Hyperplasia is the early stage development of cells to cancer cells. It increases in cells that have the capability to proliferate at a fast rate. Often times, hyperplasia is correlated with the increase in proliferation and the speed of mitosis. The increase in the number of cells with hyperplasia means that the proliferation is happening at a faster rate than normal. Hyperplasia is considered to be the early stage of dysplasia, though not all hyperplasia leads to dysplasia.
In this experiment, both BALB/c and C3H mice are induced with azoxymethane (AOM) and dextran sodium sulphate (DSS). The inflammation is caused by the administration of dextran sodium sulphate to the drinking water of the mice. While azoxymethane induction plays a role in the development to colon cancer. In this project, the development of colon cancer through the inflammation pathway is being researched. The process first starts with the of inflammation foci. Over time, it develops into hyperplasia due to the increasing capacity of cell proliferation.
The hyperplasia foci can be seen as early as 2 months, as depicted by the histological picture. The number of cells with hyperplasia is then
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calculated per total number of cells in each field, for 10 power field. The average percentage of the hyperplasia foci is then calculated to find the amount of hyperplasia in each month group. The next step of analysis is to use the Kolmogorov-Smirnov test to find out if the distribution of data obtained is normal or not. Once the distribution of data is found to be normal, T-test is then used to analyze if there is a difference of hyperplasia between BALB/c and C3H mice. However, the p value is more than 0.05 and thus it is not significantly different. This suggests that there is no significant difference between the hyperplasia foci in both strains of mice. Thus the T-test is not used for the analysis. Anova one-way is then used to see if there is a significant difference between the month-group of both BALB/c and C3H mice. The p result obtained is less than 0.05, which means that it is significantly different. The result of anova one-way suggests that there are differences in the of hyperplasia between the month groups. However, which group is significantly different from another can not be found by this method of analysis. Further analysis includes the post hoc method.
This is especially useful to find out exactly which of the month group is significantly different from each other. Data which are not significantly different from each other are written in the same column, while different column means that they have a difference. Thus it is obtained that 2-months and 4-months group are not significantly different from each other. The same is true for 4-months and 6-months group. The significant difference is between 2-months and 6-months group. However, even if the groups are listed in the same column, there are still differences in the of hyperplasia in each group. The post hoc method also analyzes the value of in each group. From the analysis, there is an increase of hyerplasia foci from 2-months until 6-months
groups. The increase in hyperplasia foci can also be seen from the histological specimen. In which, the percentage of cells with hyperplasia is highest in the 6-months group, and lowest in the 2-months group. In conclusion, the result of the research project fulfills the hypothesis that the number of hyperplasia foci increases with time. The development of colon cancer through the inflammation pathway by administering AOM and DSS is clearly seen from the result of this project.
...ozzi E, Biffoni M, Todaro M, Peschle C, et al. Identification and expansion of human colon-cancer-initiating cells. Nature. 2007;445(7123):111-5.
Vicki is a 42-year-old African American woman who was diagnosed with Hypertension a month ago. She has been married to her high school sweetheart for the past 20 years. She is self-employed and runs a successful insurance agency. Her work requires frequent travel and Vicki often has to eat at fast food restaurants for most of her meals. A poor diet that is high in salt and fat and low in nutrients for the body and stress from her job are contributing factors of Vicki’s diagnosis of hypertension. This paper will discuss the diagnostic testing, Complementary and Alternative Medicine treatments, the prognosis for hypertension, appropriate treatment for Vicki, patient education, and potential barriers to therapy that Vicki may experience.
How does this history of high blood pressure demonstrate the problem description and etiology components of the P.E.R.I.E. process? What different types of studies were used to establish etiology or contributory cause?
Congenital Adrenal Hyperplasia (CAH) is an inherited condition that affects hormone production in the adrenal gland. The individual lacks enzymes to make cortisol, and hormones are instead are shifted away to make other hormones, specifically androgens. This results in the deficiency of cortisol and the abundance of testosterone.
Chemotherapy is the treatment of a tumor with chemical agents to reduce mass or eradicate a tumor completely. There are certain mechanisms by which chemotherapy inhibits cancer. The first mechanism is cell death by cytotoxicity. Some chemical agents in certain amounts are toxic to cells. The cells die due to the toxic...
