DNA and cancer treatment
Wade, N. (2010). Speed-reading of DNA may help cancer treatment. Retrieved on June 7, 2011, from
The Johns Hopkins University has initiated a method of investigating the progress of a patient’s cancer treatment by means of modern technology for rapid succession, or decoding, huge quantities of DNA. The author in this article states clearly that individuals have a unit account of the DNA within their mitochondria, which are the several energy stores inside each cell. It states that apart form the mutations or modifications, in DNA present in cancer patients, even health individuals are known to have differences in their mitochondrial DNA, although in small amounts. The article illustrates that a cell turns to cancerous if the genes, which stop runaway development are damaged by mutations. When the cell’s anticancer defenses are damaged, genetic disorder breaks in, coming with more mutations and complete reorganization of DNA in the chromosomes takes place.
If these changed, components of DNA can be removed in the patient’s bloodstream, they can be used as direct and responsive identifiers of cancer. A surgeon could establish if the tumor has been successfully removed and the chemotherapists may inspect the achievement of some treatment by testing for the reoccurrence of the cancer cells. The DNA reorganizations are distinct to cancer cells, ensuring they are unique identifiers. The article further identifies mitochondria as another identifier of cancerous cells. Mitochondria are previous bacteria, which were enclosed eons formerly to \produce energy for bigger cells. They are placed outside the nucleus, which envelops the major human genome, and since they could be thousands of them within every cell, their DNA is certainly simple to locate.
This article is too brief in explaining how cancer can be detected and be effectively treated especially when it has developed and the cells distribute themselves across the whole body. Treatment can be difficult since not all affected cells would be destroyed. In addition, the information given in the article does not explain the sequences needed to be followed when two mitochondrial DNA series vary by a unit scale. Instead, it illustrates that it needs the direction of the analyst to present the associations as inconclusive. This is not a standard test and may result to false omission, or more significantly may result to false insertion. Hence, the articles needs further study for it to relevant in the detection and supervision of the cancerous growth.
Wade, N. (2010). DNA test may speed colon cancer diagnosis. Retrieved on June 7, 2011, from
The article discuss on current development of DNA tests for colon cancer. According to the author, this is possibly going to enhance the detection of both cancers and of the precancerous polyps, which comes first. The examination, when certified could minimize the weight of illness considerably by sensing tumors at the initial stages of cancer development in addition to those taken up by a colonoscopy. The article illustrates that colorectal cancers inclines to develop slowly and are removed simply when detected early. However, the colonoscopy procedure is being ignored by most people because it consumes a more time and involves a tube threaded up the intestines and the test do not detect everything. Colorectal cancer has been rate second among the commonly known cancer in the United States, annually causing deaths of more than 50, 000 people. Colon tumors offer significant proofs of their existence by flaking blood and cells, which are visible in the stool. Inspections of blood have minimized deaths from colorectal cancer just moderately since they are not very reactive to precancerous polyps, the phase during which cancer is highly prevented.
DNA tests are appropriate because they give precise sequences of the mutation that the colon polyp takes to full cancer. However, a patient’s risk cannot be predicted by a single mutation, but the mutation tests can be more reliable than blood tests. A current test that is under investigation is based on the various procedures in cancer cells. All cells are known to change the genes they do not require by fixing some chemicals referred to as methyl groups to a given sites together with their DNA. In cancer cells, there is usually reduced methylation, excluding some pars of the DNA where the methylation procedure is considered to overload maybe because the cells require removing tumor suppressor genes.
This article, although it gives some comparisons with other forms of tests, it does not provide an exhaustive explanation on how the tests can be carried out to detect all the cancerous cells. For colon cancer, there are several enzymes, which digest DNA, thus if such cancers can be identified effectively by way of further experiments. The colonoscopy process is also tedious for an ordinary person to get the concepts.
Grady, D. (2008). Experts decode cancer patient’s genes, seeking treatment clues. Retrieved on June 7, 2011, from http://query.nytimes.com/gst/fullpage.html?res=9804E6D9123DF935A35752C1A96E9C8B63
The article, talks form the researcher point of view where they have decoded all the genes of cancer victims and get a set of mutations, which could have been the cause or facilitated the disease development. Comparing cells of an infected victim with the cells of a healthy person, the researchers found out that the cancer cells stimulate abnormal growth, averting the cells from containing that growth and allowing it to control chemotherapy. These studies cannot support current victims, but could result to new therapies and would probably help experts develop appropriate selections on the available treatment, depending on the genetic image of each victim’s cancer. This research is first of many of such entire cancer genomes to be examined, and can be used as a primary study tat can give more clues on what takes place in DNA when cancer starts to develop.
It is confirmed that the mutations-genetic mistakes discovered in the research were not inborn, but grow later in life, just like other mutations, which causes cancer, i.e. about 5 percent to 10 percent of all cancers are considered to be hereditary. The research shows that the mutations present in a given cancer vary significantly from other researches that have examined fewer genes. The study also takes into consideration several other genes that might be involved in the mutation and development of cancer. This study although it is based on current technology, it is quite expensive and takes more time for it to come up with an excellent method that can be used by doctors in the treatment of cancer. The idea of using healthy human’s DNA in the experiments for decoding makes the study unethical because humans sacred and their lives should not be played with, especially in experimental practices.
Saretzki, G. (2010). Cellular Senescence in the Development and Treatment of Cancer. Current Pharmaceutical Design, 16 (1), pp. 79-100.
