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
    A bacterial protein enhances the release and efficacy of liposomal cancer drugs (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-25
    Description: Clostridium novyi-NT is an anaerobic bacterium that can infect hypoxic regions within experimental tumors. Because C. novyi-NT lyses red blood cells, we hypothesized that its membrane-disrupting properties could be exploited to enhance the release of liposome-encapsulated drugs within tumors. Here, we show that treatment of mice bearing large, established tumors with C. novyi-NT plus a single dose of liposomal doxorubicin often led to eradication of the tumors. The bacterial factor responsible for the enhanced drug release was identified as a previously unrecognized protein termed liposomase. This protein could potentially be incorporated into diverse experimental approaches for the specific delivery of chemotherapeutic agents to tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheong, Ian -- Huang, Xin -- Bettegowda, Chetan -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- Zhou, Shibin -- Vogelstein, Bert -- CA062924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and the Ludwig Center for Cancer Genetics and Therapeutics, Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antineoplastic Agents/*administration & dosage/pharmacokinetics/therapeutic use ; Bacterial Proteins/chemistry/genetics/*metabolism ; Base Sequence ; Camptothecin/administration & dosage/analogs & ; derivatives/pharmacokinetics/therapeutic use ; Cell Line, Tumor ; Cloning, Molecular ; Clostridium/*chemistry/genetics ; Colorectal Neoplasms/*drug therapy ; Doxorubicin/*administration & dosage/pharmacokinetics/therapeutic use ; Drug Carriers ; Humans ; Lipase/chemistry/genetics/*metabolism ; Lipid Bilayers/chemistry ; Liposomes/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Protein Structure, Tertiary
    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
    Requirement for p53 and p21 to sustain G2 arrest after DNA damage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-20
    Description: After DNA damage, many cells appear to enter a sustained arrest in the G2 phase of the cell cycle. It is shown here that this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21. After disruption of either the p53 or the p21 gene, gamma radiated cells progressed into mitosis and exhibited a G2 DNA content only because of a failure of cytokinesis. Thus, p53 and p21 appear to be essential for maintaining the G2 checkpoint in human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bunz, F -- Dutriaux, A -- Lengauer, C -- Waldman, T -- Zhou, S -- Brown, J P -- Sedivy, J M -- Kinzler, K W -- Vogelstein, B -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA 62924/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1497-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Howard Hughes Medical Institute and The Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9822382" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; CDC2 Protein Kinase/antagonists & inhibitors/metabolism ; Cell Line ; Cyclin B/metabolism ; Cyclin B1 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/*physiology ; DNA/analysis ; *DNA Damage ; *G2 Phase/drug effects ; Gamma Rays ; Gene Expression Regulation ; Genes, p53 ; Humans ; Mitosis ; Mutation ; Nocodazole/pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*physiology
    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
    Cancer genome landscapes (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-30
    Description: Over the past decade, comprehensive sequencing efforts have revealed the genomic landscapes of common forms of human cancer. For most cancer types, this landscape consists of a small number of "mountains" (genes altered in a high percentage of tumors) and a much larger number of "hills" (genes altered infrequently). To date, these studies have revealed ~140 genes that, when altered by intragenic mutations, can promote or "drive" tumorigenesis. A typical tumor contains two to eight of these "driver gene" mutations; the remaining mutations are passengers that confer no selective growth advantage. Driver genes can be classified into 12 signaling pathways that regulate three core cellular processes: cell fate, cell survival, and genome maintenance. A better understanding of these pathways is one of the most pressing needs in basic cancer research. Even now, however, our knowledge of cancer genomes is sufficient to guide the development of more effective approaches for reducing cancer morbidity and mortality.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749880/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749880/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogelstein, Bert -- Papadopoulos, Nickolas -- Velculescu, Victor E -- Zhou, Shibin -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- CA 121113/CA/NCI NIH HHS/ -- CA 43460/CA/NCI NIH HHS/ -- CA 47345/CA/NCI NIH HHS/ -- CA 62924/CA/NCI NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- R01 CA057345/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1546-58. doi: 10.1126/science.1235122.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ludwig Center and The Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21287, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539594" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Transformation, Neoplastic/*genetics ; *Genes, Neoplasm ; Genetic Heterogeneity ; *Genome, Human ; Humans ; *Mutagenesis ; Mutation ; Neoplasms/*genetics ; Signal Transduction/genetics
    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...