DNA Defects that Cause Cancer - Case Study Example

DNA Defects that cause Cancer Student name: Institution: Part A: Defects in DNA replication cause cancer Introduction DNA replication refers to the progression through which a dsDNA copies itself to generate two DNA molecules that are alike. DNA replication is a fundamental process inside the cell. Every DNA strand participates in the replication process because the new DNA molecules should have similar genetic components (Dyer, 2011). DNA repair incapability may be inherited, and such individuals have high chances of developing cancer. When there are mutations in DNA repair gene, the gene expression may be hindered. Hence, the repair purpose will be incomplete, and injures will build up. If left unrepaired, these damages lead to faults during DNA synthesis causing alterations that lead to cancer development (Pories & Moses, 2009). Cancer is a name used in describing illnesses in which irregular cells divide uncontrollably and have the capability to affect other cells. There are many diverse kinds of cancer and most of them are named according to the cell types they begin; for example cancer that starts in the colon is referred to as colon cancer (Dyer, 2011). Other wider cancer groupings include; Leukemia, which is cancer of cells that form blood. Replication of DNA DNA replication takes place in three main steps. During the first step, the double helix opens up and the DNA strands separate. The template DNA strand undergoes priming, and new DNA molecules gather (Dyer, 2011). Diagram showing unwinding of DNA double –helix During the unwinding process, the double strands untwist at a region known as the origin. Various proteins and enzymes play a part in priming the strands. At last, DNA polymerase assembles the new DNA molecules (Dyer, 2011). The replication process is initiated in two rates. Firstly, the initiator protein opens up the small section of the DNA double helix. After that, helicase, a protein, joins to the hydrogen bonds between DNA bases and disintegrates them. Therefore, the two strands open up. The helicase continues moving along the double helix separating the two strands. For the moment, as the helicase unwind, primase joins to each strand and initiates the replication process by stretching nucleotides known as primers. After the primer gets on position on a single-stranded DNA, DNA polymerase enfolds with the strand and causes attachment of fresh nucleotides to the nitrogenous bases previously exposed. The building of new strands depends on the collection of available nucleotides (Pories & Moses, 2009).The nucleotides that compose the fresh strands match up with complementary bases in the template strand. A and T bases join up with each other, and G and C join up with each other. This occurrence is called complementary base pairing. Subsequently, the fresh strand gets duplicated. The complementary strand includes similar sequences as the novel strand. Complementary base pairing ensures that the novel DNA coding is preserved (Dyer, 2011). Diagram showing the DNA complementary base pairing Defects in DNA replication Replication protein A, RPA, is a compound that binds to ssDNA and comprises of four subunits. It is vital for DNA copying in eukaryotes. Current studies indicate that it has an important role initiation of cell division after DNA is exposed to replication pressure. Additionally, RPA activates the ATM-Rad3- associated protein kinase (Pories & Moses, 2009). Also, it is involved in the transmission of checkpoint signs by phosphorylating the downstream effectors. RPA deficiency during DNA copying has effects on the cell endurance. RPA-deficient cells show increased levels of DNA destruction, and less permanence of the genome. Replication pressure whether externally or internally induced has high chances of resulting to genomic instability and increases vulnerability to cancer and abnormal cell growth. studies show that mutations and polymorphisms resulting to slight decline of MCM levels contributes to cancer, birth imperfections and growing old (Dyer, 2011). Causes of Cancer Almost 90% of all cancer cases result from exposure to one or various carcinogens, but inherited gene also hold a significant task in cancer development. Carcinogens are agents that result to DNA disruption or mutation. Mutations lead to cancer by causing cells to proliferate uncontrollably and become eternal (Dyer, 2011). There are physical, biological and chemical carcinogens. Physical DNA mutagens may be ionizing energy, U.V radiation and elements. Ionizing energy puts pores in the DNA, damaging the right genetic coding. This energy may result from X-rays and cosmic rays. U.V radiation is from the sun and lead to mutation by binding collectively some DNA regions. This binding leads to mutation because the sequences are misread during replication. Various mineral fibres may lead to DNA mutations due to their magnitude. Chemical carcinogens cause mutation through strange agents attaching onto the DNA, resulting to a misread. They include; benzopyrene and aflatoxins. Biological carcinogens may be either viruses or bacteria. Viruses that have high cancer risks in human are the human papilloma virus, and the hepatitis B. Helicobacter pylori is known to cause stomach cancer (Dyer, 2011). Treatment of cancer Surgery is the most ancient and most common applied method of cancer treatment. About 60% of individuals who test positive to cancer go through surgery. If growths are noticed early, physicians opt to eliminate the whole tumor before it affects other cells. Usually, it is used together with chemotherapy and radiation therapy (Dyer, 2011). When a patient is undergoing radiation therapy, the affected tissue is put open in radiation energy to kill the cancerous cell. Nevertheless, the radiation affects normal cells; hence they are only used to shrink cancerous cells for surgical elimination. Chemotherapy uses drugs. The most recent advances in cancer treatment include the hormone