This starts with the definition of senescence, which is the irreversible growth arrest being described by alteration of morphology, gene appearance structure, and chromatin pattern together with stimulated DNA damage reaction. Senescence has two functions in tumor growth. First, it functions as a tumor smother to avoid the propagation of seriously injured cells. Essential approaches for controlling the genomically changed cells to propagate are the stimulation of ATM, p53, and DNA damage response (DDR). Furthermore, it surfaced in the past years that oncogene stimulation functions as a genetic suppress and forces senescence alongside applying same downstream elements: DNA damage activation, alteration in gene appearance, and chromatin pattern. Thus, senescence acts a strong tumor suppressor, which defends cells portraying stimulated oncogenes in vivo from being neoplastic and malignant.
The idea that oncogene forced senescent cells were mostly discovered in early, premalignant tumor levels suggest that this senescent condition has to be outplayed at the tumor genesis for the tumor to develop to malignancy. On the other hand, senescence is rapidly identified as likely result for treatment of individual tumors since it is initiated by cells reaction to therapeutic treatment, like drugs and irradiation. This method of cancer treatment is not widely used because tissue culture growth is not well established and it needs some time for it to be verified. The senescence induction cannot be fully adapted because experimental evidences are still at the infant stages and will take some time before the mechanism becomes fully incorporated into the system.
Siegelin, M., Dohi, T., Raskett, C., Orlowski, G., Powers, C., Plescia, J., and Altieri, D. (2011). Exploiting the mitochondrial unfolded protein response for cancer therapy in mice and human cells. Journal of clinical investigation. Pp. 1349-1360.
For this article, discusses the development and environment in which the cancer tumors may develop. Adjusting the protein folding surrounding in subcellular organelles, which include the mitochondria, are essential for the acclimatize homeostasis and could contribute in human illness. However, the regulators of this procedure are still complex. In this case, the selective target of heat shock protein-90 (Hsp90) chaperones in mitochondria of human tumor cells activated reimburse autophage and an organelle unfolded protein (UPR) focused on up regulation of CCAAT enhancer binding protein (C/EBP) text aspects. On the other hand, this textual UPR illustrates NF-kB based gene expression, improved tumor cell apoptosis created by death receptor ligation, and taken by intracranial glioblastoma development in mice without notice.
This information show what can be understood as novel role of Hsp90 chaperones in the moderation of the protein-folding surrounding within the mitochondria of tumor cells. This article gives a general pathway that could be possibly be used to treat cancer, but it does not give the effects of the therapy when applied to human being since the experiment was only carried out in mice. The way mice react to different conditions is not the same as the way human being would react when exposed to the same condition.
Borges, S., Cozza, K., and Werner, S. (2006). DNA Drug Sensitivity Testing™ for Cancer Medications. Clin Pharmacol, 80(1), P. 61-74.
Independent medication control such as DNA testing is highly essential for the appropriate treatment of cancer because discovering the right medication and dose is very crucial. This is not shocking to individuals who are studying genetics. Research illustrates that of the entire clinical aspects such as sex, age, general health, weight, and liver operation, which modifies a person’s response to drugs, genetic aspects contribute for fundamental rations. Three enzymes in the liver: CYP2D6, CYP2C9, and CYP2C19 metabolize almost half of the medications including most of the cancer therapies. NAT2 and 1A2 are also among the enzymes that are engaged in the metabolism of most cancer medications. The person’s genes are the key factors identifying the degree of these enzymes in the liver. If one has too much enzymes, then the process of medication is fast, while too little of the enzyme and the therapies created in the bloodstream likely result to unfavorable reactions or side effects. Without establishing one’s genetics, the physician would need several months of trial and error prescribing to get the appropriate medication and doses for the illness.
Personal healthcare provider can assist to maximize one’s response to cancer medications and various other drugs by ordering a DNA testing. The outcome will be filled into an individual medication control software, GeneMedRx, where individual or private doctor can log in to view if the present or future drugs are detected to cause drug-drug or drug-gene relations in order for dosage and choice can be addressed to one’s needs. This can be the best since the health care provider monitors an individual health from the time of detection all through the medication process. However, the cost of maintaining a private healthcare provider is high and most people cannot afford. In addition, this system depends on the DNA testing, which can sometimes shows false information on the cell mutation. Too much drugs in human bloodstream can have diverse side effects that can also be difficult to diagnose posing great dangers to the individual.
References:
Borges, S., Cozza, K., and Werner, S. (2006). DNA Drug Sensitivity Testing™ for Cancer
Medications. Clin Pharmacol, 80(1), P. 61-74.
Grady, D. (2008). Experts decode cancer patient’s genes, seeking treatment clues. Retrieved on
June 7, 2011, from
http://query.nytimes.com/gst/fullpage.html?res=9804E6D9123DF935A35752C1A96E9C
8B63.
Saretzki, G. (2010). Cellular Senescence in the Development and Treatment of Cancer. Current
Pharmaceutical Design, 16 (1), pp. 79-100.
Siegelin, M., Dohi, T., Raskett, C., Orlowski, G., Powers, C., Plescia, J., and Altieri, D. (2011).
Exploiting the mitochondrial unfolded protein response for cancer therapy in mice and
human cells. Journal of clinical investigation, Pp. 1349-1360.
Wade, N. (2010). DNA test may speed colon cancer diagnosis. Retrieved on June 7, 2011, from
Wade, N. (2010). Speed-reading of DNA may help cancer treatment. Retrieved on June 7, 2011,
from
