The Potential And Its Effects On Cancer Cells

Most telomere are no more that the simple repetition of the DNA nucleotide sequence TTAGGG — two thymine bases, an adenine base, and three guanine bases. With a full length telomere containing more that 15,000 base pairs, telomeres can perform their functions of preventing chromosome from losing coding regions of the genome during replication for many replications before reaching what Dr. Jerry Shay describes as their “critical length” (Shay & Wright). When the telomeres of a cell reach this critical length and can no longer replicate without damaging the base pair sequences of the chromosomes themselves, programmed cell death occurs in the form of apoptosis. However, the length of a chromosome’s telomere is not only a linear function of erosion, but also a function of how often telomerase rebuilds the strands by adding the TTAGGG base pair sequence. It is this way to “cheat” the critical point that provides medicine with the possibility to extend our

The functions of telomeres includes protection of chromosomes from degradation and end to end fusions, maintains the stability of chromosomes, acts as a mitotic clock to understand the replicative history of a cell.Telomerase is a ribonucleoprotein DNA polymerase that helps in maintaining the telomeres by adding TTAGGG repeats at the ends of chromosomes (Greider and Blackburn,1989). Telomerase consists of two main subunits: telomerase RNA (hTR) and catalytic component human telomerase reverse transcriptase (hTERT). The enzymatic activity is usually absent in somatic cells but remains active in germ line cells,embryonic stem cells and tumor cells. Almost 80 to 90% of human cancers are characterized by the presence of telomerase activity.Studies on glioma shown that more than 50% of tumors have telomerase activity and its detection rate increases with the grades of malignancy (Tchirkov et al 2003). Therefore knockdown of hTERT expression may help in the development of novel therapeutic strategies. In the present study we evaluate the effect of siRNA to downregulate hTERT in LN18 cells and also investigated the effect on apoptosis and cell

What is cancer? Cancer is a disease where cells split uncontrollably and can invade other tissues, causing cells in the other tissues to have cancer. Where can cancer occur? Cancer can occur practically anywhere in the body. This is because cancerous cells can move anywhere in the amatomy through blood paths and lymph systems (lymph systems are lattice of organs, lymph intersections (nodes), tubes, and vessels that move lymph, a clear fluid containing white blood cells, from place to place. (- http://www.cancer.gov/cancertopics/cancerlibrary/what-is-cancer )

Targeting these Telomere/Shelterin compounds may be useful to suppress the tumour cells, killing it off.Grueber CE et al. 2015

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

The efficient delivery of drugs and energy to tumors faces several difficulties and obstacles that need to be overcome for effective cancer treatment. Nanoparticles administrated through intravenous injections accumulate at a tumor site due to the enhanced permeability and retention (EPR) effect, but only a small quantity of the injected particles can actually “reach the tumor” (Su et al, 2016). The majority of the nanoparticles interact with “cancer cells at the periphery of a tumor” which presents a “physiological barrier” that prevents most of the injected particles from reaching the tumor (Su et al, 2016). In addition to this barrier, there is also another significant obstacle, “cancer-associated fibroblasts”, which can also

Cancer is the uncontrolled division and growth of cells within the body. (Appendix 1) These cells are usually abnormal and are caused by mutations in genes that control the cell growth and replication. These cells damage the normal function of organs and can form tumours. Anti-cancer drugs work using number of strategies that interferes with the mitosis of the body cells, which in turn slows down the growth of the cancerous tissues. Anticancer drugs have distinct mechanisms of action which may vary in their effects on different types of cancer cells. These mechanisms of action are divided into three main categories. Anticancer drugs generally do one of the following, stop the synthesis of the pre-cursors of the DNA synthesis, damage the nucleic acid of the cell or affect the formation of the mitotic spindle. This is displayed in appendix 2. All three interfere with the division of the cells, which in turn slows down the growth of the cancerous tissue.

ImageCancer cells are the production of abnormal cell division. Our bodies have an order in which they replace worn-out cells because each of our cells have instructions that tell our bodies how fast the cells should grow and divide and when they should die. This balance between the division of cells and the death of cells keeps our bodies functioning properly. The difference between cancer cells and healthy cells is that when our cells start to develop without this balance between growth and death, small lumps of benign or harmless cells will form, it can occur anywhere on your body.

