Bio 241 Hmwrk 1

FAP is caused by mutations on the APC (adenomatous polyposis coli) gene, a tumor suppressor gene on chromosome 5 that occurs in an autosomal dominant pattern. The ACP gene controls cell growth, so a mutation on that gene develops polyps in the colon that when left untreated, will develop into colon cancer and can only be prevented by removing the colon. FAP is very rare, associated with less than 1 percent of colon cancers . Familial adenomatous polyposis can also be a result of mutations on the MUTYH gene (U.S. Library of Medicine 2013). Then, it is inherited in an autosomal recessive pattern, where both copies of the gene in each cell are mutated. Both parents may carry a single copy of the gene without showing symptoms. HNPCC, or Lynch syndrome, is a result of mutations in the genes that repair DNA. Lynch syndrome is inherited in an autosomal dominant pattern, so a single copy of the mutation will increase cancer risk. Most cases of Lynch Syndrome are caused by mutations in two genes, MLH1 and MSH2. Both FAP and HNPCC have a 50% chance of offspring inheritance, and are inherited in an autosomal dominant pattern. A mutated, inherited gene that is related to HNPCC causes an 80% chance of developing colorectal cancer (U.S. Library of Medicine 2013). So even when an HNPCC-related gene is inherited, there is not a definite future of colon cancer.

Cellular Differentiation is when a less specific cell becomes a more particular cell. Each tissue has their own type of cell.

Cancer is the disease caused by an uncontrolled division of abnormal cells in a part of the body.

To perform this task, however, the cells must specialize by a process called cell differentiation. Cells that are

Usually cells grow and divide at a specific pace that keeps the body working healthy but

Not all cancers are a result of rapid and abnormal cell growth within the body. Cancers of the blood, for example leukaemia's, do not form tumours, but they make many abnormal blood cells build up in the blood. Unlike normal cells, under a microscope, it becomes clearly evident how different cancer cells look in comparison to regular body cells. Cancer cells often exhibit much more variability in cell size, some are larger than normal cells and some are smaller. In addition, cancer cells often have an abnormal shape, both of the cell, and of the nucleus. The nucleus is both larger and darker than those of normal cells. The dark nucleus is due to excess DNA and an abnormal number of chromosomes that are arranged in a disorganised fashion. These mutations can either drive the cell to transform and become cancerous, or act as passenger mutations which develops the cell without it being able to perform any specific function. Normally, each cell has a specialised function within the body, but unlike normal cells, cancer cells do not have any function at all (Rykaj et al. 2015). For example, the white blood cells of leukaemia function a lot differently

Cell differentiations is how generic embryonic cells become specialised cells. This occurs through a process called gene expression which is a specific combination of genes that are turned on and off and this is what dictates how a cell functions. This is in order for the cell to perform a specific function. Cell differentiation is presented during multiple stages of development. During this process the cell size and shapes changes dramatically as its ability to respond to signaling molecules. Differentiated cells can be red and white cells, sperm cells, egg cells, bone cells, hair cells and muscle cells. Differentiated cells are specific to suit their function in the body and they work together in a particular organ or an organ system. Cell

These subpopulations area unit called sub clones. every of those increasing sub clones undergoes Darwinian evolution and natural action (Figure one.1), which means these clones bear positive choice once advantageous mutations arise and negative choice once hurtful mutations arise. The well positive mutations, called “driver mutations”, area unit the most actuation behind the expan- two Figure one.2: Example showing emergence and progression of cancer. sion of the clones. Alternative sorts of mutations, called “passenger mutations”, ride on the increasing clones however area unit assumed to be not below selective pressure. an easier pictorial read of initiation and progression of cancer is given in Figureone.2. in a very healthy tissue, mutations could arise in sure genes in one among the cells that end in that cell’s effort higher proliferative potential as compared to the healthy cells. This cell (as shown by D1 in Figure one.2) grows, divides quicker and quickly overpopulates the healthy cells within the tissue. As tumour cells generally acquire injury to the deoxyribonucleic acid replication system, that makes them at risk of additional mutations, alternative mutations could arise leading to another cell population (as shown by D2 cell sort within the

Cancer is a disease that is developed by our cells and how they grow and divide. Yes, our cells are supposed to divide but the dividing rapidly and abnormally is what causes the cancer. Researchers claim that this disease is genetic but can also be triggered from mishaps that happen as cells divide over a person’s lifetime. Cancer can very well be started in almost every part of your body because of the millions of cells our body is made up of.

A person’s diet, as well as lack of physical activity and obese citizens is severely large risk factors too. Inflammatory bowel disease, which is often mistaken for colorectal cancer, too, plays a part in the risk factor. Smoking, which most people think would be the most common cause of lung cancer, has a higher colorectal cancer rate than the average person, as well as African American citizens. Colorectal cancer affects not only the colon itself, as well as a person’s genes. The APC, p53, and K-ras genes are commonly involved. The APC gene stands for the Adenomatous Polyposis Coli gene. It is known as a tumor suppressor gene, and mutations of it are found in common colon polyps or cancers. Furthermore, in the p53 gene, cells that have damaged DNA are repaired by this gene. As well as the APC gene, it is a tumor suppressor. When it’s mutated, it no longer functions, leaving damaged DNA cells in the body. Lastly, the K-ras gene helps with cellular growing and signaling. In the abnormal state, it can result in a continually growth-simulated state. The treatments for colorectal cancer may not help the mutation of these

Cells have the ability to grow, have particular functions, and replicate during their life. Although cell enlargement is part of organismal growth, cell replication is also required and allows growth without each cell becoming too large. All of these activities are part of a repeating set of events known as the cell cycle. The major feature in the cell cycle is cellular replication and what enables for cellular replication is the process of mitosis. Mitosis is the only part of the cell cycle, and the remainder of the cycle consists of interphase, cytokinesis, gap 1, synthesis, and gap 2 phases. But cell division and reproduction can occur in two ways mitosis (which I just

Other factors to understand are oncogenes, which are the result from the turning on of proto-oncogenes, but tumor suppressor genes cause cancer when they are turned off. A proto-oncogene is a normal gene that can turn into an oncogene, if this happens it can cause a change in protein structure since proto-oncogenes code proteins.

These tumours are a result of mutation that occurs in the DNA of normal cells. Because of these mutations, the cells grow and divide at an increased rate. Gradually the healthy cells die while the abnormal cells continue to grow, thrive and gradually form a tumour.

There is one kind of cell that never specializes during development. They are called stem cells and they are the only known cells that can renew themselves. When they are in danger of dying they can divide into two new cells. These cells are referred to as daughter cells. The parenting stem cell has a choice to make as to what kind of cells

All cancerous tumors have a basic structure of a large group of cells with a small cluster of cells in the center of the tumor that are responsible for the growth and recurrence of cancer. These central cells are the most difficult part of the tumor to destroy. Mutations in tumor suppressor genes are essential for promoting and allowing tumors begin forming, through spontaneous or even hereditary forms of cancer (Collins, 1997). Cancer is caused by mutation in genes, however not all mutations can cause cancer but certain combinations of genetic mutations do cause cancer (Blanpain, 2015). Cancer cells are cells that divide uncontrollably due to mutations in genes; the mutations in oncogenes and tumor suppressor genes largely affect the aggressiveness of cancer (Yokota, 2000). Through lots of research it has been proven that cancers are heterogeneous and show different functions and phenotypic traits at cell level