Prostate Cancer Essay

of a higher grade and most of them show a signature ofbasaloid gene expression (Mayer et al., 2014).

The F-value is high enough at the 5% level of significance to suggest a significant difference between the control and treatment groups. The p-value 0.005 < 0.05 hence this suggests a rejection of the null hypothesis, meaning that the control and treatment groups are found to be different.

Testing allows the p-value that represents the probability showing that results are unlikely to occur by chance. A p-value of 5% or lower is statistically significant. The p value helps in minimizing Type I or Type II errors in the dataset that can often occur when the p value is more than the significance level. The p value can help in stopping the positive and negative correlation between the dataset to reject the null hypothesis and to determine if there is statistical significance in the hypothesis. Understanding the p value is very important in helping researchers to determine the significance of the effect of their experiment and variables for other researchers

A key characteristic of cancer cells is that they are no longer constrained by the standard cell cycle controls that normally coordinate cell division activity. Consequently the timing of mitosis in cancer cells is altered. You may

B. The test is valid if all of the estimated cell frequencies are at least five

The prostate gland is an egg-sized organ that rings the male urethra. The secretions of the prostate give nutrients to the semen. Prostate cancer is the most commonly diagnosed cancer and the second most common cause of cancer death in men. (Ernstoff,Heaney,Peschel,1998,pviii) Like all cancers, prostate cancer is an uncontrolled cell production in a particular organ or area of the body. In the case of prostate cancer, these cells begin to split impulsively in the prostate and form tumors. As these tumors begin to grow they begin to use up oxygen from other healthy cells and surrounding tissue. Not only do these tumors take up oxygen from other cells, they secrete protein signals that initiate the formation of new

Mutations (for most cancers) must appear in both tumour suppressing genes and oncogenes for cancers to form. The tumour suppressing genes and oncogenes act in complementary fashion to one another; one pulls forward, and the other pushes back ensuring that the cell cycle occurs in a controlled manner (Sherr, 2004).

A quantitative allelic imbalance assay was developed to determine differences in gene expression from individual BRCA1/2 alleles. Allele-specific assays quantify gene expression specific to the allele being tested. For the BRCA1 gene, two individuals homozygous for the BRCA1-c.4308T/T or BRCA1-c.4308C/C polymorphism were tested. Complementary DNA (cDNA) was created from reverse-transcription polymerase chain reaction (RT-PCR) using RNAs extracted from blood lymphocytes. RT-PCR uses reverse transcriptase to form an RNA/cDNA heteroduplex that is then amplified by normal polymerase chain reaction techniques to produce a large quantity of cDNA. Ratios of the cDNA from the two alleles were mixed for use in real-time PCR (qPCR). qPCR uses fluorescent probes that anneal to the cDNA during PCR. These probes contain a reporter and a quencher; the reporter fluoresces when separated from the quencher, allowing a computer to measure the number of cycles needed for the fluorescence to exceed background levels (cycle threshold or CT). Using the ratios of cDNAs and ∆CT, a linear regression was computed to form an allelic expression standard curve that can be used to evaluate allelic imbalance. These same methods were repeated with BRCA2 with two individuals homozygous for the BRCA2-c.3396A/A or BRCA2-c.3396G/G allele.

Cyclin D1 (CCND1) is known to be a prominent part of the cell cycle in humans by regulating the cell cycle. In this research paper, the CCND1 was examined for other things. Researchers believed that an access amount of the CCND1 was causing breast cancer, which is a wide spread problem across the country. The research consisted of 147 patients and eight different tissue cores from 4-8 tumors were taken. It was found that a high degree of homogeneity is the beginning development for breast cancer.

| * located on chromosome 17p13.1, is the single most common target for genetic alteration in human tumors * tumor suppression protein that is dysfunctional in many types of cancer. One highly studied function of pRb is to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide. It is also a recruiter of several chromatin remodelling enzymes such as methylases and acetylases.

This rapid cell growth is caused by a mutation in the DNA. The two most common genes that risk the chance of cancer are the p53 gene and the BRCA1 gene. The p53 gene is also known as “the guardian of the genome.” The function includes the ability to control cell cycles. This gene is mutated in more than half of cancers in humans. The Breast Cancer Gene, or BRCA1 is normally supposed to suppress tumor functions, but when this backfires, a tumor can begin to form.

Inferential statistics: Paired‘t’test, chi square test and independent‘t’ test . P value less than 0.05 used to indicate significance.

Cell replication and division is vital for growth and development. The mechanisms associated with replication of DNA are very precise. However, there can be errors at times and when these errors occur there could be problems in reproduction process. Some of these errors can cause uncontrolled cell growth causing tumor formation. There are genes within the human genome that prevent this uncontrolled growth from occurring. These genes are known as tumor suppression genes. They work in a very specific way and are vital for proper growth. Though they fix errors, the tumor suppression genes can malfunction or be malformed at times as well. When these errors occur, there can be serious consequences.

1. Proto-oncogenes and tumor suppression genes are both used to help regulate the cell cycle. Tumor suppression genes produce proteins that inhibit cell division, and proto-oncogenes produce proteins that stimulate cell growth and division. The balance between the activities of these two genes ensure cells are dividing at a suitable rate for their body. Mutations affect these cells in two different ways. When mutation occurs, proto-oncogenes become oncogenes. Oncogenes promote excessive growth and causes the cells to divide excessively, even when it is unnecessary for the cell to keep dividing. When mutation occurs for tumor suppression genes, the tumor suppression genes can become inactive. Because tumor suppression genes inhibit and lessen

The cancer specific genes can be identified by Differential display. This is a powerful technique for analyzing differences in gene expression. This technique used to compare mRNA expression patterns of tumor and adjacent non neoplastic tissue in radical prostate ectomy specimens. This can be useful in identifying novel genes and gene functions.