Telomeres are appendages of non-coding, repetitive sequences of nucleotides located at the ends of linear DNA molecules such as those in eukaryotic cells. These protective "caps" found at chromosomes ends prevent the shortening of genes during DNA replication, make it possible for our cells to divide without the erosion of genetic units and ensure that genetic material is successfully passed down from one generation to the next. They also protect the chromosomes from fusing and connecting DNA with each other. Recent studies have also shown that telomeres correlate to aging and that telomeres play a significant role in the immortality of cancer cells.

El-Aneed, A. (2004). An overview of current delivery systems in cancer gene therapy. Journal of Controlled Release, 94(1), 1-14.

Telomerase extends the telomeres of the chromosomes, and it is important during the development period. Although, telomerase activates in 90% of tumors. The function of the enzyme telomerase is when the enzyme extends the telomeres of the chromosomes. The enzyme is making the DNA using RNA as a template (Telomeres and Telomerase). The binding of the enzyme goes to a special RNA molecule to contain a sequencing which is complementary to the telomere repeat. It then extends an overhanging strand of the telomere DNA using the complementary RNA as a template. The overhang then becomes long enough, and the matching strand is made by a normal DNA replication. This finally produces a double-stranded DNA.

Throughout the past years, research of this unexpected instability has created a number of surprising discoveries. As a matter of fact, it has led to the findings of a great enzyme named telomerase that acts on telomeres and is thought to be required for the maintenance of many human cancers. Telomerase, the ends of the chromosomes, are eukaryotic ribonucleoprotein complex, which contains both an essential RNA and a protein reverse transcriptase subunit. They are meant to protect the chromosomal ends. They basically cap the ends of the chromosomes, thus protecting the ends. Unlike viral or retroviral reverse transcriptase’s, like the ones on HIV-1, the cellular enzyme telomerase focuses in making the multiple short tandem repeats that are at

In particular: a) species which show no aging (“animals with negligible senescence”) show the same telomerase activity at any age and have no cancer problem, as demonstrated by their constant mortality rate at any age; b) in our species, studied in wild conditions, the increase in age-related mortality is precedent to cancer-related deaths cases and it is impossible that defenses against cancer kill before cancer can develop; c) shortened telomeres, as a result of telomerase inactivity, cause dysfunctional telomere-induced instability and so the likelihood of cancer increases; d) in normal mice, telomerase expression delays aging but does not increase cancer risk.

During each and every cell replication, chromosomes shrink by a small, but noticeable amount. Because of this, telomeres cap the ends to protect the coding regions of the chromosomes. With each generation of DNA, more and more of the telomere disappears. An enzyme slowly rebuilds them, but it cannot keep up with the degradation during chromosome replication. Eventually the shortened telomeres cause the cell to go through apoptosis (Pierce 2014). Because telomeres are one cause of cell death, it is hypothesized that telomere size can determine the health and age of an individual. Research has shown a correlation between telomere length and chronic disease. Those with chronic diseases usually have significantly shorter telomeres. This raises the questions of what the correlation means. Chronic disease could shorten the telomeres, or short telomeres could cause chronic disease. Another hypothesis exists that shortened telomeres and chronic disease are both caused by another force; they occur simultaneously, but one does not necessarily cause the other. Researchers have also seen a correlation between telomere length and age. Physical age may be derived from the number of cells that have undergone apoptosis. There are a number of things that we can do to prevent telomere reduction. Diet and exercise both play a key role in this. Things that are “bad” for us, such as smoking and stress, increases the rate at which telomeres shorten. By

Throughout my experience with cancer, I have gained a little more knowledge than I had before I was diagnosed with this nasty disease. This paper gives me the chance to explain some of the causes and effects that cancer has on those afflicted with the disease and those who are constantly around them. I am glad to be the one writing this paper. I believe that if people read more papers like this one that there would not be as much tormenting or misunderstanding of what people with cancer actually have to go through. Some of the effects that cancer has are not only on the patient but also on the family and friends that are near and far. There are so many causes and effects of the many types of cancer I can only touch trying to be able to explain them. So I am going to explain what I know about lung, brain, and breast cancer to the best of my ability because most people do not know much about cancer since most have not had the personal experience.