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.
Several methods such as surgery, radiation, and chemotherapy have been used to treat cancers. The cancer patients who are not helped
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It may be possible to correct an abnormality in a tumor suppressor gene such as P53 by inserting a copy of the wild-type gene; in fact, insertion of the wild-type P53 gene into P53-deficient tumor cells has been shown to result in the death of tumor cells (3). This has significant implications, since P53 alterations are the most common genetic abnormalities in human cancers. The over expression of an oncogene such as K-RAS can be blocked at the genetic level by integration of an antisense gene whose transcript binds specifically to the oncogene RNA, disabling its capacity to produce protein. Experiments in vitro and in vivo have demonstrated that when an antisense K-RAS vector is integrated into lung cancer cells that over express K-RAS their tumorigenicity is decreased (4).
Despite the promise of such approaches, a number of difficulties remain to be overcome, the most important of which is the need for more efficient systems of gene delivery. No gene transfer system is 100% efficient, unless germ-line therapy is contemplated. During the past two decades, there have been major advances in our understanding of how cancer develops, proving that cancer has a genetic basis (2). A series of genetic abnormalities that accumulate in one cell may result in a pattern of abnormal clonal proliferation. Our growing understanding of the genetic basis of cancer offers new opportunities for the molecular prevention and treatment of cancer. There has been a
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.
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
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).
Roughly fifty years ago, scientists thought that the use of genetic modification by exogenous DNA would be effective. This idea could offer curative and long lasting benefits, in a single treatment.
The modified cells would then continue to replicate as normal cells. The in vivo approach involves the gene being directly injected into the affected tissues or into the bloodstream(Health Canada, 2012).. Although both these approaches involve the gene entering a patient’s cell in one way or another, the gene itself cannot just be entered into a cell. To be able to enter a cell the gene must use a carrier known as a vector in order for the gene to effectively enter the cell and start producing the correct proteins. A vector is a type of virus (usually adenoviruses, retroviruses and herpes simplex virus) where the virus’ DNA is removed and replaced with the gene that is required(U.S National Library of Medicine,2018). The vector can then either be applied to body cells which is called somatic gene therapy, or more controversially the gametes of the patient which is called germline gene therapy(legal in the US but banned in Canada under Section 5 of the Assisted Human Reproduction Act and other countries like Germany, Australia and UK) (Legislative Services Branch,2004). Both types of gene therapy will cause the vector to enter the
There are many types of cancer treatment. The types of treatment that a patient receives will depend on the type of cancer that they have and how advanced it is. The main types of treatment are surgery, radiotherapy, hormone therapy, chemotherapy and bone and stem cell transplants.
If there are mutations of the oncogene, then there will be uncontrolled cell division and therefore tumour formation will occur. However, the chances of the tumour developing into a benign tumour is unlikely as the tumours must break free and invade nearby tissue and this is life threatening. The chances of this happening is slim, however, due to the increased longevity of humans in the recent century, the chances of cancer will therefore increase. The signs of growth are practical abilities that permit malignancy cells to survive, duplicate and spread. Harm to cell DNA is included in mutagenesis and the improvement of malignancy. The DNA in a human cell experiences a few thousand to a million harming occasions for every day, created by both outside (exogenous) and inside metabolic (endogenous) forms. Changes to the phone genome can produce blunders in the interpretation of DNA and resulting interpretation into proteins
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.
Tumor suppressor gene tells the when to die, repair the mistakes made in the DNA, and slow down cell division. If a tumor suppressor gene gets mutated the cells will grow out of control with nothing to stop them. The mutation can be caused when this gene isn’t activated. Two common example of a tumor suppressor are the p53 and NF1. Proto oncogenes codes for protein which helps with the cell cycle, prevents differentiation in cell, and programs cell death. If a proto oncogenes gets mutated there would be change in the protein sequence which would interfere normal cell regulations. The name of the proto oncogene was oncogene. DNA repair identifies incorrections and damages and fixes them. These three genes are mostly used to find cancer because
This can be by way of in vivo or ex vivo. In vivo is when the gene is put into a medium that is directly inserted into the patient, allowing the transfer of the gene in question into the tissue where the necessary protein can be expressed.1 Ex vivo is when the functional gene is put into cells that have been taken from the patient and are outside the body, then these new cells are put back into the patient, where the new protein can be expressed. The physical delivery of the medium and monitoring the progress of the therapy is facilitated with different kinds of medical imaging, such as ultrasound, computed and positron emission tomography, and magnetic resonance.1
The transformation of somatic cells to cancerous cells is usually a slow and accumulative process, brought about by external sources causing mutations to the genetic material of the cells (DNA or RNA). Many intrinsic mechanisms, such as the mismatch repair system, are implemented to reverse
Deoxyribonucleic acid (DNA) was discovered in 1944 by Avery and colleagues. Avery identified DNA as the primary genetic material. Watson and Crick later discovered the double helix structure of DNA. Leder and co-workers deciphered the triple nucleotide code that designated the amino acids from which proteins were built. The science of molecular biology was born (Sokol, Gewirtz, 1996). In 1990 a four year old girl who was suffering from severe combined immunodeficiency (SCID) was the first to undergo gene therapy. White blood cells were removed from the girl and the cells were inserted with normal copies of the defective gene and returned into the girls circulation. Her condition improved with four treatments and
Parents can now pick a kid’s sex and screen for genetic illness. Will they someday select brains and beauty too?
More than twenty different types of cancer have been found to exist in the world today. Cancer is referred to an ailment characterised by an unrestrained growth of abnormal cells which if untreated, can lead to death. According to the National Cancer Institution, cancer is the second biggest leading disease in the United States of America and accounts for twenty-two per cent of the deaths in the country. There are many different types of treatments for cancer and the treatment type varies according to the individual. Some of the commonly known treatments may are known as: surgery to remove the cancer, chemotherapy and radiation biological therapy. There are many, many more types of treatment that are not at all well known in the world and an