Skin Neoplasia
Mostrando 13-24 de 41 artigos, teses e dissertações.
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13. Skin and lung carcinogenesis in mice Selected for acute inflammatory response (AIR). / Carcinogênese de pele e pulmão em linhagens de camundongos selecionados segundo a reatividade inflamatória aguda.
AIRmax mice are resistant and AIRmin susceptible to skin carcinogenesis by repeated DMBA doses. AIRmin mice developed initial contact hypersensitivity reaction (CHS) and late skin and lung tumors. The aryl hydrocarbon receptor (AHR) plays important roles in DMBA metabolism. Upon binding to agonist this transcription factor induces the expression of CYP P450
Publicado em: 2007
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14. Estudo dos fatores prognosticos do carcinoma espinocelular de pele de cabeça e pescoço / A study of the prognostic factors of the squamous cell carcinoma of the skin of the head and neck
O carcinoma espinocelular ou de células escamosas constitui a segunda neoplasia de pele mais freqüente e apresenta índice de cura superior a 90%, quando tratado na fase mais inicial. Tumores maiores e uma pequena fração dos tumores iniciais costumam apresentar evolução desfavorável, representada pelas recidivas loco-regional e a distância, apesar do
Publicado em: 2005
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15. Early onset of neoplasia in the prostate and skin of mice with tissue-specific deletion of Pten
PTEN is a tumor suppressor gene mutated in various advanced human neoplasias, including glioblastomas and prostate, breast, endometrial, and kidney cancers. This tumor suppressor is a lipid phosphatase that negatively regulates cell survival and proliferation mediated by phosphatidylinositol 3-kinase/protein kinase B signaling. Using the Cre–loxP system, w
National Academy of Sciences.
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16. A monoclonal antibody against basal cells of human epidermis. Potential use in the diagnosis of cervical neoplasia.
A murine monoclonal antibody was generated against human skin cells obtained from psoriatic plaques. The antibody, called VM-2, recognizes an epitope expressed on the basal cell layer of human skin and other epithelia. VM-2 also binds to cultured cells from a variety of human carcinomas including HeLa cervical carcinoma, A-431 vulvar carcinoma, A-549 lung al
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17. Bmx Tyrosine Kinase Transgene Induces Skin Hyperplasia, Inflammatory Angiogenesis, and Accelerated Wound Healing
The Bmx gene, a member of the Tec family of nonreceptor protein tyrosine kinases, is expressed in arterial endothelium and in certain hematopoietic and epithelial cells. Previous in vitro studies have implicated Bmx signaling in cell migration and survival and suggested that it contributes to the progression of prostate carcinomas. However, the function of B
The American Society for Cell Biology.
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18. Clues to epidermal cancer proneness revealed by reconstruction of DNA repair-deficient xeroderma pigmentosum skin in vitro
Sun exposure has been clearly implicated in premature skin aging and neoplastic development. These features are exacerbated in patients with xeroderma pigmentosum (XP), a hereditary disease, the biochemical hallmark of which is a severe deficiency in the nucleotide excision repair of UV-induced DNA lesions. To develop an organotypic model of DNA repair defic
The National Academy of Sciences.
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19. 8-Cl-Adenosine Inhibits Proliferation and Causes Apoptosis in B-Lymphocytes via Protein Kinase A-Dependent and Independent Effects: Implications for Treatment of Carney Complex-Associated Tumors
Context: Carney complex, a multiple neoplasia syndrome, characterized primarily by spotty skin pigmentation and a variety of endocrine and other tumors, is caused by mutations in PRKAR1A, the gene that codes for the RIα subunit of protein kinase A (PKA). PKA controls cell proliferation in many cell types. The cAMP analogue 8-Cl-adenosine (8-Cl-ADO) is thoug
The Endocrine Society.
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20. Id2 Is Dispensable for Myc-Induced Epidermal Neoplasia
We have previously described a transgenic mouse model of epidermal neoplasia wherein expression of a switchable form of c-Myc, MycERTAM, is targeted to the postmitotic suprabasal keratinocytes of murine epidermis via the involucrin promoter. Sustained activation of c-MycERTAM results in a progressive neoplastic phenotype characterized by aberrant ectopic pro
American Society for Microbiology.
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21. EVIDENCE THAT XERODERMA PIGMENTOSUM CELLS DO NOT PERFORM THE FIRST STEP IN THE REPAIR OF ULTRAVIOLET DAMAGE TO THEIR DNA*
Xeroderma pigmentosum (XP) is a recessively transmitted disorder of man characterized by increased sensitivity to ultraviolet light. Homozygous, affected individuals, upon exposure to sunlight, sustain severe damage to the skin; this damage is characteristically followed by multiple basal and squamous cell carcinomas and not uncommonly by other malignant neo
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22. Targeted expression of the E6 and E7 oncogenes of human papillomavirus type 16 in the epidermis of transgenic mice elicits generalized epidermal hyperplasia involving autocrine factors.
The E6 and E7 early genes of human papillomavirus type 16 have been shown in vitro to play a central role in the transforming capability of this virus. To explore their effects on differentiating epithelial cells in vivo, we used a bovine cytokeratin 10 (K10) promoter to target the expression of E6 and E7 to the suprabasal layers of the epidermis of transgen
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23. NF-κB RelA opposes epidermal proliferation driven by TNFR1 and JNK
NF-κB inhibition promotes epidermal tumorigenesis; however, whether this reflects an underlying role in homeostasis or a special case confined to neoplasia is unknown. Embryonic lethality of mice lacking NF-κB RelA has hindered efforts to address this. We therefore generated developmentally mature RelA–/– skin. RelA–/– epidermis displays hyperplasi
Cold Spring Harbor Laboratory Press.
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24. Differential effects of human papillomavirus type 6, 16, and 18 DNAs on immortalization and transformation of human cervical epithelial cells.
The human papillomaviruses (HPVs) are associated with specific benign and malignant lesions of the skin and mucosal epithelia. Cloned viral DNAs from HPV types 6b, 16, and 18 associated with different pathological manifestations of genital neoplasia in vivo were introduced into primary human cervical epithelial cells by electroporation. Cells transfected wit