SOFT TISSSUE SARCOMA; Study data from Ohio State University provide new insights into soft tissue sarcoma. (2007, December 3). Biotech Business Week, 1033.
Chen, C., Cen, L., Chan, C., Hsieh, F., Chen, G., et al. (2007 June 28). Signal transducer and activator of transcription factor 3 is involved in cell growth and survival of human rhabdomyosarcoma and osteosarcoma cells. BMC Cancer, (7) 111.
The articles address certain types of soft tissue sarcomas. Soft tissue sarcomas are malignant tumors that can develop from fat, muscle, nerve, fibrous tissues surrounding joints, blood vessel, or deep skin tissues. They can develop in any part of the body. They include oesteosarcomas (ca. of the bone); rhabdomyosarcomas (ca. of the voluntary muscles) which includes alveolar and embryonal; and also leiomyosarcoma cell lines which is soft tissue cancer of the smooth or involuntary muscles.
Stat3 is a proto-oncogene that is highly regulated; therefore it is not always turned on. However, a mutation in its pathway can lead to its constant activation, which then contributes to uncontrolled cell proliferation and cancer. Researchers noticed the constitutively activation of Stat3 in cancer cells.
However, they did not know if the signaling pathway of constitutive Stat 3 plays any role in the survival and growth of osteosarcomas, rhabdomyosarcomas, and other soft tissue sarcomas. In order to find out if constitutive Stat3 was activated, in the cancers listed above, researchers examined sarcoma tissues and sarcoma cell lines using immunohistochemistry and western blot analysis with a specific phosphor-Stat3 antibody. Through studies, researchers found that the activated Stat3 pathway is important for cell growth and survival of human sarcoma cells; the study also showed that Stat3 phosphorylation is elevated in human rhabdomyosarcoma, osteosarcoma and other soft tissue sarcomas.
My summary article is from Biotech Business Week, Dec. 3, 2007. This summary is not a typical newspaper article because it contains mostly direct quotes from the abstract of the primary article. The words are those of the principal researchers. Therefore, because nothing has been reworded, trust is not an issue; however the article does not provide complete data. The complete article was easier to understand because it provided extensive background information and gave details on the methods. Because the secondary article summarizes the basic information in only two paragraphs, some important findings were left out. For example, in the primary study, the authors stated that further research must be done to determine the mechanism of the constitutive Stat3 phosphorylation; the study showed mainly the relationship, but not the mechanism. Furthermore the discussion section mentions that the activated Stat 3 pathway could be useful in developing new chemotherapy drugs because blocking Stat 3 signaling in sarcoma cells induces apoptosis, which can stop growth. I checked Google Scholar and Highwire Press, and this article has not yet been cited.
My reaction to the two articles was that the primary source was clearer and gave more substantial information. I enjoyed seeing the charts and being able to understand them and think about the implications as described in the Discussion section. The primary article motivated me into wanting to know more about the constitutive Stat3 and find out more about their future research. The two questions I have remaining are: have researchers made any progress to developing chemotherapy agents and how many subjects were involved in the study and how old were they?
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This post relates to PattyD's post on soft tissue cancers and stat3. I have done a large screen of thymomas (cancer of they thymus; this is a cancer of lymphoid cells) in rats to identify possible genes involved in the initiation and/or progression of these tumors in the rat. Stat3 is one of the genes that has been identified. It was not surprising to me that stat3 would be a potential oncogene, when de-regulated (given its normal role in the cell); but now I am even more interested in this gene, given PattyD's post. Did they mention in the article that stat3 had been published as associated with any other cancers?(my work has not been published yet). also, are there stat3 "knockout mice" or mice over expressing stat3 that people use for looking at the effects of a gene in vivo?
nice post, Patty
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