Research Paper: Gene Expression Analysis in Cancer

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Gene Expression Analysis in Cancer Cells

Perhaps one of the most critical links in cancer research was the discovery that certain cancers have a strong genetic component and that cancer was not simply a random occurrence. As a result, it is now well established that the presence of certain genes can be highly predictive of whether a person will or will not develop cancer and this fact is considered in some prevention, detection, and treatment guidelines. However, genetic predisposition is only one factor to examine when looking at whether or not someone will develop cancer and the prognosis of a cancer if it develops. In addition to genetic predisposition, exposure to certain environmental factors, most notably carcinogens, can promote the mutations underlying cancer development. The relationship between environmental exposure and genetic predisposition is a complicated one, but understanding how environmental factors impact gene expression in cancer cells may be the key to understanding who develops particular types of cancers and under what circumstances they develop those cancers.

Gene expression analysis provides a way of examining the genes in a cell. More importantly, gene expression analysis provides a way of examining which genes are expressed in a cell. Gene expression is not solely about cancer. For example, most of the cells in a person will contain that person's entire genome, but not all of that genome will be activated in each cell. Instead, the function of the cell determines what parts of the genome are activated. As a result, cells containing the same genetic code can engage in vastly different functions. The messenger RNA (mRNA) helps determine which genes are expressed in each cell, and, though the exact mechanism is not yet fully understood, it appears that environmental factors can impact how mRNA impacts a cell.

Furthermore, genetic information can be useful in the preventative treatment of cancers. For example, when a person has a harmful mutation in either their BRCA1 or BRCA2 gene, this mutation can indicate a higher risk of developing breast cancer, as well as other cancers, most notably ovarian cancer. Combined with the family and personal history of the patient, the presence of this gene may cause a patient to choose a preventative mastectomy or oophorectomy in order to reduce the chances of developing breast cancer. In other cases, the use of hormones, hormone blockers, or preventative drugs like tamoxifen. Even in cases where preventative surgeries are not available, and where the patient does not have lifestyle risk factors that can be altered to change cancer risk, knowing that a patient is at an increased risk of developing a cancer can guide a doctor's screening guidelines. For example, there is a genetic component to many colorectal cancers, and patients in high risk groups may begin routine colonoscopies younger than indicated by general screening guidelines and have them on a more frequent basis than people who are not at risk.

However, one of the most fascinating elements about cancer and genetic risk is that the presence of these high-risk genes does not mean that a patient will necessarily develop cancer. Genes are not a determining factor, although they have a tremendous influence on likelihood of development. Instead, some people with high-risk genetic profiles do not develop cancer within the course of a normal lifetime. This has led to the conclusion that the mere presence of a gene is not enough to predict cancer development; instead, there needs to be a combination of genetic predisposition and some type of environmental triggering factor that activates the gene. Cancer appears, in most cases, to be a combination of environment and genetics, although the environment being discussed may be the environment inside the body, and not within the control of the patient.

Perhaps even more compelling than the fact that environmental triggering factors play a role in activating genes in largely genetic cancers is the notion that genetics may play a role in predisposing people to certain cancers that have been considered non-genetic. For example, exposure to the carcinogens in cigarettes is known to be a significant risk factor for the development of various types of cancers, most notably lung cancer. However, the correlation between smoking and lung cancer is not a one-to-one correlation. Some people can be heavy smokers their entire lives without ever developing lung cancers, while others may develop smoking-related lung cancer after relatively minimal exposure to cigarette smoke. The idea that some people appear to have some type of natural resistance to particular carcinogens may be explained by the presence or absence of certain genes and the environmental triggers required to activate those genes.

The purpose of this overview is to examine the current research in gene expression analysis in cancer cells. The research focuses on several different ways that various environmental factors can help determine gene expression in cancer cells, or in potential cancer cells. Some of this research focuses on the microenvironment and how laboratory growth conditions can impact a cancer cell's resistance to both radiation therapy and chemotherapy. Other research linked chemosensitivity, not only to the likelihood of genetic expression of cancer, but also to other factors that can greatly impact prognosis at diagnosis including: cell adhesion, tumor growth, tumor progression, and invasiveness. Taken together, these factors can not only help predict who will develop cancer, but also help determine appropriate treatment regimes, and help predict metastasis and recurrence rates. Eventually, this research should allow doctors to more accurately determine when aggressive, risky therapies are appropriate and when to stick to less aggressive treatments, not only increasing survival rates, but also reducing some of the horrific side effects that accompany cancer treatment.

Literature Review

The idea that the extracellular matrix (ECM) could have a significant impact on gene expression is not a new one; it is has been established for more than 30 years. The idea was that ECM molecules might provide a means of regulating the cell within the context of its microenvironment. This has proven to be true, and it is now well established that the ECM is linked to changes in both tissue and organ structure, in both malignant and non-malignant cells (Spencer et al., 2007). In malignant progression, structure is impacted on multiple levels: chromatin, nuclear, cellular, and tissue (Spencer et al., 2007). Spencer et al. verified that ECM controls, or at least has a significant impact upon, both gene expression and tissue function. When cells transition from the 2D monolayer to a 3D environment, their structure and shape change. This change in structure has an impact on genetic expression (Spencer et al., 2007). Furthermore, these changes are cumulative; the longer the cells are exposed to ECM, the greater the changes in cell shape, so that the cells undergo morphogenic events and form acinar structures (Spencer et al., 2007). These results make is clear that tissue structure has an impact on genetic expression, which, in turn, has an impact on tissue function and health (Spencer et al., 2007).

Zschenker et al. may not have built directly upon Spencer's research, but they did begin their research with the fundamental perspective that the microenvironment is critical to regulating cell behavior, and, further, that the nature of the extracellular matrix (ECM) can impact gene expression (2012). For example, cells grown in 3D growth conditions had been demonstrated to have greater radiation and chemotherapy resistance than cells grown in 2D growth conditions. They decided to investigate whether the differences in gene expression that were due to growth conditions being either 3D or 2D were linked to DNA repair pathways by comparing basal gene expression of cancer cell lines under both 3D ECM scaffold growth conditions and 2D monolayer conditions (Zschenker et al., 2012). The experiment was repeated with two human cancer cell lines from different origins to ensure that the results were not specific to a single cancer cell line. Their results did not support the idea that 3D growth conditions impacted DNA repair pathways, but did underline a significant difference in cells grown under the two types of growth conditions. What they found was that growth conditions did, indeed, impact gene expression. Moreover, the found that 3D cell cultures could make cancer cells more resistant to both radiation therapy and chemotherapy. Their findings suggested that cell shape and cell to cell contact helped determine cellular responsiveness to external stress, which, in turn can provide cues for therapy resistance. However, they did not find the expected link between cell culture growth dimensions and DNA repair pathways; the transition to the 3D structure does not appear to inhibit or promote the creation of DNA repair pathways (Zschenker et al., 2012).

Martin et al. did not compare 2D and 3D models, but instead used the 3D culture model to examine breast cancer outcomes across different datasets (2008). Breast cancer is not only prevalent in the female population, but, even with aggressive treatment, remains the second deadliest cancer for women in the United States. It is well established that early detection impacts survival rates, though screening guidelines may… [END OF PREVIEW]

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Cite This Research Paper:

APA Format

Gene Expression Analysis in Cancer.  (2013, October 29).  Retrieved June 25, 2019, from

MLA Format

"Gene Expression Analysis in Cancer."  29 October 2013.  Web.  25 June 2019. <>.

Chicago Format

"Gene Expression Analysis in Cancer."  October 29, 2013.  Accessed June 25, 2019.