![]() | Henry HenningsLaboratory of Cancer Biology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland | Laboratory of Cancer Biology and Genetics, National Cancer Institute, NIH, ... |
KOL Resume for Henry Hennings (epidermal thickening, nigricans, acanthosis, skin, acanthosis nigricans)
Year | |
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2007 | Laboratory of Cancer Biology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland |
2005 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Building 37, Room 4054B, 37 Convent Drive, Bethesda, MD 20892 |
2002 | Drug Discovery Program, Department of Neurology, Georgetown University Medical Center, 3970 Reservoir Road, NW, Washington, D.C. 20007-2197, NeuroLogic, Inc., 15010 Broschart Road, Suite 200, Rockville, Maryland 20850, and Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Institutes of Health, Bethesda, Maryland 20892 |
2000 | National Institutes of Health, National Cancer Institute, Building 37, Room 3B12, 37 Convent Drive MSC4255, Bethesda, MD 20892‐4255. |
1998 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland |
1997 | National Cancer Institute, Building 37, Room 3B26, Bethesda, MD 20892 |
1996 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer InstituteBethesda, MD 20892, USA |
1995 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892 |
1993 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD. Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. |
1992 | National Cancer Institute, Bethesda, MD, USA |
1991 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA National Cancer Institute, Bethesda 20892. |
1990 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. |
1988 | Laboratory of Cellular Carcinogenesis and Tumor Promotion Building 37, Room 3B25 National Cancer Institute Bethesda, Maryland 20892 |
1987 | Vitro Pathogenesis Section, Laboratory of Cellular Carcínogenesis and Tumor Promotion, Nation Cancer Institute, National Institutes of Health, Bethesda, Maryland, U.S.A. |
1986 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland, U.S.A. |
1983 | In Vitro Pathogenesis Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, 20205, Bethesda, Maryland, USA |
1982 | Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Building 37, Room 3A21, Bethesda, MD 20205 U.S.A. Department of Biological Structure, University of Washington, Seattle, Washington |
1981 | In Vitro Pathogenesis Section, Laboratory of Experimental Pathology National Cancer, Institute, Bethesda, Maryland, U.S.A. Laboratory of Cellular Carcinogenesis and Tumor Promotion, Bethesda, MD 20205, USA |
1980 | Vitro Pathogenesis Section, Laboratory of Experimental Pathology, National Cancer Institute, Bethesda, Maryland, U.S.A. |
1977 | In vitro Pathogenesis Section, Experimental Pathology Branch, Division of Cancer Cause and Prevention, National Cancer Institute, Bethesda, Md. 20014 U.S.A. |
1976 | In Vitro Pathogenesis Section, Experimental Pathology Branch (Carcinogenesis), Division of Cancer Cause and Prevention, National Institutes of Health, Bethesda, Maryland, U. S. A. |
1973 | National Cancer Institute, Bethesda, Md., USA |
1971 | Institutt for Generell og Eksperimentell Patologi, Universitetet i Oslo, Rikshospitalet, Oslo, Norway |
1970 | Institute for General and Experimental Pathology, Rikshospitalet, University of Oslo |
Prominent publications by Henry Hennings
Mouse skin carcinomas arise from a small subpopulation of benign papillomas with an increased risk of malignant conversion. These papillomas arise with limited stimulation by tumor promoters, appear rapidly, and do not regress, suggesting that they differ in growth properties from the majority of benign tumors. The transforming growth factor beta (TGF-beta) proteins are expressed in the epidermis and are growth inhibitors for mouse keratinocytes in vitro; altered TGF-beta expression ...
Known for Malignant Conversion | Skin Tumors | Factor Beta | Transforming Growth | Loss Expression |
Inducible Cutaneous Inflammation Reveals a Protumorigenic Role for Keratinocyte CXCR2 in Skin Carcinogenesis
[ PUBLICATION ]
Transgenic mice that overexpress PKCalpha in the epidermis (K5-PKCalpha mice) exhibit acute CXCR2-mediated intraepidermal neutrophilic inflammation and a strong epidermal hyperplasia in response to application of 12-O-tetradecanoylphorbol-13-acetate (TPA). We now show that hyperplasia is independent of infiltrating neutrophils. Furthermore, when K5-PKCalpha mice were initiated with 7,12-dimethylbenz(a)anthracene (DMBA) and promoted with a low dose of TPA, 58% of K5-PKCalpha mice ...
Known for Skin Carcinogenesis | Cxcr2 Ligands | Oncogenic Ras | Cutaneous Inflammation | Transformed Keratinocytes |
Chelation of intracellular Ca2+ inhibits murine keratinocyte differentiation in vitro
[ PUBLICATION ]
The role of intracellular Ca2+ in the regulation of Ca(2+)-induced terminal differentiation of mouse keratinocytes was investigated using the intracellular Ca2+ chelator 1,2-bis(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA). A cell permeable acetoxymethyl (AM) ester derivative BAPTA (BAPTA/AM) was loaded into primary mouse keratinocytes in 0.05 mM Ca2+ medium, and then the cells were induced to differentiate by medium containing 0.12 or 0.5 mM Ca(2+) Intracellular BAPTA ...
