Dr. Richard D. Wood

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  www.promisingminds.com/AwardDetails.aspx?ProgramID=308& - [Cached Version]
  Published on: 7/1/2007    Last Visited: 7/1/2007  

  Richard D Wood, PhD Visiting Professor: Hillman Cancer Center

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  DNA enzyme patches genetic potholes -... - [Cached Version]
  Published on: 10/22/2004    Last Visited: 10/22/2004  

  "Over the years, we've studied how DNA damage is taken out of DNA by enzymes through a cut-and-splice mechanism," said Richard Wood, head of the molecular and cellular oncology program at the University of Pittsburgh Cancer Institute and one of the study's authors.
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  POLQ comes to the rescue in a different way that Wood likened to a wooden plank or metal board being placed over a pothole.
  
  "Instead of taking the damage out, POLQ seems to bypass it while the DNA is being copied," said Wood, who is also a pharmacology and molecular oncology professor at the University of Pittsburgh School of Medicine.
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  POLQ isn't always perfect, but it is the only known enzyme to single-handedly perform this type of DNA repair, Wood said.
  
  "POLQ's two-step actions of insertion and extension, essentially the work that would be performed by two enzymes, are the most efficient of any known DNA polymerase," Wood said."While a mispaired base may in turn result in mutation after replication, it seems to be a small price to pay for the cell's survival."
  
  Wood and his cancer institute colleague Mineaki Seki teamed with researchers in Japan and Pitt computational biology experts Lee Wei Yang and Ivet Bahar to find out what makes POLQ work.
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  For example, disabling POLQ might make radiation therapy more effective because it would allow the radiation to disrupt the division of cancer cells without resistance from DNA repair enzymes, Wood said.

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  A look at duct tape, cellular style - [Cached Version]
  Published on: 10/25/2004    Last Visited: 10/26/2004  

  The enzyme is by no means perfect when it makes its repairs, said molecular oncologist Richard Wood.In fact, it often makes mistakes ---- genetic mutations ---- that need to be corrected later.But POL-Q can rapidly fill in gaps in DNA or quickly replace damaged areas in the DNA strands, mistakes that otherwise would halt the process of DNA replication and virtually ensure the cell's death.
  
  "You trade mutation for survival," said Wood, who heads the Molecular and Cellular Oncology Program at the University of Pittsburgh Cancer Institute.
  
  Wood, research associate Mineaki Seki and colleagues at Pitt and Osaka University reported this newly discovered function of POL-Q in a paper published online last week by The EMBO Journal, a publication of the European Molecular Biology Organization.
  
  POL-Q is one of 15 such enzymes that are involved in repairing the damage that occurs routinely in cellular DNA, the molecule that encodes genetic information.Failure to repair this damage, or mistakes made in repair, can lead to cancer.
  
  While Wood's group has been characterizing the enzyme, a research team headed by John Schimenti, a geneticist at Cornell University, has developed a mouse without an active gene for producing POL-Q.
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  Wood emphasized that it's too soon to say where this basic research might lead.

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  ASM Meetings - [Cached Version]
  Published on: 11/29/2001    Last Visited: 10/9/2004  

  Errol Friedberg, Robert Fuchs, Jan Hoeijmakers, Maria Jasin, Joe Jiricny, Alan Lehmann, Tomas Lindahl, Leona Samson, John Tainer, Kiyoji Tanaka, Sam Wilson, Rick Wood
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  Rick Wood, University of Pittsburgh Cancer Institute

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  Abilene Reporter News: Nation / World - [Cached Version]
  Published on: 10/26/2004    Last Visited: 10/27/2004  

  The enzyme is by no means perfect when it makes its repairs, said molecular oncologist Richard Wood.In fact, it often makes mistakes -- genetic mutations -- that need to be corrected later.But POL-Q can rapidly fill in gaps in DNA or quickly replace damaged areas in the DNA strands, mistakes that otherwise would halt the process of DNA replication and virtually ensure the cell's death.
  
