ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Reversibility of progression of the transformed phenotype in Ad5-transformed rat embryo cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: The carcinogenic process is extremely complex and is affected by diverse environmental and host factors. The mechanism for the gradual development of the transformed phenotype (a process termed "progression") was studied in type 5 adenovirus (Ad5)-transformed rat embryo cells. Progression was not correlated with major changes in the pattern of integration of viral DNA sequences. Instead, it was associated with an increased methylation of integrated viral sequences other than those corresponding to the E1 transforming genes of Ad5. A single exposure of progressed cells to the demethylating agent 5-azacytidine (Aza) resulted in a stable reversion to the unprogressed state of the original parental clone. A further selection of cells after growth in agar allowed the isolation of Aza-treated clones that had regained the progressed phenotype. These observations indicate that progression is a reversible process and suggest that progression may be associated with changes in the state of methylation of one or more specific genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babiss, L E -- Zimmer, S G -- Fisher, P B -- CA-33434/CA/NCI NIH HHS/ -- CA-35675/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1099-101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2581317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*genetics ; Animals ; Azacitidine/*pharmacology ; Cell Division ; Cell Transformation, Viral/*drug effects ; Cells, Cultured ; DNA, Neoplasm/genetics ; DNA, Viral/genetics ; Gene Expression Regulation ; Genes, Viral ; *Methylation ; Mice ; Neoplasms, Experimental/*pathology ; Rats ; Rats, Inbred Strains/embryology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Recombinant interferon enhances monoclonal antibody-targeting of carcinoma lesions in vivo (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: Heterogeneity in the expression of tumor-associated antigens, as defined by the binding of monoclonal antibodies, is a characteristic common to most, if not all, human carcinoma cell populations. Antigen-negative cells within the population can escape detection and therapy by their failure to bind the appropriate antibody. Therefore, the extent of antigenic heterogeneity is an important consideration when designing protocols for the management of cancer by administration of monoclonal antibodies. One approach to counteracting the effect of antigenic heterogeneity is the use of clone A of recombinant human leukocyte interferon (Hu-IFN-alpha A). Administration of Hu-IFN-alpha A in vivo effectively increased the amount of tumor antigen expressed by a human colon xenograft in situ and augmented the localization of a radiolabeled monoclonal antibody to the tumor site. Concomitant administration of Hu-IFN-alpha A and monoclonal antibody may thus be effective in overcoming the antigenic heterogeneity of carcinoma cell populations and in enhancing the efficacy of monoclonal antibodies in the detection and treatment of carcinoma lesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greiner, J W -- Guadagni, F -- Noguchi, P -- Pestka, S -- Colcher, D -- Fisher, P B -- Schlom, J -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):895-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3580039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*administration & dosage ; Antigens, Neoplasm/*immunology ; Antigens, Surface/immunology ; Carcinoma/*immunology ; Colonic Neoplasms/*immunology ; HLA Antigens/immunology ; Humans ; Interferon Type I/*administration & dosage ; Mice ; Mice, Nude ; Neoplasm Transplantation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Control of cytochrome P1-450 gene expression by dioxin (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-22
    Description: The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may produce its effects by altering gene expression in susceptible cells. In mouse hepatoma cells, TCDD induces the transcription of the cytochrome P1-450 gene, whose product, aryl hydrocarbon hydroxylase, contributes both to the detoxification and to the metabolic activation of carcinogenic polycyclic aromatic hydrocarbons. A DNA fragment containing sequences flanking the 5' end of the cytochrome P1-450 gene was isolated and analyzed. This DNA fragment contains a cis-acting control element with at least three functional domains: a putative promoter, an inhibitory domain upstream from the promoter that blocks its function, and a TCDD-responsive domain still farther (1265 to 1535 base pairs) upstream of the promoter. These findings, together with results from earlier studies, imply that transcription of the cytochrome P1-450 gene is under both positive and negative control by at least two trans-acting regulatory factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, P B -- Galeazzi, D R -- Fisher, J M -- Whitlock, J P Jr -- CA09302/CA/NCI NIH HHS/ -- CA32786/CA/NCI NIH HHS/ -- GM07149/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1499-502.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856321" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/biosynthesis/genetics ; Animals ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Cytochrome P-450 Enzyme System/*genetics ; DNA, Recombinant ; Dioxins/*pharmacology ; Enzyme Induction ; Gene Expression Regulation/*drug effects ; *Genes, Regulator ; Liver Neoplasms, Experimental ; Mice ; *Promoter Regions, Genetic ; Tetrachlorodibenzodioxin/*pharmacology ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...