Known for Intracellular Ca2 | Keratinocyte Differentiation | Cell Membrane | Increase Cai | Egtazic Acid |
Disaggregated epidermal cells, sheets of epidermis, and explants of partial and full-thickness skin have been grown in cell, organ, and explant cultures. Each type of epidermal sample has also been "cultured" as a graft on a living animal host. The extent of tissue-specific phenotypic expression by the epidermal cell varies with the type of culture and the culture conditions: medium, biologic and pharmacologic additives, substrate, cell density, pH, and temperature. Specific culture ...
Known for Epidermal Cells | Phenotypic Expression | Cell Culture | Basement Membrane | Microscopy Electron |
Phorbol esters stimulate DNA synthesis and ornithine decarboxylase activity in mouse epidermal cell cultures
[ PUBLICATION ]
TUMOUR-PROMOTING agents have been defined by their ability to promote tumour formation on carcinogen-initiated mouse skin. The most potent of these agents are the diesters of phorbol which are the active components of croton oil, the classic promoting substance. Phorbol esters can be chemically modified in a number of positions to form molecules with a wide range of promoter potency1. Such modifications have been useful in determining structure-function relationships2. A good correlation ...
Known for Phorbol Esters | Dna Synthesis | Decarboxylase Activity | Mouse Epidermal | Cell Cultures |
Calcium regulation of cell-cell contact and differentiation of epidermal cells in culture An ultrastructural study
[ PUBLICATION ]
Calcium modulation of keratinocyte growth in culture was studied by both transmission (TEM) and scanning electron microscopy (SEM). Under standard culture conditions (1.2-1.8 mM calcium), cells were connected by desmosomes and stratified to 4-6 cell layers. Many aspects of in vitro epidermal maturation were analogous to the in vivo process, with formation of keratohyalin granules, loss of nuclei, formation of cornified envelopes and shedding of cornified cells containing keratin ...
Known for Epidermal Cells | Electron Microscopy | Calcium Regulation | Ultrastructural Study | Keratin Filaments |
Modification of the ionic calcium concentration in the culture medium markedly alters the pattern of proliferation and differentiation in cultured mouse epidermal cells. When medium calcium is lowered to 0.05--0.1 mM, keratinocytes proliferate rapidly with a high growth fraction and do not stratify, but continue to synthesize keratin. The cells grow as a monolayer for several months and can be subcultured and cloned in low Ca++ medium. Ultrastructural examination of cells cultured under ...
Known for Epidermal Cells | Calcium Regulation | Culture Medium | Mice Mice | Protein Synthesis |
Henry Hennings: Influence Statistics
Concept | World rank |
---|---|
mitotic rate vinblastine | #1 |
mitotic rate 8–10 | #1 |
maximum reduction 12 | #1 |
intervals treated skin | #1 |
vinblastine 34 | #1 |
regression tumour size | #1 |
chemical carcinogenesis12 | #1 |
single mutational event7 | #1 |
retinoids tumor promoters | #1 |
depressed 80 | #1 |
actinomycintreated skin | #1 |
g2 inhibitory effects | #1 |
carcinogen3 | #1 |
kinetics precede | #1 |
endogenous mitotic | #1 |
promoted mezerein | #1 |
dimethylbenzaanthracene binding | #1 |
labelled interfollicular cells | #1 |
skin intraperitoneal liver | #1 |
neoplasms urethane animals | #1 |
urethane 910 | #1 |
individual tpa applications | #1 |
24 actinomycintreated skin | #1 |
papillomas rate | #1 |
papillomas urethane | #1 |
acid 20 weeks | #1 |
51 micrograms acid | #1 |
00201 mm | #1 |
tpapromoted papillomas | #1 |
8 chalone injection | #1 |
chalone injection | #1 |
urethane 4 | #1 |
exposure tumor promoters | #1 |
calcium inbred balb | #1 |
labelling mitotic rate | #1 |
extracts inhibiting activity | #1 |
cell flux g1 | #1 |
initial 40–50 inhibition | #1 |
hamsters epidermal chalone | #1 |
dmba urethane | #1 |
epidermal chalone decision | #1 |
tumor promoters consideration | #1 |
initiation single treatment | #1 |
mice carcinomas | #1 |
actinomycin skin | #1 |
aqueous extract liver | #1 |
papillomas develop | #1 |
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Key People For Epidermal Cells
Henry Hennings:Expert Impact
Concepts for whichHenry Henningshas direct influence:Epidermal cells, Malignant conversion, Mouse skin, Dna synthesis, Inbred balb mice, Intracellular ca2, Tumor promotion, Terminal differentiation.
Henry Hennings:KOL impact
Concepts related to the work of other authors for whichfor which Henry Hennings has influence:Protein kinase, Human keratinocytes, Epidermal cells, Mouse skin, Keratinocyte differentiation, Growth factor, Cell proliferation.
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