therapy and the immunotherapy. Hormone therapy involves disruption of hormones in the body, in treatment of the cancerous cells. This method involves the use of drugs and hormones. The hormonal glands may also be surgically eliminated to prohibit further proliferation of the cancerous cells. Immunotherapy acts in a similar manner, disrupting the body’s regular task. It involves giving medication that fuels the ability of the body to battle cancerous cells (Pories & Moses, 2009). Difference between Normal Cells and Cancer Cells Normal cells usually stop reproducing when enough cells are produced while cancerous cells grow indefinitely, resulting to a tumor. Normal cells respond to signals while cancer cells do not interact with other cells. Normal cells undergo maturation with time whereas cancer cells do not mature. Normal cells are functional, but cancer cells are un-functional (Dyer, 2011). Diagram Showing the Differences between Normal Cells and Cancer Cells Part B: Commonly Diagnosed Cancers in Australia Cancers Diagnosed in Australia An estimate of new cancers that were diagnosed in Australia added up to 120,710 in the year 2012. Out of this, 67260 were males while 53,460 were females. The highest diagnosed cancer were the cancer of the prostate (15,560), breast cancer was diagnosed with 14,680 cases while the bowel cancer 15,840 cases (“Cancer in Australia”). Melanoma was 12,510. In 2010, more than 42,844 deaths were caused by cancer. Out of this, 24,328 included males whereas the rest were females. In this year, 8,099 of the total deaths were from lung cancer, 3,982 -bowel cancers, 3,235 -prostate cancers, 2,864-breast cancer, and pancreatic cancer-2,434. Between the years 2006-2010, the percentage 5-year survival was 65% for the males whereas in females, the percentage was 67% (“Cancer in Australia”). This result showed that females diagnosed with cancer had higher chances of surviving the next five years compared to males. The rate of breast cancer in male is unusual; nevertheless, 110 cases were recorded in the year 2009. Between the years 2010-2012, there were a total of 880,432 had been hospitalized due to cancer. The NMSC had the highest number of hospitalized patients followed by the prostate cancer. In my own opinion, the reason for high cancer rates in men than in women lies in lifestyle differences. Men have a tendency to take alcoholic drinks and become overweight, and are more prone to smoking. The three increase the susceptibility to cancer development. Men are mostly diagnosed with cancer types that are hard to treat, so this could be reason of high cancer-death rates in males. Such cancers that are common in males affect organs such as the liver, bladder and the oesophagus (Dyer, 2011). Steps for Cancer Prevention Cancer prevention tips are still in development. It is believed that apart from inherited defects, cancer development is stimulated by poor lifestyles. Tobacco is linked to several cancer types such as; lung cancer, kidney, and cancer of the cervix. Healthy diet is believed to reduce cancer risk; Abundance of fruits, low fat foods, and low alcohol intake. Healthy-weight maintenance is believed to reduce the chances of cancer development of breast, colon, and prostrate. Minimal changes in a person’s lifestyle can have a great impact on the person’s cancer risk (Pories & Moses, 2009). Part C: Techniques of focusing slides Steps of focusing a light microscope Firstly, the microscope should be plugged in and the light revolved to medium high strength. Ensure that the low power objective lens is down way and make low the stage. Ensure the image is in the centre; beneath the objective lens and along the light pathway. The aperture of the condenser is then set to the minimum opening. Carefully adjust the coarse adjustment knob to locate specimen. The condenser knob adjusts the light for perfect observation (Dyer, 2011).The fine adjustment is not necessary when using the 400X and the 100X lenses. To switch to high power objective lens, bring it in place and focus again by use of the fine adjustment knob. Light-bending as it moves from air to glass can be avoided by use of immersion oil at high magnification (100X). When viewing specimen using the oil-immersion, the condenser ought to be lifted to a place closer to the stage to produce the best resolution (Pories & Moses, 2009). Diagram showing the parts of a light microscope Focusing a Wet-mount of Human Cell Slide Wet mounts are vital for observing live biological specimens. They appear superior in presences of a water drop in the microscope slide. The water holds up the specimen and covers the gap in between the glasses, hence, allowing easier light passage. A drop of water is added on the sample and the other side gently lowered using a toothpick to prevent trapping bubbles. The slide is then observed using the low power magnification lens (Dyer, 2011). Conclusion Defects in DNA replication lead to cancer development in humans. Cancer development is also be triggered by inherited defects. DNA replication is a complex process and requires various proteins and enzymes. Absence of any of the required proteins lead to replication defects, which in turn cause mutation that lead to cancer. Cancer is also caused by physical, biological, and chemical agents. Such mutagens cause defects in the DNA that lead to misread of the coding sequence during replication, which in turn lead to mutation that cause cancer. In Australia, studies have shown that men are more prone to cancer risks compared to women. The survival rate of males diagnosed with cancer is lower than the females diagnosed with cancer. This rate is attributed to the different lifestyles between males and females. References Cancer in Australia: key facts. (n.d.). (AIHW). Retrieved from http://www.aihw.gov.au/cancer/cancer-in-australia/ Dyer, M. A. (2011). Cancer and development. San Diego, Calif.: Academic Press. Pories, S., & Moses, M. A. (2009). Cancer. Santa Barbara, Calif.: Greenwood Press. Read More