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The article by Esteva and Hortobagyi (2008) discusses breast cancer from the aspect of increased survival rates, the novel treatments that have necessitated this and the promise in even more enhanced management of breast cancer. The authors identify that North America, as well as Canada, have particularly enjoyed higher breast cancer survival rates due to advanced research in cancer therapy among other reasons. It has been possible to tailor cancer therapy for patients in addition to the ability to mix treatments to effectively handle cancer at any stage.
Esteva and Hortobagyi (2008) have highlighted that tumor growth highly proliferates if there is the production of the HER2 protein. This protein has now become a target molecule for newly developed cancer drugs such as trastuzumab. The molecular targeting is being advanced to attack other cells that are known to lead to breast cancer initiation and progression. While these authors acknowledge the great impact of novel cancer therapies, they also emphasize the use of earlier therapies as well as the provision of supportive care, better and widespread screening, and awareness campaigns as important factors that are combined to realize better results.
The knowledge that the presence of BRCA gene mutations increases the likelihood of breast cancer development has necessitated the development of MRI screening. Screening is done annually especially among families with a history of breast cancer. Current surgical removal of affected breast tissue is less damaging; the same with current radiation therapy which is highly focused. Esteva and Hortobagyi (2008) also note that systemic therapies come in handy in targeting metastatic cells which may be missed by other treatment approaches. Localized breast cancer which is dependent on female reproductive hormones is handled using antiestrogen or antiprogesterone medications, with direct targeting of the hormonal cell receptors improving efficacy. This approach was adopted after realizing that receptors for sex hormones can exacerbate cell growth, including cancerous cells.
The authors also indicate that the discovery of oncogenes explains the differences in breast cancer presentation among different patients. This realization opens the door for developing even more customized therapy if an individual’s tumor were to be profiled. This promise is indicated by the success of therapies such as trastuzumab which targets the HER2 gene. Future drugs should aim at interfering with the pathway leading to the generation of the HER2 gene or directly suppressing the HER2 receptor by initiating antibody attack. According to the authors, there is high promise in breast cancer treatment if researchers pursue “molecular targeting of breast cancer and individualized therapy” (Esteva & Hortobagyi, 2008, p. 63).
Having realized that HER2 genes are involved in the proliferation of breast cancer cells, it is possible to utilize the understanding of the cell cycle to arrest breast cancer development. Interfering with the cell cycle of breast cancer development cells is one of the promising approaches that can be taken. In fact, some drugs have been shown to interfere with the cell cycle effectively thus appearing promising in the treatment of breast cancer. Zhuang and Miskimins (2008) indicate that metformin “inhibit cyclin D1 expression and proliferation of some cultured cancer cells” (p.18). In specific, the G0/G1 phase is arrested. Drugs can also target other stages of the cell cycle. For instance, it has been shown that TAM67 “inhibits breast cancer growth predominantly by inducing inhibitors of cyclin-dependent kinases (such as p27) and by reducing expression of cyclins involved in transitioning from G1 into S phase of the cell cycle” (Liu et al., 2004, p. 8238).
References
Esteva, F. J. and Hortobagyi, G. N. (2008). Gaining ground on breast cancer. Scientific American, 298, 58-65.
Liu, Y. Lu, C., Shen, Q., Munoz-Medellin, D., Kim, H. and Brown, P. H. (2004). AP-1 blockade in breast cancer cells causes cell cycle arrest by suppressing G1 cyclin expression and reducing cyclin-dependent kinase activity. Oncogene, 23, 8238–8246.
Zhuang, Y. and Miskimins, W. K. (2008). Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1. Journal of Molecular Signaling, 3:18.
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