"Red meat and colon cancer." Harvard Health Publications. Harvard, Mar. 2008. Web. 1 Apr. 2014.
Li, Y., Wicha, M. S., Schwartz, S. J., & Sun, D. (2011, February 4). Implications of Cancer Stem Cell Theory for Cancer Chemoprevention by Natural Dietary Compounds. Retrieved December 12, 2013, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248810/
Several risk factors can be linked with the incidence of colorectal cancer. Age and hereditary factors are the most important factors on which an individual’s cannot able to manage. The probability of being affected by colorectal cancer is increases after the age of 40. More than 90% of colorectal cancer cases reported among people in the age greater than 50 and older (Fairley TL , 2006). In addition, a large number of environmental and behavioral risk factors can also contribute for the development of colorectal cancer; among these dietary factors are the major one (Fatima AH, 2009).
The next stage is transformation of mutated cells to cancerous cells; 5-20 years may require for the transition of benign carcinogenic phase to the fully developed malignant stage where the cancer can be detected clinically. The last stage called progression where further genetically changes take place leading to increase the proliferation and metastasis (Weinberg, 1996, Compagni and Christofori, 2000).
The patients in the Chen, et al., 2003 study suffered from damaged colonic epithelium because of “elevated levels of reactive oxygen species (ROS) and reduced oxidative defenses” (Chen et al., 2003). ROS are chemical species containing oxygen. This is another cause of genomic instability, in turn, this will lead to tumor formation and progression. Not only did the reactive oxygen species cause damage to the colonic epithelium but it also induces genetic damage to the DNA. The DNA received acute damage from base alterations, abasic sites, and strand breaks.
Cancer develops when cells in a part of the body begin to grow out of
Cancer is a disease that affects human somatic cells. It causes the cells to divide uncontrollably and form masses known as tumors. There are two different types of cancer tumors. Some tumors are benign and other tumors are malignant. Benign tumors look similar to the tissues that they came from and develop slowly. The tumor remains in the same area that the tumor originated in. Malignant tumors are formed from cells that do not resemble the tissue that they came from. They vary in shape and size. This enables pieces of the tumor to break off and spread to other places in the body. Over the past few decades cancer has become a very prominent disease. There are many different types of cancer and many different causes for the the disease. Most cancers are because of a genetic mutation. The most common type occur when a cell is dividing. Proto-oncogenes, which are alleles in a normal cells, mutate to form oncogenes. These oncogenes cause cancer because they do not allow the cells to self destruct or become epistatic. There have been several research projects which have been testing epistatis.
Tumors are formed by the alteration of the body’s own cells. This can be caused by environmental factors such as radiation, like UV exposure, chemicals or viruses 1. These can disrupt genes that control growth and cause an increase in cell division and proliferation. Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells. One of these is a deficiency of natural killer (NK) cells, which are able to kill cancer cells by creating a pore in the cell membrane with perforin and releasing granzymes into the cell. Low levels of perforin allow for tumor growth 1. Chronic inflammation can also ...
Cozy Mystery Short Story The Park Street Murder The suburbs are often filled with kids laughing and playing in the streets while the neighbourhood dogs bark continuously with moms driving up and down all day long. I often stay with my grandmother in quieter side of the suburbs where the tree stumps are growing out of the tarred roads and the houses are surrounded by bushes and trees to maintain a little privacy. “It is a little like Pleasantville and too quiet sometimes if you ask me.” Said Monica’s grandmother as she stared out into the street towards the cul-de-sac that ends their street.
To create a chronic inflammatory state, DSS, an agent with direct toxic effects on the colonic epithelium will be administered in drinking water to mice in multiple cycles. With sufficient duration, some of these mice will develop tumors. Tumor development is hastened in this model if administered in a pro-carcinogenic setting. These include mice pre-treated with genotoxic agent (azoxymethane [AOM]). The combination of DSS with AOM as a model for colitis associated cancer has gained popularity for its reproducibility, potency, low price, and ease of use. Mice injected with AOM and subsequently treated with DSS develop adequate tumors in as little as 7-10 weeks (Thaker et al, 2012). Hence, we use both AOM and DSS in our study. Then, EO will be orally-administered into the mouse model to test the production of mucin from the goblet cells in proximal colon and compared to the disease control. The production of mucin is crucial in protecting the intestinal barrier function from