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  • 1
    Publication Date: 2011-10-29
    Description: Cytotoxic chemotherapy targets elements common to all nucleated human cells, such as DNA and microtubules, yet it selectively kills tumor cells. Here we show that clinical response to these drugs correlates with, and may be partially governed by, the pretreatment proximity of tumor cell mitochondria to the apoptotic threshold, a property called mitochondrial priming. We used BH3 profiling to measure priming in tumor cells from patients with multiple myeloma, acute myelogenous and lymphoblastic leukemia, and ovarian cancer. This assay measures mitochondrial response to peptides derived from proapoptotic BH3 domains of proteins critical for death signaling to mitochondria. Patients with highly primed cancers exhibited superior clinical response to chemotherapy. In contrast, chemoresistant cancers and normal tissues were poorly primed. Manipulation of mitochondrial priming might enhance the efficacy of cytotoxic agents.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280949/" 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/PMC3280949/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ni Chonghaile, Triona -- Sarosiek, Kristopher A -- Vo, Thanh-Trang -- Ryan, Jeremy A -- Tammareddi, Anupama -- Moore, Victoria Del Gaizo -- Deng, Jing -- Anderson, Kenneth C -- Richardson, Paul -- Tai, Yu-Tzu -- Mitsiades, Constantine S -- Matulonis, Ursula A -- Drapkin, Ronny -- Stone, Richard -- Deangelo, Daniel J -- McConkey, David J -- Sallan, Stephen E -- Silverman, Lewis -- Hirsch, Michelle S -- Carrasco, Daniel Ruben -- Letai, Anthony -- P01CA068484/CA/NCI NIH HHS/ -- P01CA139980/CA/NCI NIH HHS/ -- R01 CA129974/CA/NCI NIH HHS/ -- R01 CA129974-05/CA/NCI NIH HHS/ -- R01CA129974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 25;334(6059):1129-33. doi: 10.1126/science.1206727. Epub 2011 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22033517" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; Antineoplastic Agents/*therapeutic use ; *Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Child ; Disease-Free Survival ; Drug Resistance, Neoplasm ; Female ; Humans ; Leukemia, Myeloid, Acute/drug therapy/physiopathology ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Mitochondria/*physiology ; Multiple Myeloma/drug therapy/physiopathology ; Neoplasms/*drug therapy/*physiopathology ; Ovarian Neoplasms/drug therapy/physiopathology ; Peptide Fragments/metabolism ; Permeability ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/physiopathology ; Proto-Oncogene Proteins c-bcl-2/chemistry/metabolism ; Remission Induction ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2013-04-13
    Description: Type I interferons (IFN-I) are critical for antiviral immunity; however, chronic IFN-I signaling is associated with hyperimmune activation and disease progression in persistent infections. We demonstrated in mice that blockade of IFN-I signaling diminished chronic immune activation and immune suppression, restored lymphoid tissue architecture, and increased immune parameters associated with control of virus replication, ultimately facilitating clearance of the persistent infection. The accelerated control of persistent infection induced by blocking IFN-I signaling required CD4 T cells and was associated with enhanced IFN-gamma production. Thus, we demonstrated that interfering with chronic IFN-I signaling during persistent infection redirects the immune environment to enable control of infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704950/" 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/PMC3704950/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Elizabeth B -- Yamada, Douglas H -- Elsaesser, Heidi -- Herskovitz, Jonathan -- Deng, Jane -- Cheng, Genhong -- Aronow, Bruce J -- Karp, Christopher L -- Brooks, David G -- 8UL1TR000077-04/TR/NCATS NIH HHS/ -- AI060567/AI/NIAID NIH HHS/ -- AI082975/AI/NIAID NIH HHS/ -- AI085043/AI/NIAID NIH HHS/ -- HL108949/HL/NHLBI NIH HHS/ -- P30 AI028697/AI/NIAID NIH HHS/ -- P50 AR063020/AR/NIAMS NIH HHS/ -- R01 AI047868/AI/NIAID NIH HHS/ -- R01 AI056154/AI/NIAID NIH HHS/ -- R01 AI085043/AI/NIAID NIH HHS/ -- R01 HL108949/HL/NHLBI NIH HHS/ -- U01 AI082975/AI/NIAID NIH HHS/ -- UL1 TR000077/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):202-7. doi: 10.1126/science.1235208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology and Molecular Genetics and the UCLA AIDS Institute, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Antigens, CD274/metabolism ; Arenaviridae Infections/*immunology/*virology ; CD4-Positive T-Lymphocytes/immunology ; Cytokines/immunology/metabolism ; Dendritic Cells/immunology ; Gene Expression Profiling ; Immune Tolerance ; Interferon Type I/genetics/*immunology/*metabolism ; Interferon-gamma/immunology/metabolism ; Interleukin-10/metabolism ; Lymphocytic choriomeningitis virus/*immunology/*physiology ; Mice ; Oligonucleotide Array Sequence Analysis ; Receptor, Interferon alpha-beta/antagonists & inhibitors/genetics/metabolism ; *Signal Transduction ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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