Normal Cell Function Research Paper

Cancer is a genetic disease caused by certain changes to genes that control the way our cells function, especially how they grow and divide. Genes carry the instructions to make proteins, which do much of the work in our cells. Certain gene changes can cause cells to evade normal growth controls and become cancer. Genetic changes that promote cancer can be inherited from our parents if the changes are present in germ cells, which are the reproductive cells of the body (eggs and sperm). Such changes, called germline changes, are found in every cell of the offspring. In general, cancer cells have more genetic changes than normal cells. But each person’s cancer has a unique combination of genetic alterations.

level? A mutation in just one allele of proto-oncogenes can cause over production of cells tumor, and thus tumor formation, because they are dominant. Tumor suppressor genes require mutations of both alleles to inhibit function because they are recessive.

Our genes regulate cell growth and cancer occurs due to abnormal changes in these genes. Genes are in each cell's nucleus and control the cells growth in relation to our genetic make up. The cells grow and replace themselves in a natural

Therefore, the most notable P53-induced mechanisms in mediating this response are cell cycle arrest and apoptosis [18], which activation depends on the cellular context and the extent of damage [20].

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

In order to become cancerous a cell has many molecular changes that can occur including: tumor suppressor gene inactivation, oncogene activation, telomerase lengthening, ability to evade apoptosis, and angiogenesis (Mechanisms in Medicine, 2012). There are a few particular

In addition to translocations and gene amplifications, deletions can occur and also result in oncogene activation. This can be by the removal of negative regulatory elements or the elimination of regulatory protein domains. However it is more common for a deletion to cause the loss of a tumor suppressor and therefore lead to a cancerous cell i.e. one which rapidly divides.

When a tumor suppressor gene is effected by a mutation, it loses its control over the cell and the cell does not stop to get inspected. When this happens, the mutation is copied, the cell divides and damage is passed down to the newly formed daughter cells. The mutation then becomes permanent and the now mutated cell will continue to divide and proliferate when it normally would not.

Cancer is a disease caused by an uncontrolled division of abnormal cells. The DNA sequence in cells can be changed as a result of copying errors during replication. If these changes whatever their cause are left uncorrected, both growing and non-growing somatic cells might gain many mutations that they could no longer function. The relevance of DNA damage and repair to the generation of cancer was obvious when it was recognized that everything that causes cancer also cause a change in the DNA sequence. Tumor suppressor genes are protective genes and normally they limit cell growth by monitoring the speed of cell division, repair mismatched DNA and control when a cell dies. When a tumor suppressor gene is mutated cells grow

There are two important type of genes responsible for the development or cancer namely tumor suppressor because their normal function is

Cells may experience uncontrolled growth and if they are damaged or mutated in the DNA.There are four types of genes that are responsible for the cell division process. Those four types of genes are Oncogenes, Tumor Suppressor genes, Suicide genes, and DNA-Repair genes. Oncogenes tell the cells when to divide. Tumor Suppressor genes tell the cells when not to divide. Suicide genes controls apoptosis and tell the cells to kill themselves if something goes wrong. DNA-Repair informs the cells to repair damaged DNA. Cancer can occur when the cells of genes mutation are not able to correct damaged DNA and are not able to commit cell suicide. If you have some DNA mutations of the oncogenes or tumor suppressor genes that can lead to pancreatic cancer. It is a Great chance that the mutation was a result of some factors that affected the DNA after you were born rather than you inheriting it from your parents.

There are two key ways in which cancerous tumors form. Within the human genome, the two primary gene classes which control cell growth are proto-oncogenes which encourage cell growth, and tumor suppressers which inhibit it. Proto-oncogenes can lead to cancerous growths if mutations in the gene cause it to produce too much growth-stimulatory protein, or a hyper-active form of it. Tumor suppresser genes can also lead to cancerous cell reproduction when mutations make the gene incapable of putting the breaks on reproduction. Normal activity of a proto-oncogene can thus be cancerous if the tumor suppresor genes are rendered incapable of carrying out their function of regulation. With this classification, it is easy to see how one might use gene therapy and recombinant DNA techniques to introduce into the system a fully-functioning tumor suppresser gene. Presumably, if cells are reproducing at a normal rate and are merely incapable of being

Tumour suppressor genes: In health this family of genes usually act as a counter balance for oncogenesis. It is thought that they may be responsible for repairing gene damage in cells, or are growth inhibitor genes. In Hodgkin’s disease, there are often evidences of mutation in tumour suppressor genes as well as other genes.

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.

PM331 Essay: Exosomes, their cell biology, normal function in the cell, and role in disease.