Biological Chemical Pathways And Its Effect On Cancer Cells Essay

Cancer, medically called ‘tumorigenesis’ (Thaker, Lutgendorf, & Sood, 2007, p.430) occurs when cells in the body orient themselves for malignant growth. Such cells show ‘self-sufficiency in growth signals’, are ‘insensitive to anti-growth signals’ and have ‘limitless replicative potential’ (Thaker, Lutgendorf, & Sood, 2007, p.430). Once a particular set of cells become malignant, the malignancy can spread to other set of cells in different organs due to ‘crosstalk’ between the affected cells and their surrounding ‘tissues’ and ‘micro-environments’(Thaker, Lutgendorf, & Sood, 2007, p.430).

Cancer is characterized by unregulated/uncontrolled growth and spread of abnormal cells. The etiological factors of Cancer include both external factors (tobacco, infectious organisms, chemicals, and radiation) and inherent factors (inherited mutations, hormones, immune conditions, and mutations that occur from metabolism). The etiological factors may act together or in sequence to trigger the development of cancer. It may take several years for the manifestation of the disease to be obvious after the initial trigger.

Cancer is described as the abnormal growth of cells. Normal cells are replaced with abnormal cells in which their deoxyribonucleic acid (DNA) has been damaged or augmented (McCance & Huether, 2014). Cancer cells with their various DNA changes are characterized by growing uncontrollably, being immortal with an unlimited lifespan

Breast Cancer is a type of cancer where in the breast cells growth are uncontrolled. To enhance our understanding of breast cancer, knowing how any cancer can develop is crucial. Cancer develops as a result of the alteration of the genes, or abnormal changes in the genes accountable for managing the growth of the cells and maintaining their health. In each nucleus, the genes operates as the “control room.” The cells in our bodies replace themselves through a process called cell growth in which the

An effective breast cancer treatment in some women can be traced to the root of the disease. Some of the most aggressive form of breast cancers are caused by a transmembrane receptor protein known as Human Epidermal Growth Factor Receptor 2 (HER2) which is a member of the HER family of receptor tyrosine kinase. Approximately 20,000 HER2 receptor are normally expressed on surface of healthy breast cell however, in about 25% of breast cancer cells the HER2 protein is overexpressed resulting in tumour cells with as many as over 2 million receptors present on their surface. This cancer is known as HER2 positive (HER2+). The effect of HER2 overexpression is an increase in receptor mediated intracellular signalling causing the cell

Cancer occurs when cells in the human body create irregularities and start to duplicate at anomalous quick rates. The outcome is the development of tumors in or on the surface of the body and organs. Tumors might be generous (not destructive) or threatening (harmful). Since ordinary cell improvement and duplication is a moderate procedure which is well controlled, it is evident when cells duplicate so rapidly.

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

Cancer cells respond to signals from other cells, and they communicate using hormones. Hormones can be small proteins or derived from steroids. To change a cell’s behavior, the target cell is sent a hormone from the signaling cell. Hormones can cause the cell to produce new proteins, or to stop producing the bad proteins. The target cells can start to grow and to reproduce.

In the research paper, Transfer of a malignant trait to BRCA1 deficient human fibroblasts following exposure to serum of cancer patients by Dana Hamam and her colleagues, the idea of any cells within the human body that contain a single oncosuppressor mutation and can assimilate cancer factors and endure a successful malignant transformation is explored. Hamam first goes into detail about the background of cancer. A person that is diagnosed with cancer, it is usually the metastasis (the spreading) of cancer that instigates the poor healthy and possible death of the individual. Due to the statistic, Dana Hamam reviewed a piece of literature that explained the possibility of that the primary tumor cells may not be the only thing spreading throughout the body of cancer patients, but cancer cell-derived factors may also be making their way through the body as well. These cancer cell-derived factors, in theory, would create a niche that would allow malignant cancer cells to take host in other organs in the body. The factors could be numerous things such as proteins or nucleic acids that may perhaps be either floating around in the bloodstream or hitching a ride in exosomes (small extracellular membrane-enclosed vesicles). This process of trait transfers through blood circulating factors is named genometastasis. Hamam actually did an experiment on human embryonic kidney cells (HEK293) that was exposed to cancer. Those embryonic kidney cells were transformed into malignant cancer

