June 2003
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New Research Breakthroughs at UHN
New Faces in Research
Breaking News from UHN Research
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New Research Breakthroughs at UHN
Cells Infected with Hepatitis C Programmed to Self Destruct
Researchers at AMDI/OCI/PMH have recently used gene therapy to kill liver cells infected with hepatitis C, revealing a promising new approach for treating this deadly
liver disease. According to lead researcher
Dr. Chris Richardson,
the key to this new treatment involves inserting a deadly but inactive form of a molecule into a harmless virus, which is picked up by liver cells. The suicide molecule is
only activated in cells infected with the hepatitis virus, causing these cells to die, while leaving the uninfected cells intact. “In a sense, we developed a genetic smart
bomb,” says Dr. Richardson.
The research group, which included colleagues in Alberta, tested the treatment successfully in a mouse model engineered to have a liver composed of human liver cells.
The treatment may be useful for treating the early stages of liver disease, or when only portions of the liver are infected. This pioneering discovery offers a framework for
the development of new treatments for hepatitis C and other viral infections.
Nat Biotech 2003 May; 21(5):519-525
[PubMed abstract]
Institute: AMDI/OCI/PMH
Division: Division of Molecular and Structural Biology
Priority Platform: Genes, Proteins and People
Molecule Offers Clues for the Treatment of Immune Disorders
The role of the protein caspase-8 in immune system function has been revealed in a new mouse strain developed by a team of researchers led by Drs.
Razq Hakem,
Pam Ohashi and
Wen-Chen Yeh
of AMDI/OCI/PMH. These mice lack caspase-8 in their T cells, the leaders of the immune system.
According to Dr. Hakem, the mice were unable to mount a successful attack against infection. “This research has helped us understand why people who have faulty
copies of this protein have a poorly functioning immune system. It also provides clues for developing therapies for people who suffer from diseases caused by an
overactive immune system.”
Type I diabetes, multiple sclerosis and rheumatoid arthritis are all autoimmune diseases caused by an immune system that works in 'overtime' and attacks healthy
tissues in the body.
Genes Dev 2003 Apr 1;17(7):883-95
[PubMed abstract]
Institute: AMDI/OCI/PMH
Division: Division of Cellular and Molecular Biology
Priority Platform: Genes, Proteins & People
Cell Surface Protein Jump Starts Immune Response
Researchers at TGRI/TGH have identified a novel mechanism which may activate immune cells to fight infections.
Selectins are special proteins that exist on the surface of our cells and have important roles in relaying messages between cells.
Drs. Greg Downey and
Tom Waddell
found that when they specifically stimulated L-selectin proteins using antibodies, the cells were activated and the CXCR4 receptor was externalized. They also found
that stimulation of L-selectin prevented the cell from internalizing the receptor.
“This is very important,” explains Dr. Waddell, “because HIV uses this receptor to enter the cell. So, in knowing how the receptor is affected we may devise a way
to prevent HIV entry into cells.” 
This work will lead to a better understanding of exactly how the immune system mounts its response to protect the body from infection.
Blood 2003 Jun 1;101(11)4245-52
[PubMed abstract]
Institute: TGRI/TGH
Division: Division of Cellular and Molecular Biology
Priority Platform: Regenerative Medicine
New Faces in Research
Peter Cheung, PhD
According to Dr. Peter Cheung—newest researcher in the Division of Experimental Therapeutics at OCI/PMH—the opinion that all cancers arise as a result
of DNA damage is too simplistic. He explains, “In every cell there are multiple proteins and cellular factors besides the DNA that make up a person's genome. Changes
in any one of these components can have a profound effect on whether or not a cell will change its normal course of development and become cancerous.”
The study of these changes is called 'epigenetics' and Dr. Cheung has undertaken to determine how structural changes to specific cellular proteins called histones
can impact cancer development.
“Some changes to histone proteins turn genes on, while others turn genes off, and some changes team together to elicit their effects,” explains Dr. Cheung. “Just as
our cells exploit this feature to regulate gene expression, we can develop drugs that favour one type of change over another to prevent cell growth going awry.”
Read more about Dr. Cheung in the next issue of Net Results.
Breaking News from UHN Research
New Stem Cells Show Promise for Cancer and Transplant Patients
Dr. John Dick—senior scientist at TGRI/TGH—has
discovered a new type of human hematopoietic stem cell (HSC) that may allow transplant patients to quickly regain their blood cells.
HSC's are blood forming cells that have been used to treat cancers of the blood such as leukemia for the past 40 years. A patient's own HSC's are killed when high
doses of radiation and chemotherapy are used to eliminate cancer cells.
The newly discovered HSC's rapidly begin producing a new arsenal of healthy immune cells when injected directly into the bone marrow of mice. HSC's are usually injected into the
blood system and don't begin re-growth until reaching the bone marrow. This process can take up to three weeks, leaving the patient vulnerable to infection.
“This is an exciting discovery because for the first time we have found human stem cells that rapidly rebuild a blood system,” says Dr. Dick, “and it might allow us to
offer bone marrow transplants to a broader range of people.”
View the article published in
The Globe and Mail
on June 9, 2003.
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