A proto-oncogene are genes that help control cell growth. The functions of a proto-oncogene can be extensive in what they can do. First, they can kick start the cell division. They play a role in differentiation of a cell. And lastly, they help with cell death (Robertson). These are also considered normal genes. Once the gene is mutated it becomes an oncogene. The gene that may possibly be mutated could be the HER-2/neu gene. This is a type of gene amplification. This is a mutation where there are more copies then normal of a gene. In this specific case it causes rapid reproduction of the cell (Porth, Carol, and Kathryn J. Gaspard). The mutated proto-oncogene could have caused the cells to grow by no longer having control of the cell proliferation. …show more content…
Tamoxifen is an antiestrogen drug that is used as a hormone therapy for breast cancer. When levels of estrogen are too high this can cause the start of cancer or help it metastasize. Hormone therapy in general is used before surgery, after surgery or for individuals at a high risk for breast cancer. With this being an antiestrogen drug, it blocks the effect of estrogen. With this drug it blocks estrogen only in the breasts. This helps the cancer to stop growing and metastasizing (Hormone Therapy for Breast Cancer). Cancer treatment where an antibody attaches to a tumor is called Monoclonal antibody drugs. The way these antibodies work can vary. They tag the cancer cell so that they can be destroyed. Monoclonal antibodies can weaken the membrane of the cancer cell and cause destruction. They can also function in many other ways (Monoclonal Antibody drugs for Cancer: How they work). In this situation we are considering toxin-linked monoclonal. This treatment still has the antibody that attaches to the cancer cell. With there being a toxin attached it has a little different of effect. Once the antibody latches to the cell the toxin attached can enter the cell. When the toxin is pushed into the cell it can help destroy it. This treatment is focusing directly on the cancer cell and not on healthy cells (Taber, Clarence, …show more content…
If the levels of p53 are decreased, then the DNA is not being fixed or disposed of. In damaged radiation or chemotherapy cancer cells the gene p53 assists in their cell death (Porth, Carol, Kathryn J. Gaspard, 138). Therefore, if there is a deficiency in this p53 protein then DNA is not being fixed or disposed of and certain cancer treatments are not going to be as effective. With the lack of p53 protein there are many dangers. There is going to be an accumulation of bad DNA in many cells. With the lack of cell death not only is the DNA bad but there will form a mass from these cells not being disposed of in the way they were meant
Specifically “TP53, p16INK4A, and SMAD4. The p53 nuclear protein activates transcription of a cyclin kinase inhibitor p21WAF1/CIP1. Following genomic stress, inappropriate growth factor stimulation or expression of oncogenic ras increased expression of p53, and thus p21WAF1/CIP1 resulted in inactivation of specific CDK/cyclin complexes” (MedScape). If this transformed cell can escape internal and external fail-safe mechanisms, receive nutrients, and activate its proliferative program, it can form a mass of cancerous cells. Tumor growth can cause the loss of pancreatic functions. Another characteristic of pancreatic cancer is metastasis happens early in tumor growth, which is most likely responsible for pancreatic cancer’s aggressive
The acquisition of an immortalized proliferative potential is very important for human tumors because, otherwise, the tumors will not grow in number nor will they metastasize. Mutations in progenitor cells would not be transmitted too far as they have limited replication and proliferation ability. Thus, the growth of the tumors will be limited. Hence, if there is even a very small population of cells with the ability to proliferate continuously, there will be a source for productions of more cells for the tumor. Clonogenic assays have shown that, though most cells in a tumor have a limited ability to proliferate, a subset of cancer cells exist in these tumors that continuously proliferate and give rise to new tumors on transplantation.
There are essentially three main types of cancer treatments; surgery, chemotherapy, and radiation. Surgery allows doctors to effectively remove tumors from a clear plane. Chemotherapy uses drugs to treat the tumor; but often the drugs affect other healthy cells in the process. Using radiation as a treatment can be either precise or vague. Many health stigmas can come from the vague forms of radiation or conventional radiation therapy. Conventional radiation treats both the unhealthy and healthy cells, therefore exposing healthy cells to harmful radiation (Radiation Oncology, 2011, p.6). When healthy cells are exposed to gamma radiation they are also exposed to ionizing radiation. The ionization can cause “breakage of chemical bonds or oxidization (addition of oxygen atoms)” in a cell; the main impact of this is on a cell’s DNA, if two strands of DNA break it can result in “mutations, chromosome aberrations, ...
..., t. t. (n.d.). Menopausal Hormone Replacement Therapy Use and Cancer - National Cancer Institute. Comprehensive Cancer Information - National Cancer Institute. Retrieved September 19, 2011, from http://www.cancer.gov/cancertopics/factsheet/Risk/menopausal-hormones/print
These changes occur in genes that are essential for development and often disrupt the development of an embryo in its earliest stages. Because these mutations have very serious effects, they are incompatible with life.
In 1896 the scientist Beatson reported that the removal of the ovaries resulted in the reduction of breast cancer tumours (Russo and Irma 1998). Breast cancer is a malignant, metastasizing cancer of the mammary gland. It is the leading cause of death in woman between the ages of 35 - 45. Breast cancer can also occur in males, although less frequent, around 400 men die each year from breast cancer in the united states. (Martini, F., 2004). Studies on rats have shown considerable evidence that rat oestrogens are mammary carcinogens. Oestrogens have shown to stimulate the hormone prolactin. Through studies involving the use of antioestrogens, for example, tamoxifen, "Tamoxifen alone or in combination with the retina all trans-N-(4 hydroxyphenyl)-retinamide (4-HPR) reduces the incidence of NMU-induced mammary tumours in Sprague-Dawley rats." (Jane M. Ussher Ph.D. 1996). This suggests that Oestrogens and Prolactin's can have the effect of the development of breast cancer since the pathogenesis of spontaneous breast cancer in humans is similar to that of chemical-induced rodent mammary cancer. (Jane M. Ussher
Women who have taken estrogen-only hormone replacement therapy (HRT) after menopause have a higher risk of ovarian cancer.
...e. These hormones have menopausal side effects. Progestins commonly known as Depo-Provera is used to shrink endometrial spots. Side effects of progestin can include weight gain, depression, and decreased bone growth.
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
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 ...
What is breast cancer? According to the National Cancer Institute at the National Institute of Health breast cancer is a, “cancer that forms in tissues of the breast" (cancer.gov). More specifically breast cancer is a malignant tumor that grows inside the breast tissue. What happens is one cell in the tissue does not get the stop signal and keeps dividing into this big mass. This big mass continues to grow and grow and could eventually taking over space that is meant for other tissue or getting into the blood stream taking the dividing cells elsewhere. Breast cancer normally starts in one of two places.
The cancer cells from gene-mutation. Scientists now know some of the risk factors for lung cancer can cause certain changes in the DNA of lung cells. These changes can lead to not normal cell growth and, sometimes, cancer. DNA is the chemical in each of our cells that makes up our genes and how our cells function. People usually look like their parents because they are the source of our DNA. But DNA affects more than how we look; it also can affect our risk for developing certain diseases, including some kinds of cancer like lung cancer etc…Some people inherit DNA mutation from their parents that greatly increase their risk for developing certain cancers.
She was very tall for her age(7). Instead of getting one copy from her father, she got two which told her body to grow and grow. The extra gene over produces a hormone that tells her body to grow. Since her body kept growing, it put her at risk for cancer in her kidney. Eventually the risk of developing tumors decreases and is the same as with any other child her age.
Cancer develops when cells in a part of the body begin to grow out of
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. Transfecting DNA To perform the experiments for this research, the researchers had to grow certain pieces of DNA.... ... middle of paper ...