This excerpt taken from the CBMX 10-K filed Mar 27, 2009.
Breast cancer is the most common malignancy in women in the United States. The American Cancer Society estimates that there will be approximately 182,000 new cases of breast cancer in 2008 and about 41,000 women will die from this disease. Recent studies have shown that approximately 21 percent of newly diagnosed breast cancer cases have extra copies of the HER2 gene on chromosome 17 (called HER2-positive), and thus, these patients have a concomitant poor prognosis due to the aggressive disease characteristics conferred by the extra dosage of the HER2 gene product. HER2-positive tumors are likely to respond to the Herceptin drug because it is designed to target the product of the HER2 oncogene. Conversely, it is important to accurately identify patients with normal copy number or loss of the HER2 gene (HER2-negative) because, for these patients, the risks of side effects, including cardiotoxicity, are greater than any potential benefit of the drug.
In 2008, we launched HerScan array services, which is the first BAC CGH array-based test for breast cancer patients. The HerScan test is designed to detect amplification of the HER2 gene in early breast cancer while simultaneously giving clinicians a complete profile of a patient's tumor genome.
The HerScan test gives pathologists and oncologists an objective measure of the HER2 gene copy number with simultaneous analysis of the entire tumor genome. As a function of the enumeration of the HER2 gene through the HerScan test, patients are assigned to one of four categories of HER2 gene status: amplification, gain, normal, or loss. As part of the validation of the HerScan test, clinical testing was completed on over 100 cases of invasive ductal and invasive lobular carcinomas. The HerScan test accurately and reproducibly determined HER2 status, and in addition, clearly revealed the genomic subtypes previously reported in the publication Cancer Research 64: 8541-8549; 2004. These subtypes include tumors showing gain of chromosome 1q; loss of chromosome 16q; amplification of the c-MYC oncogene on chromosome 8; and loss of the tumor suppressor gene P53 on chromosome 17. These additional markers, which are not simultaneously available by the conventional diagnostic techniques of immuno-histochemistry or fluorescence in-situ hybridization, provide additional relevant information, enabling the clinician to make better patient management decisions and recommendations.