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Causes of Breast Cancer

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Date added: 19-02-06


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Cancer is the most lethal and dangerous diseases for human beings. Huge resources have been spent to acknowledge breast cancer evolution, to figure out causes and to develop methods of treating breast cancer. For all these researchers main point is to understand cancer development pathway, and to increase overall survival percentage. Nowadays, scientists are faced with the hard problem, and they are inability to cure it once the breast cancer developed. The key to prevent breast cancer is to analyze and learn more about the biological mechanisms which cause it, and try to identify very early changes. Human breast cancer evolution is not clear and defined. Researchers have not been able to identify early morphological, cellular, or molecular changes which caused to develop breast cancer disease. These research article based on five different investigators scientific articles about breast cancer origin and evolution, molecular evolution of the breast cancer, gene mutations which cause breast cancer, tumor cell growth in human breast cancer.

Many research are done to find solution and prevent breast cancer in early stages. Peter T Simpson article explains invasive breast cancer evolution and development. The whole point of this article is to analyze invasive breast cancer molecules, for better understanding its development. Invasive cancer evolution begins in the lobules; women breast glands that produced milk. After developing invasive cancer cells, they break lobule and spread to the other parts of the body. According to Peter T Simpson article, breast cancer cell development a new ways described in the last a few years. Most of the research have the same result, that the Nuclear grade connected with genetic changes or mutations in breast cancer cells (Simpson, 2005). Based on “Molecular Evolution of Breast Cancer” article there are low?grade and high?grade invasive cancer development. During low?grade invasive cancer cells development, ER (estrogen receptor) and PgR (progesterone receptor) are positive and Her-2 is negative, this means that cancer cells receive signals from progesterone receptor and stop growing (Simpson, 2005). On the other hand, during high?grade development, there are nuclear abnormalities, estrogen receptor is negative and Her-2 is positive. This means that estrogen is supporting cancer cells growth and spread of (Simpson, 2005). However, even a single changes of nuclear molecules can cause breast cancer.

According to Kornelia Polyak article, researchers beginning to understand cancer cells behavior relating to tumor heterogeneity and development. “Breast Cancer: Origins and Evolution” article explains tumor cells, analyzes tumor cells, gives information about evolution of tumor cell based on genetic changes and gene expression changes in organisms (epigenetic). The two common models that this article describes are the cancer stem cell and the clonal evolution hypotheses (Polyak, 2007). As in every model, this two also sharing similarities and have differences between them. The main difference of this two hypotheses is that cancer cells are offspring of cancer stem cells, and can not undergo stem cells unlimited division (self-renewing). Also, after increasing genetic changes the cancer stem cell can control tumor cells movement. Secondary, according to the clonal evolution model, the cancer cells developed multiple phenotypes during genetic and epigenetic changes (Polyak, 2007). Phenotypes are not stable and can change when the tumor cell developed. All tumor cells have the function to undergo cells unlimited division. So, the important difference between the models is describing same types of tumor cell behavior in every case with different mechanisms: either tumor cell genetic or epigenetic changes or tumor cells different phenotypes. Based on Kornelia Polyak scientific research article, both models sharing similarities as well. The most important function that connects both models is tumor cell origination from a single cell that had multiple mutations and variations.

“Breast Tumor Heterogeneity” article discusses the same topic with different views. Lauren L. Campbell & Kornelia Polyak article describes tumor cells morphologies and behaviors in a human breast. The evolution of tumor heterogeneity is not clear; mutations and changes in the nature can effect tumor heterogeneity. As described in a previous article, “Breast Cancer: Origins and Evolution”, this article also explains tumor cells evolution based on two most popular concepts: the cancer stem cell hypothesis, and the clonal evolution model (Campbell, 2007). A lot of research and scientific findings support one of these two hypothesis. These two models are very different, but still sharing some similarities. Based on this article information, breast tumor heterogeneity caused by the clonal evolution hypothesis (Campbell, 2007). The main concept of this article is analyzing breast cancer cells, the most common hypothesis, and the role of clonal evolution model in tumor heterogeneity. These processes are key to develop new effective ways to solve and prevent breast cancer problem worldwide.