Cancer occurrs by the production of multiple mutations in a single cell that causes it to proliferate out of control. Cancer cells often different from their normal neighbors by a host of specific phenotypic changes, such as rapid division rate, invasion of new cellular territories, high metabolic rate, and altered shape. Some of those mutations may be transmitted from the parents through the germ line. Others arise de novo in the somatic cell lineage of a particular cell. Cancer-promoting mutations can be identified in a variety of ways. They can be cloned and studied to learn how they can be controlled.

The human epidermal growth factor receptor-2 (HER-2)/neu, (erbB-2) gene is localized to chromosome 17q and encodes HER2, is a 185 kDa protein (p185) and 1255 amino acids with an intracellular tyrosine kinase domain and an extracellular ligand binding domain. However, HER family is dysregulated and/or show abnormal signaling activity in a broad range of human tumors and, in particular, the HER2 receptor plays a critical role in disorders. The primary cause of HER2 overexpression in cancers is the amplification of the HER2 gene, an event rarely identified in other malignancies. The essential role of HER2 in the HER signaling cascades leads to the development of anti-HER2 monoclonal antibodies (mAbs) for cancer therapy. In particular, the humanized

RAS proteins are well understood in terms of their function, molecular structure and most importantly their prevalent role in carcinogenesis. Oncogenic RAS is the single most abundant phenotype seen in cancers seen in almost 30% of human tumours screened (Stafford, Walker and Webb, 2012); with certain mutations in RAS being the single determining factor for carcinogenesis. The role of RAS in signal transduction pathways involved in cellular proliferation, apoptotic evasion and cell survival make RAS a key proto-oncogene vulnerable to oncogenic mutations. (Weinberg, 2014) The structural indications of certain mutations in RAS is widely understood however the preference of different RAS mutational isoforms in certain cancers still requires

High level of Aluminum in the brain causes the formation of neurofibrilar tangles (the main characteristics of the

Jiang-Tao Li, Jiu-Liang Zhang, Hui He, Zhi-Li Ma, Zhi-Kui Nie, Zhen-Zhen Wang, and Xiao-Gen Xu are affiliated with the College of Food Science and Technology, Huazhong Agricultural University & Key Laboratory of Environment Correlative Dietology, and the Ministry of Education, all in China. Their study of corn peptide effects on liver tumors in mice was funded by a grant from China’s National Natural Science Foundation and National “863” Program. They undertook this study to examine the effects of plant-derived chemicals on cancer. Cancers can be a result of any combination of dietary insufficiency, environmental factors, and/or genetic components. However, up to 95% of cancers are thought to be the result of diet and other lifestyle factors rather than the result of genetic factors (Bhanot et al 2011). The authors recognize this fact and there is a proliferation of naturally based products to boost immune function and combat tumor growth and development. Corn proteins (CPs) are widely and readily available as they are by-products of the expansive corn products market. Because previous work with CPs had shown positive physical affects (such as lowering blood pressure and mitigating the harmful effects of alcohol on the liver), the authors chose to examine how CPs might modulate tumors and the immune systems of mice.

The human epidermal growth factor receptor 2 has been established in most of the clinical and the preclinical settings. HER2 has the strongest kinase activity as compared with the other HER family proteins in the protein and its functions are the most active because they signal the complexity of the HER2 family after dimerization (Liu et al., 2014). The overexpression of the HER2 in the breast cancer tissues can lead to increased levels of the hetero-dimerization as well as high levels of homo-dimerization. This initiates pro-tumorigenic in the tissues which signal a cascade. There is a transformation of the cell cultures because of increased overexpression of the HER2 proteins in the body of the various patients used in any experimental study. The same overexpression of HER2 leads to transgenic mouse