  "You trade mutation for survival," said Wood, who heads the Molecular and Cellular Oncology Program at the University of Pittsburgh Cancer Institute.
  
  Wood, research associate Mineaki Seki and colleagues at Pitt and Osaka University reported this newly discovered function of POL-Q in a new paper published online by The EMBO Journal, a publication of the European Molecular Biology Organization.
  
  POL-Q is one of 15 such enzymes that are involved in repairing the damage that occurs routinely in cellular DNA, the molecule that encodes genetic information.Failure to repair this damage, or mistakes made in repair, can lead to cancer.
  
  While Wood's group has been characterizing the enzyme, a research team headed by John Schimenti, a geneticist at Cornell University, has developed a mouse without an active gene for producing POL-Q.
  ...
  Wood emphasized that it's too soon to say where this basic research might lead.

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  Albert P. Knowles Research Fund | Giving and... - [Cached Version]
  Published on: 8/8/2008    Last Visited: 8/8/2008  

  The Research Fund greatly enhanced UPCI's recruitment of Richard Wood, Ph.D., one of the most accomplished molecular scientists in the world, who now leads our Molecular and Cellular Oncology Program.
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  --Rick Wood, PhD
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  Dr. Wood and Mary Knowles McClintock
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  Dr. Rick Wood and Mary Knowles McClintock.

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  Amoena Aviana Post Mastectomy Breast Forms Prosthesis... - [Cached Version]
  Published on: 12/18/2002    Last Visited: 6/25/2004  

  Richard Wood, a cancer specialist at the University of Pittsburgh, says this commonality shows how vital DNA repair has been throughout evolution: Species that could fix damaged DNA survived; those that couldn't perished.
  
  "The human genome encodes information to protect its own integrity," Wood said.
  
  Medical applications of DNA repair are undergoing preliminary tests, Wood said, although therapies aren't ready for general use.

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  BIO.COM: Biotechnology Pharmaceutical Therapeutics,... - [Cached Version]
  Published on: 11/19/2004    Last Visited: 1/7/2006  

  In this study, Dr. Wittschieben--working in the laboratory of Richard D. Wood, Ph.D., professor of pharmacology, the Richard M. Cyert Chair in Molecular Oncology and director of the molecular and cellular oncology program at the University of Pittsburgh Cancer Institute--sought to determine pol zeta's key role in mice cells.
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  To do this, Drs. Wittschieben and Wood disabled, or "knocked out," the gene for pol zeta's Rev3L subunit, the part with the lesion-replicating capabilities.
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  According to Dr. Wood, these findings have significant implications for human cancer research, in that such a high degree of chromosomal instability is a characteristic of cancer cells.Furthermore, the human Rev3L gene is located in a segment of chromosome 6 where multiple tumor suppressor genes are believed to reside and a slew of human cancers, including a number of leukemias and lymphomas, are associated with chromosomal instabilities in this particular region of chromosome 6.
  
  "Although it requires further investigation, we believe that mutations in this part of chromosome 6 could occur during the development of some cancers and this may have prognostic and therapeutic implications.We are now investigating this hypothesis by selectively deleting the Rev3L gene in adult mouse cells to study how the loss of DNA polymerase zeta influences the development and progression of spontaneous cancers," explained Dr. Wood.

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  Congregational Church of Austin Texas Monthly... - [Cached Version]
  Published on: 2/24/2006    Last Visited: 1/1/2008  

  For information, please stop by the Shop at 5335 Burnet Road, Monday through Saturday, 10 a.m. to 4 p.m., or call Shop manager Richard Wood at 512-459-1288. (e-mail: sales@next2new.org

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  EMS 2003 Annual Meeting Program - [Cached Version]
  Published on: 9/18/2008    Last Visited: 9/18/2008  

  Richard D. Wood, University of Pittsburgh

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