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  • A chemotherapy drug packs a one-two punch | Newswire
    published online this week by the journal Blood Dhodapkar postdoctoral fellow Radek Spisek and their colleagues show that unlike radiation or other chemical therapies bortezomib can kill multiple myeloma cells in culture in such a way that it elicits a response by memory and killer T cells The results suggest the drug has the potential to enhance patients immunity to tumors helping their bodies fight the disease more effectively Multiple myeloma is a cancer of immune cells in the bone marrow Dhodapkar s experiments show that when treated with bortezomib in tissue culture multiple myeloma cells die in such a way that a heat shock protein called hsp90 migrate to their surface When another group of immune cells called dendritic cells encounter hsp90 on the dying tumor cells the protein acts as a signal for their activation The dendritic cells then ingest them for presentation to memory and killer T cells a progression that in humans could potentially lead to enhanced immunity If you could directly target the drug to these cells Dhodapkar says it may be sufficient enough to create a vaccine The exposure of heat shock proteins on dying cells represents an immunogenic form of cell death When the researchers tested other standard treatments for multiple myeloma such as radiation or the corticosteroid dexamethasone the therapies failed to increase levels of hsp90 on the surface of dying cells and so couldn t activate dendritic cells to the degree that bortezomib did And their findings aren t limited to a single cancer After treatment with bortezomib dying lymphoma and breast cancer cells experienced the same increase in hsp90 How well this research will translate to increased survival rates depends on how applicable these tissue culture studies are to the actual immune system response in people So Dhodapkar plans to

    Original URL path: http://newswire.rockefeller.edu/2007/02/15/a-chemotherapy-drug-packs-a-one-two-punch/ (2016-02-13)
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  • Kavita Dhodapkar | Newswire
    of undetermined significance or MGUS which sometimes progresses to multiple myeloma But new research suggests that MGUS patients who naturally develop an immune response to an embryonic stem cell protein called SOX2 appear to be protected from developing the blood cancer More Tags Kavita Dhodapkar MGUS myeloma February 15 2007 Science News A chemotherapy drug packs a one two punch How cancer cells are killed could turn out to be

    Original URL path: http://newswire.rockefeller.edu/tag/kavita-dhodapkar/ (2016-02-13)
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  • myeloma | Newswire
    SOX2 appear to be protected from developing the blood cancer More Tags Kavita Dhodapkar MGUS myeloma February 15 2007 Science News A chemotherapy drug packs a one two punch How cancer cells are killed could turn out to be an important element in activating a patient s immune system A new study shows that one chemotherapy drug may kill tumor cells in such a way that the immune system can

    Original URL path: http://newswire.rockefeller.edu/tag/myeloma/ (2016-02-13)
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  • Malignant Cells Survive-and Replicate-Because Cancer-causing Molecule Jams Normal p53 Cell-suicide Trigger | Newswire
    is a tumor suppressor which prevents cancer much as a spell check in a word processor catches and repairs mistakes In the case of p53 the mistakes are mutations in a cell s DNA genetic code If the mistake cannot be repaired p53 activates the cell s suicide program However when p53 is blocked by WISP 1 as is shown to occur by Levine s new research mutations are not caught Instead cells with mutations survive and replicate unchecked resulting in the uncontrolled cell growth that characterizes cancer Faulty p53 is responsible for some 55 percent of all human cancers various studies have revealed Previous research by Levine and his colleagues showed WISP 1 promotes growth of cancer cells and is overproduced or amplified in colon cancer cells In the Genes and Development paper Levine and his Rockefeller colleagues found that WISP 1 thwarts the cell s suicide mechanism by binding to the surface of cells damaged by chemotherapeutic drugs thereby blocking p53 initiated cell death Michael Overholtzer Fei Su and Daniel Besser have begun to elucidate the role of WISP 1 in cancer Most proteins that contribute to cancer either promote cell growth or block cell death says Levine Now we know that WISP 1 does both and the second activity preventing cell death is dependent on p53 WISP 1 works by activating Akt and Bcl XL two other proteins that interfere with the cell death program and disabling a third molecule called cytochrome c Akt and Bcl XL operate in two separate pathways to promote a cell s survival and block cell death respectively Under normal conditions cytochrome c leaks out of mitochondria the cell s energy storage houses and triggers cell death Su showed that WISP 1 inhibits the release of cytochrome c from mitochondria in response to DNA damage The researchers propose that WISP 1 inhibits cytochrome c by increasing production of Bcl XL which blocks the release of cytochrome c even though p53 has been activated This is the first time a link between p53 and Bcl XL has been documented The researchers also found that WISP 1 works only in cells that contain p53 and it doesn t work if the p53 gene is mutated According to Levine this finding helps explain the failure of chemotherapy in the 45 percent of cancers like colon cancer in which p53 is functioning properly and a positive response to chemotherapy would be expected This may explain the poor correlation between response to chemotherapy and presence of p53 which we did not understand before now says Levine Levine and his colleagues also developed an antibody for WISP 1 and showed that the antibody can block WISP 1 We may be able to give an antibody against WISP 1 to cancer patients to enhance the effectiveness of chemotherapy says Levine WISP 1 is a member of the WNT pathway which is involved in embryonic development and stimulates cell growth Other researchers have shown that several proteins in the Wnt

