New vector delivers genes to lung cells
Article Abstract:
A genetically engineered virus has been introduced into the lungs of rats; the virus contains a gene which encodes a protein that can treat respiratory infections such as colds. This work is being done by scientists at the National Heart, Lung, and Blood Institute and those at the Institut Gustave-Roussy and Transgene in France. This is the first time a foreign gene has been successfully introduced into the lungs. This research differs from other work, as it uses a different type of virus, an adenovirus rather than retroviruses, which have been used in the past. Adenoviruses naturally infect lung cells and produce and secrete foreign proteins in large quantities. These techniques may be further developed to treat pulmonary diseases in humans, such as cystic fibrosis and a form of emphysema that is inherited. In hereditary emphysema, the gene coding for the protein alpha 1-antitrypsin is defective. Alpha 1-antitrypsin blocks the enzyme elastase, which can destroy the tissue of the lung, causing emphysema, if uncontrolled. The gene which encodes alpha 1-antitrypsin can be introduced into the lungs of humans and can be used to treat hereditary emphysema. Further experiments need to be done to establish the safety of the use of the genetically engineered adenovirus. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1991
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Tumor suppressor genes: the puzzle and the promise
Article Abstract:
The links between gene function and cancerous tumor growth have been investigated in recent years. In cancer, cell growth is abnormally rapid. Scientists have discovered that certain genes, called oncogenes, must be activated to produce accelerated growth. But for malignancy to develop, other genes, called suppressor genes, must be inactivated; these genes normally limit cell proliferation. Loss of suppressor gene activity appears to be as crucial as stimulation of oncogenes in changing a normal cell to a cancerous one. When oncogenes and suppressor genes function normally, they form a system of checks and balances that controls cell growth and prevents cancer. Researchers have detected a loss of suppressor gene activity in every type of solid tumor. Several suppressor genes may need to be inactivated for a certain cancer to form, and one specific suppressor gene may be implicated in more than one type of cancer. Lung, breast and colon cancer appear to share certain mutations of suppressor genes. Tumor suppressor genes constitute a very important area of research; they may reveal effective ways to prevent and treat cancer. When functioning normally, tumor suppressor genes are the body's natural protection against cancer; for many individuals they prevent carcinogenesis throughout most or all of the life span.
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1989
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One Wilms' tumor gene is cloned; are there more?
Article Abstract:
Researchers now believe that human cells become cancerous through a series of many steps; each step is apparently caused by a specific genetic mutation. Ten separate abnormalities may need to accumulate before a cell becomes cancerous. In cancer, cell growth is abnormally rapid. Scientists have discovered that certain genes, called oncogenes, must be activated to produce accelerated growth. But for malignancy to develop, other genes, called suppressor genes, must be inactivated; these genes normally limit cell proliferation. Loss of suppressor gene activity appears to be as crucial as stimulation of oncogenes in changing a normal cell to a cancerous one. Scientists have cloned a gene that may cause Wilms' tumor, which is responsible for 85 percent of kidney cancer in children. A clone is an identical reproduction of the original cell. While the suspected gene appears to be critical in the development of Wilms' tumor, other genes may also be involved. The one gene cloned so far is involved in suppressing cell growth; if its action is stopped by a mutation, and certain other mutations occur simultaneously, rapid cancerous growth may result. Researchers are working to identify the exact role of the cloned gene; they suspect it has a specific place in a sequence of mutations that eventually causes Wilms' tumor.
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1989
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