A Good Biomarker Is Hard to Find
17/08/10 20:32 Filed in: GenomeWeb Daily Scan
Submitted by S. Pelech - Kinexus on Tue, 08/17/2010 - 20:32.
The major reason why robust cancer biomarkers are difficult to find is that over a hundred oncoproteins and probably a greater number of tumour suppressor proteins can contribute to neoplastic growth. The gain of function of just a few oncoproteins in combination with the loss of function of a couple of tumour suppressor proteins may be sufficient for full blown cancer. In view of the astronomical number of complimenting combinations of mutations of the genes encoding these growth control proteins, each cancer in a patient may be unique. If one views cancer as an organ-specific disease, then it will be impossible to find a biomarker that correlates in high frequency with cancers of a specific tissue and not to cell proliferation in general. However, if one considers cancer as a disease-specific to particular combinations of defective proteins, then it becomes possible to not only provide an accurate diagnosis but also to develop an effective strategy for therapeutic intervention. Presently, it is feasible to identify thousands of mutation sites in oncogenes and tumour suppressor proteins with gene microarray technology. However, it is difficult to ascertain whether these actually underlie the problem in a particular cancer due to numerous feedback controls and redundancy in the regulatory proteins that control cell growth and death. Antibodies and enzyme assays are the best way to assess the functional states of regulatory proteins, but the reagents available at this time are often non-specific and impotent. As improved reagents are developed and we better understand how these regulatory proteins interact in control systems, much more accurate cancer diagnoses will become feasible.
Link to the original blog post.
The major reason why robust cancer biomarkers are difficult to find is that over a hundred oncoproteins and probably a greater number of tumour suppressor proteins can contribute to neoplastic growth. The gain of function of just a few oncoproteins in combination with the loss of function of a couple of tumour suppressor proteins may be sufficient for full blown cancer. In view of the astronomical number of complimenting combinations of mutations of the genes encoding these growth control proteins, each cancer in a patient may be unique. If one views cancer as an organ-specific disease, then it will be impossible to find a biomarker that correlates in high frequency with cancers of a specific tissue and not to cell proliferation in general. However, if one considers cancer as a disease-specific to particular combinations of defective proteins, then it becomes possible to not only provide an accurate diagnosis but also to develop an effective strategy for therapeutic intervention. Presently, it is feasible to identify thousands of mutation sites in oncogenes and tumour suppressor proteins with gene microarray technology. However, it is difficult to ascertain whether these actually underlie the problem in a particular cancer due to numerous feedback controls and redundancy in the regulatory proteins that control cell growth and death. Antibodies and enzyme assays are the best way to assess the functional states of regulatory proteins, but the reagents available at this time are often non-specific and impotent. As improved reagents are developed and we better understand how these regulatory proteins interact in control systems, much more accurate cancer diagnoses will become feasible.
Link to the original blog post.