Cancer and Cell Cycle Project

You would expect for the normal lung cells to not have to divide as often because those cells are not exposed to many things through out the day. The normal stomach cells on the other hand would be expected to divide more because there is a lot of acidity in the stomach and therefore those cells are exposed to a lot of things on a daily basis. As for the ovaries you would expect that there would be a little more cell division because that is where new life is formed and all of the things that come along with that which means that there should be more division going on.

Oncogenes can also be activated by the amplication of proto-oncogenes. Gene amplification is an increase in the cellular copy number of a gene or genomic region relative to the rest of the genome. An amplication in a proto-oncogene would cause an increase in cell division, a decrease in cell differentiation and an inhibition of cell death – the phenotype of a cancer cell.

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.

PC3 (8×104  cells/well) and LNCaP (3×105  cells/well) cells were seeded in 6-well plates in 1.5  mL of complete growth media. Cells were treated with 2.5 μM of free sorafenib or an equivalent sorafenib concentration of SMA-Sor, 3 μM of free nilotinib or an equivalent nilotinib concentration of SMA-Nilo, DMSO or SMA for 48  h. Cell cycle distribution was assessed using propidium iodide staining, as previously described {Somers-Edgar, 2011 #82}. Samples were analysed using a FACScalibur flow cytometer (BD Biosciences, San Jose, CA, USA) and the proportion of cells in each of G0/G1-, S- and G2/M-phases were determined using CellQuest Pro software (BD Biosciences, San Jose, CA, USA).

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.

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).

He believes that circular DNA carries many copies of oncogenes increasing the tumors growth. During cell division eccDNA replicates like any other cell, but unlike chromosomal DNA. Circular DNA may not be evenly apportioned between daughter cells during cell division. As a result, eccDNA can massively increase the number of oncogenes in some cells and if the oncogenes give the cell a growth boost than oncogenes cells can take over the tumor cells.

Cancer cell growth is distinct from normal cell growth. Cancer begins when cells in begin to grow and develop out of control. Instead of dying like the normal cells, cancer cells keep to grow and produce new abnormal cells.

Cancer cell divide by bypassing the three cell checkpoints, G1, S, and G2. (Seitz) The cancerous cells can pass through the checkpoints by tricking the cell into the next phase, where a normal cell would have caught the error and stopped the cell cycle. ("Karyotyping Cancer Cells.") Cancerous cells are not reserved by size, allowing them to grow and replicate. (Seitz) Cancerous cells are extremely dangerous and can trick cells into creating more.

Brain cancer affects the cell cycle by causing the cells to go out of control. It starts out normal but the cells in the brain start going though the cell cycle and rapidly dividing the cancerous cells. Therefore, the immune system thinks that the cells are doing their job so the immune system does nothing. The cell cycle is the natural and orderly progression that cells take to undergo proper division. The cell cycle is a series of four steps which are G1, S, G2, and M. G1 phase is prepares cells for copying, S phase directs the copying of the DNA, G2 phase leads to further cell growth. The M phase represents the stage where the single mother cell divides into two daughter cells.

Many question, “What does the Cell cycle have to do with cancer?”The cell cycle is a process in which cells develop and go on to divide.The cell cycle lies in the metaphorical heart of cancer. The cell cycle is a series of pathways by which a cell is signaled and continues to grow, the cell the replicates and divides.The process also includes different additional systems to make sure any problems that occur are corrected.If the problems are not corrected the cells fail and “commit suicide” in other words,(apoptosis).The only thing is, after apoptosis happens, cancer begins, as a result of genetic cells changing, the process then malfunctions which then causes uncontrollable cell growth.

The cell cycle of a normal cell and a cancer cell have many similarities and differences. The main similarity is that both sets of cells undergo the four phases of the cell cycle: G1, S, G2, M. There are three checkpoints within the cell cycle that tell the cell to move to the next phase or die, but cancer cancer cells do not obey the checkpoints. During the first phase, G1 phase, normal cells double in size and the number of organelles double as well. The G1 checkpoint ensures that proper doubling has occurred and allows cells to move forward to S phase. However, cancer cells that are too small or have too few organelles will not die. During the second phase, S phase, DNA replication (an identical copy of all the cell’s DNA is made)

Millions of families and individuals are affected each and every day with the diagnosis of cancer. Cancer can form anywhere in the body and it can take the life of a person in a blink of an eye. The body forms new cells all the time, then your old cells die. Although, sometimes the old cells will not die when they are suppose to. These extra cells can form a tumor. Tumors can be benign or malignant. Benign tumors are noncancerous and malignant tumors are cancerous. The parts of tumors can easily break away from the tissue that they have grown on and spread on to other parts of the body. This causes the cancer to be far more aggressive than if it were just in one area. The cancer spreading causes the cancer be in different stages. Stage 0

Cancer cells are characterized by unlimited cell growth, inefficient apoptosis and excessive anabolism. The process of becoming cancer cells includes gene activation, micro-environmental changes and metabolic reprogramming. All of which compound upon one another and lead the cancer cells to continue with their overwhelming growth and activity. Malignant cancer cells invade and destroy organ infrastructure and replace it with disorganized and damaging cells. (1) The metabolic preference of cancer cells is wide ranging with cervical and glioma cells maintaining a normal oxidative phosphorylation and others exhibiting the switch to glycolysis. (2) This metabolic switch exhibits the adaptation to environmental changes and the tumor’s energy needs and activity. Overall, the carcinogenic process that defines each malignant tumor determines the metabolic profile of the cells. For the purpose of examining the metabolic switch, this paper will focus primarily on the Warburg principle with only slight examination of other cancer cell metabolic profiles.

Uncontrolled proliferation, immortalization, tissue invasion, and metastasis. Incipient cancer cell mounts up mutations in their genome due to damage caused by endogenous processes such as errors in replication or interference of metabolic products with the stability of DNA or exogenous factors such as ionizing radiation, UV radiation, and chemical. All these events