Genetic engineering is currently being used to direct the natural ability of some T-lymphocytes to destroy viruses toward the destruction of breast cancer cells. The drug CX 5461 has been shown to block ribosome biogenesis and protein production. Excess Human Epidermal Growth Factor Receptor 2 protein (HER2) has been found in up to 30% of breast cancer patients, thereby making it a major risk factor and a negative survival indicator. It has been understood that ER (Estrogen Receptor) and PR (Progesterone Receptor), which tend to be increased along with HER2, are not as reliable as the latter for risk estimation. HER2 status measurement has become mandatory for proper diagnosis and treatment planning.
Women who have positive for HER2 protein have also been found to have a lot of female hormone receptors that make them very sensitive to estrogen and progesterone. These hormone sensitive breast tumors have been found to have the tendency to be the lobular type. Breast tumors that are not hormone-sensitive are known to have a greater tendency to spread, and therefore prove more difficult to treat. Tumors that test negative for HER2, ER and PR, have been identified and designated 'triple negative'.
HER2-negative tumors have been shown to be mostly ductal carcinomas and very hard to treat. It has been understood that only the 15% to 20% of breast malignancies caught in their very early (carcinoma-in-situ) stage prior to spreading to lymph nodes can be surgically eradicated. Ductal carcinoma-in-situ (DCIS) is now known to be the precursor (preceding stage) for invasive carcinoma. Lobular carcinoma-in-situ (LCIS), on the other hand, is now known to be just an indicator of high risk for breast cancer development.
Tamoxifen, an aromatase inhibitor (AI) that blocks the conversion of other hormones to estrogen has been successfully used to limit their growth. Researchers in London have shown that the drug AT 13148 can block multiple breast cancer targets - HER2 positive and PIK3CA-mutated BT474 receptors. Researchers at Cinergy Health in New York have shown that the drug poly adenosine diphosphate ribose polymerase (PARP) enzyme inhibitors can shrink BRCA gene mutation positive tumors. The drug CX 5461 has also been shown to block ribosomal biogenesis and protein synthesis in cancer cells. The drug herceptin (trastuzumab) has been successfully used to inhibit the overproduction of HER2 in some patients.
Given this rapid explosion of the understanding of how these tumors develop, the various possible intervention targets, and potential drug treatment options, there is good reason to look forward to an imminent final breakthrough in the search for a cure for breast cancer. (See Part I)