c-src Structure in Human Cancers
Author Information
Author(s): P. Wang, F. Fromowitz, M. Koslow, N. Hagag, B. Johnson, M. Viola
Primary Institution: State University of New York at Stony Brook
Hypothesis
Is mutational activation the mechanism of enhancement of pp60C-src-specific kinase activity found in human cancers?
Conclusion
Mutational activation is not the mechanism of enhancement of pp60C-src-specific kinase activity in various human cancer types.
Supporting Evidence
- No mutations were detected at codons 98, 381, 444, and 530 in the tumors tested.
- Elevated pp60C-src activity was observed in various human cancers, but not due to mutations.
- The study analyzed 169 human tumors using two different mutation detection methods.
Takeaway
The study looked for mutations in a gene related to cancer but found none, suggesting that other factors might be causing increased activity in cancer cells.
Methodology
RNAase protection and restriction fragment length polymorphism assays were used to detect activating mutations of c-src in human tumors.
Limitations
The study may not have detected all possible mutations due to the specific sites tested.
Participant Demographics
The study included a variety of human tumors, including colon cancers, B-cell lymphomas, and chronic myeloid leukemias.
Want to read the original?
Access the complete publication on the publisher's website