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Query: UNIPROT:P04626 (
erbB-2
)
5,251
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The distribution of several markers of keratinocyte differentiation was studied in normal epidermis, basal cell carcinomas (BCCs), and squamous cell carcinomas (SCCs) using the immunoperoxidase technique on frozen sections of punch biopsy specimens. As markers a panel of chain-specific monoclonal antibodies (MoAbs) directed against cytokeratin (CK) 4, 8, 10, 13, 18 and 19, a polyclonal antiserum against
involucrin
, as well as a MoAb against the
epidermal growth factor (EGF) receptor
were used. In 15 out of 19 BCCs tested, expression of CK 8 was seen. Only a few individual cells in a limited number of BCCs showed positive staining for CK 4, 18, or 19. No expression of CK 10 was seen except for some foci of cell keratinization. Involucrin was not found in BCCs except for some squamous horn cysts. In all BCC cells expression of EGF receptor was found. In the suprabasal layers of normal epidermis from SCC patients, positive staining for CK 10 was seen. A few individual cells in a limited number of SCCs showed positive staining for CK 4, 8, or 18. Involucrin was expressed in the center of SCCs and in the upper layers of normal epidermis. Expression of EGF receptor was found in all SCC cells. These results demonstrate differences in cellular origin and differentiation between BCC and SCC.
...
PMID:Expression of EGF receptor, involucrin, and cytokeratins in basal cell carcinomas and squamous cell carcinomas of the skin. 247 80
Two epithelial cell lines were established from human papilloma virus (HPV) 18 or 16 associated tumours, characterised as poorly and well differentiated squamous cell carcinomas of the cervix uteri (EC) and the vulva (GC), respectively. The cell lines are described by their morphology, biological parameters, and immunological markers. Both cell lines have undergone approximately 35 passages in vitro. HPV16 and 18 DNA are maintained integrated into the host cell DNA. Expression of epithelial cell markers--cytokeratins K1, K10, K13, K14 and
involucrin
, proliferation-specific proteins, proliferating cell nuclear antigen (PCNA) and Ki67 as well as the
epidermal growth factor (EGF) receptor
were monitored by indirect immunofluorescence studies. The cytoplasmic and membrane-associated locations of EGF receptor molecules in EC and GC cells, respectively, suggest a differently regulated expression. Studies of the HPV18 oncogene transcription revealed marked differences of amplimers between HeLa and EC cells, such as an additional fragment, probably corresponding to a E6**--E7 splice product, and a radical shift in transcription pattern observed in various sections of the tumour tissue. Injected subcutaneously into nu/nu mice both cell lines were non-tumorigenic.
...
PMID:Properties of two epithelial cell lines derived from HPV-associated cervical and vulvar lesions. 810 42
Transforming growth factor beta (TGF-beta) inhibits proliferation of keratinocytes cultured from normal anogenital epithelia; however, human papillomavirus (HPV)-immortalized cell lines often exhibit increased resistance. Present results demonstrate that TGF-beta 1 (1-10 pM) stimulates growth of multiple HPV-immortalized cell lines when cultures are maintained under conditions promoting squamous differentiation (MCDB153-LB medium with 1.0 mM calcium and without epidermal growth factor and bovine pituitary extract). Growth stimulation by TGF-beta 1 was not due to altered expression of type I or II receptors, but was increased after extended passage of cells in culture. Differentiation of immortal keratinocytes resulted in induction of RNAs encoding two markers of squamous differentiation,
involucrin
and keratin 1, and decreased expression of RNAs for the
epidermal growth factor (EGF) receptor
and two ligands, amphiregulin and TGF-alpha. Growth stimulation by TGF-beta 1 occurred indirectly via establishment of an autocrine loop. TGF-beta 1 increased expression of RNAs encoding the EGF-R and amphiregulin, and also increased numbers of cell-surface EGF-Rs without altering their affinity. In contrast, TGF-beta 1 inhibited autonomous growth and transcription of amphiregulin RNA in normal keratinocytes. Growth stimulation by TGF-beta 1 could be blocked by a monoclonal antibody that competes for binding to the EGF-R or by a mixture of monoclonal antibodies that neutralize amphiregulin activity, confirming the importance of this autocrine pathway. Thus, partial abrogation of the growth inhibitory response to TGF-beta 1 sensitizes HPV-immortalized keratinocytes to a growth stimulatory signal mediated by an EGF-R-dependent pathway involving autocrine stimulation by amphiregulin.
...
PMID:Transforming growth factor beta 1 supports autonomous growth of human papillomavirus-immortalized cervical keratinocytes under conditions promoting squamous differentiation. 878 Aug 94
This work concerns the effect of low frequency electromagnetic fields (ELF) on biochemical properties of human oral keratinocytes (HOK). Cells exposed to a 2 mT, 50 Hz, magnetic field, showed by scanning electron microscopy (SEM) modification in shape and morphology; these modifications were also associated with different actin distribution, revealed by phalloidin fluorescence analysis. Moreover, exposed cells had a smaller clonogenic capacity, and decreased cellular growth. Indirect immunofluorescence with fluorescent antibodies against
involucrin
and beta-catenin, both differentiation and adhesion markers, revealed an increase in
involucrin
and beta-catenin expression. The advance in differentiation was confirmed by a decrease of expression of
epidermal growth factor (EGF) receptor
in exposed cells, supporting the idea that exposure to electromagnetic field carries keratinocytes to higher differentiation level. These observations support the hypothesis that 50 Hz electromagnetic fields may modify cell morphology and interfere in differentiation and cellular adhesion of normal keratinocytes.
...
PMID:Low electromagnetic field (50 Hz) induces differentiation on primary human oral keratinocytes (HOK). 1473 62