the exact role of
Conditional TPM3-ALK and NPM-ALK transgenic mice develop reversible ALK-positive early B-cell lymphoma/leukemia.
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NPM-ALK (nucleophosmin-anaplastic lymphoma kinase) and TPM3-ALK (nonmuscular tropomyosin 3-anaplastic lymphoma kinase) are oncogenic tyrosine kinases implicated in the pathogenesis of human ALK-positive lymphoma. We report here the development of novel conditional mouse models for ALK-induced
Increased level of c-erbB-2/neu/HER-2 protein in cutaneous squamous cell carcinoma.
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Overexpression of c-erbB-2/neu/HER-2 oncoprotein, a receptor tyrosine kinase, has been demonstrated in a variety of human cancers. To elucidate the involvement of c-erbB-2 in human skin carcinogenesis, we examined expression of the protein in skin samples from five cases of keratoacanthoma (KA), 10
[Squamous cell carcinoma in a patient receiving sorafenib].
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BACKGROUND
Sorafenib is a multikinase inhibitor approved for the treatment of renal cell carcinoma and hepatocellular carcinoma. Associated short-term cutaneous adverse events are well known. Regarding long-term adverse events, keratoacanthoma has been reported more recently and, more rarely,
The novel protein PTPIP51 is expressed in human keratinocyte carcinomas and their surrounding stroma.
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BACKGROUND
The novel protein PTPIP51 (SwissProt accession code Q96SD6) is known to interact with two non-transmembrane protein-tyrosine phosphatases, PTP1B and TCPTP in vitro. Overexpression of the full-length protein induces apoptosis in HeLa and HEK293T cells (Lv et al. 2006). PTPIP51 shows a
Eruption of squamous cell carcinomas after beginning nilotinib therapy
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Chronic myelogenous leukemia (CML) is characterized by a reciprocal translocation between the long arms of chromosomes 9 and 22 leading to the formation of a constitutively active tyrosine kinase. Tyrosine kinase inhibitors (TKIs) are the treatment of choice for patients diagnosed with CML and have
Dermatologic toxicities to targeted cancer therapy: shared clinical and histologic adverse skin reactions.
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BACKGROUND
Dermatologic toxicities (DT) to targeted cancer therapy may present as inflammatory dermatoses, keratoses, and as benign and malignant squamous proliferations.
METHODS
Published reports of DT with cancer therapy with epidermal growth factor receptor (EGFR), tyrosine kinase (TK), MEK,
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