    Original URL path: http://newswire.rockefeller.edu/2002/01/08/malignant-cells-survive-and-replicate-because-cancer-causing-molecule-jams-normal-p53-cell-suicide-trigger/ (2016-02-13)
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  • WISP-1 | Newswire
    while others with the same form of cancer respond to the treatment according to researchers at The Rockefeller University The findings reported in the Jan 1 issue of Genes and Development suggest that drugs designed to block WISP 1 may increase the effectiveness of chemotherapy in colon cancer and perhaps other cancers More Tags Arnold J Levine chemotherapy James E Darnell Jr WISP 1 Search for Categories Science News Awards

    Original URL path: http://newswire.rockefeller.edu/tag/wisp-1/ (2016-02-13)
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  • New Rockefeller faculty member studies mechanisms of DNA repair | Newswire
    understanding how the DNA repair pathway in patients with Fanconi anemia works the function of the proteins in that pathway and their contribution to cancer prevention Dr Smogorzewska honed her interest in molecular biology and biochemistry as an undergrad at the University of Southern California where she also received a summer research scholarship in biological research sponsored by the Howard Hughes Medical Institute and a science and engineering research scholarship sponsored by the United States Department of Energy After receiving her Ph D and M D she did a clinical pathology residency at Massachusetts General Hospital and then joined the genetics department at Harvard Medical School where she has been a postdoc since 2005 in the laboratory of Stephen Elledge As a postdoc Dr Smogorzewska identified and characterized FANCI a gene that is mutated in a subset of Fanconi anemia patients Dr Smogorzewska s research further revealed that this gene affects the repair of DNA Without the proper protein DNA isn t repaired and the outcome is full blown Fanconi anemia a genetic disorder characterized by bone marrow failure skeletal anomalies and increased incidence of tumors Dr Smogorzewska also completed two whole genome genetic screens using RNA interference in human cells one that yielded a list of proteins necessary for survival after DNA cross link damage and a second that resulted in a list of proteins important for induction of replicative senescence Both screens identified many novel components of these critical cellular processes At Rockefeller Dr Smogorzewska will focus her research on understanding how several of these proteins regulate the activity of the Fanconi anemia pathway and other pathways necessary for DNA repair and on identifying factors that promote survival in Fanconi anemia cells in the setting of DNA damage When a cell is confronted with DNA damage it can

    Original URL path: http://newswire.rockefeller.edu/2009/05/27/new-rockefeller-faculty-member-studies-mechanisms-of-dna-repair/ (2016-02-13)
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  • Researchers solve structure of an enzyme vital for DNA repair | Newswire
    Rtt109 The results published today in the Proceedings of the National Academy of Sciences include a description of Rtt109 s structure and a theory of how it works During the first phase of cell division tightly wrapped DNA unwinds itself from around the spool like histones that help control its gene activity and provide structural support The DNA is duplicated and the new strands coil themselves around a freshly manufactured histone complex But when DNA damage occurs the cell recognizes the damage and uses Rtt109 to modify the nearest histone The modification prevents the damaged bit of DNA from wrapping around it too tightly creating slack that provides access for DNA repair It s a very essential process to be able to repair the DNA says André Hoelz senior author of the paper and a research associate in Günter Blobel s Laboratory of Cell Biology Our study addresses one step of this very complicated process We figured out how a critical enzyme is regulated Determining the structure of Rtt109 and understanding its regulation is key to understanding the complex DNA damage repair machinery which involves dozens of other proteins working together Solving one structure gives you just a snapshot But if you have several structures you can understand how they work says Hoelz who collaborated with first author Pete Stavropoulos a former graduate fellow in the Blobel lab And by amassing enough data researchers can begin to understand how other enzymes may be regulated as well The research could ultimately lead to the development of drugs for conditions such as cancer in which rapid cell division goes unchecked and DNA damage from chemotherapy is quickly repaired If we can find a way to target the machinery that corrects damage happening during cell division we could specifically kill those cells undergoing

    Original URL path: http://newswire.rockefeller.edu/2008/08/11/researchers-solve-structure-of-an-enzyme-vital-for-dna-repair/ (2016-02-13)
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  • Seth Darst | Newswire
    RNA is transcribed from DNA has been elected to the National Academy of Sciences one of the highest honors given to a scientist or engineer in the United States More Tags Seth Darst U S National Academy of Sciences October 15 2007 Science News Newly solved structure reveal how cells resist oxygen damage Cells have evolved multiple lines of defense to protect themselves from the effects of singlet oxygen a toxic byproduct of photosynthesis After five years of study Rockefeller University researchers have become the first to solve the structure of a protein complex that regulates this process using a zinc ion to quench singlet oxygen s harmful properties More Tags Seth Darst December 1 2006 Science News Structure shows how a key protein in gene activation is controlled Using the structure of the protein σ28 bound to its inhibitor as inspiration a new structural study finds that this gene activator can also inhibit itself from binding to and expressing the wrong gene at the wrong time More Tags gene activation RNA Seth Darst February 21 2006 Science News Modular structure enables TRCF protein to both halt transcription and repair DNA Using x ray crystallography Rockefeller scientists have now solved the structure of a protein called Transcription Repair Coupling Factor or TRCF that plays a dual role in DNA transcription repair The results show that TRCF employs a modular structure which would allow for conformational changes so that TRCF s recruitment of the repair machinery doesn t interfere with its interruption of transcription More Tags DNA repair Seth Darst transcription factors TRCF May 17 2002 Science News Three D images shed light on first steps of RNA synthesis The first three dimensional images of the initiating form of the molecular machinery in bacteria that transcribes genetic information from DNA into

    Original URL path: http://newswire.rockefeller.edu/tag/seth-darst/ (2016-02-13)
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