There are a few similarities that the cancer stem cell hypothesis and the clonal evolution model share it. According to the authors, in each case, tumor cell originate from a single cell that has mutations. Also, in each case, genetic and environmental changes can increase the risk, as well. Finally, both the cancer stem cell hypothesis, and the clonal evolution model have stem cell: cells within a tumor that can dividing and give rise many tumor cells. These two models have differences as well. First of all, they explain tumor heterogeneity with different mechanisms. Second, according to the cancer stem cell hypothesis, normal stem cells are the most effective of changes, while non of the normal cells are identified by the clonal evolution model. Lastly, according to the cancer stem cell hypothesis, only a small amount of cancer stem cells present during tumor growth, while the clonal evolution model expects that any tumor cell has high risk to be involved in this process.

Researchers are working to figure out the main cause of breast cancer that is still undefined. The previous articles discuss breast cancer evolution, molecular changes, tumor heterogeneity and tumor cell evolution the most common concepts. But this article has different view to the same problem. It discusses the role of genetics to determine breast cancer rick in advance. The main concept of this article is using family history to determine breast cancer risk. According to the American Journal of Human Genetics research study results in 2002, women who had BRCA1 and BRCA2 (BReast CAncer gene 1and 2) genes mutations in their history have huge risk to get breast cancer (more than 80% ), than women without carrying mutation gene (Antoniou, 2003). Also, according to the same article research, children who have mutant gene transferred from parents, develop breast cancer during their life (Antoniou, 2003). The main point of this article is to discuss BRCA1 and BRCA2 gene mutations, which causes both breast cancer and ovarian cancer. Males and females, who are carriers of BRCA1 and BRCA2 gene mutation, were tested and the results are very different. BRCA1 gene mutation does not develop breast cancer among males, but BRCA2 genes have high risk to develop breast cancer. For females, BRCA1 gene mutation have high risk factor to evolve breast cancer, and with BRCA2 gene mutation both breast cancer and ovarian cancer. Lastly, according to the American Journal of Human Genetics, a father with gene mutations can pass the abnormal gene to his children. If the child is a girl, she already has high risk of developing Hereditary breast cancer; gene mutation transferred from parent to child, which developed in very early ages.

Based on “New England Journal of Medicine” report, after Breast Cancer 1 and Breast Cancer 2 gene mutation, the second gene mutation which causes breast cancer is PALB2 gene. The main concept of this scientific article is to explain PALB2 gene importance, and the side effects of PALB2 gene abnormal function. A study founds that breast cancer risk increases of PALB2 gene abnormal function. According to this article, PALB2 gene localized of the BRCA2 gene, and it’s main function is to repair damaged DNA and stop tumor growth (Antoniou, 2014). Also, PALB2 gene makes protein that works with the BRCA2 gene. Unlike the previous articles research, for this experiment researchers collected information from 362 family members (Antoniou, 2014). The half of the family members had an abnormal PALB2 gene, but they did not have an mutant BRCA1 or BRCA2 gene in their family history (Antoniou, 2014). As of result, 229 women out of 311 had been detected with breast cancer, because of PALB2 gene mutation. For men’s, seven out of 51 identified with breast cancer. Based on this study results, the risk to develop breast cancer with PALB2 gene mutation is 14% among women. But the percentage of developing breast cancer increases by age 50 and above.

In conclusion, this research paper based on five different scientific articles with the same view of the problem; understand causes and find solutions to overcome breast canes. In order to prevent breast cancer, researchers analyzing and developing more knowledge about the biological mechanisms, and trying to identify breast cancer during very early stages. Based on the research articles, the evolution of human breast cancer is not clear, very little is known about it. Scientists have not been able to identify early morphological, cellular, or molecular changes which developed breast cancer disease. This research paper analysis breast cancer origin and evolution, molecular evolution of breast cancer, breast tumor heterogeneity, BRCA1 and BRCA2 gene mutation and breast cancer risk during PALB2 mutation. This research paper explains two main well defined pathways to the evolution of low?grade and high?grade invasive disease, the two most common models: the cancer stem cell and the clonal evolution and selection hypotheses, compared and contrasted human tumor cells, as well as used family history to explain breast cancer.

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