1. Methyl Mismatch Repair (MMR)
To repair mismatched bases, the system has to know which base is the correct one. In order to recognize the parental strand, the characteristic than can be detect isi it is a DNA strand that has been methylated. Once in a while, there will be times when the polymerase would accidentally place the wrong base across the template DNA strand during the replication of DNA. Usually it would detect it mistakes, and correct itself. But, if polymerase failed to fix its mistakes, there are some types of repair enzymes that would scan the DNA strand and proof reed the strand again. However, there might still be a wrongly placed base pair of the new strand compare to the parental strand. Figure 7 in page 15 show the pathways
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Nucleotide Excision Repair (NER)
NER is more complex biochemical complex than BER. The problem that needs NER system to repair the cell is when pyrimidine dimers occur. The nuclease will detect the mutation and remove the lesion on the DNA strand. Then polymerase will go through the DNA strand again and add new and correct base needed on that stand. Then ligase will seal the strand, and a new healthy DNA strand is born. Figure 9 in page 19 show the pathways in illustration of the process of MMR.
Consequences of DNA damages, cancer could be develop. This is because an unrepaired DNA damages, can cause errors when the cell is dividing. The cells will synthesis wrong code in DNA strand that lead to mutation and eventually to cancer. First and foremost, the DNA was damaged through exogenous or endogenous sources. When the damaged DNA were failed to be repair when it replicates in a new cell with a proliferative capacity (ability to spread rapidly), mutation conferring cellular growth will take advantages. Then, large areas of cells at a tissue surface or within any organ will be affected by the damaged DNA (Pre-malignant field defect). This damaged DNA is called as carcinogenic alteration, where, normal cells were converted into cancer cells. Figure 10 in page 21 explains on the process of cancer cell development. It all started with DNA damages that lead to mutation. Eventually, it leads to cancer if it is failed to be repair or remove the mutated DNA
On December 10, 2015, three profound individuals received the Nobel Prize in chemistry for their work on DNA repair systems. Paul Modrich, Thomas Lindahl, and Aziz Sancar studied how the cell repairs and protects the information held in its DNA; specifically, Paul Modrich focused on DNA mismatch repair. Since DNA constantly replicates, damage and incorrect pairings are expected, but enzymes watch over DNA as it replicates and repair any errors that occur. In the mismatch repair system, enzymes find the mismatch in the copy of DNA, cut the incorrect section out, and replace it with the correct sequence. Paul Modrich’s study of the mismatch repair system has provided the medical field with important information regarding cancer growth and the possibility of a cure.
A mother of a gay student that faced bullying stated in an article, that anyone who has “‘’hate in their hearts’” should accept people with differences because they are “‘going to be who they are’” (James, Boy Assaults Gay Student as Cellphone Captures Attack). In a perfect society, everyone would accept each other and not judge others based on appearance or social status. However, today many people still face the problem of acceptance. Harper Lee’s novel, To Kill A Mockingbird, illustrates how others can learn to be accepting from the characters in the novel. Scout leaves her naïve childhood behind and changes to into an accepting young adult through
Prometheus was a titan who did not like Zeus. One day he asked Zeus why he made man, but why did he not help mankind. Zeus says that he is not not helping, but he is letting them be able to find out how to do certain things.
Moreover, it’s important to understand that gene mutation occurs in our cell all the time. Accordingly, the prevention of cancer is profoundly dependent on the p53 tumour suppressor protein, which is the process to eliminate excess, damaged or infected cells by apoptosis (Haupt 2003). But if the cell doesn’t die in the process of apoptosis, it may lead a person to developing a cancer. Oncogene are a sequence of deoxyribonucleic acid (DNA) that has been altered or mutated from its original form and induces cancer (Encyclopaedia Britannica 2017). Some people have high risk of developing cancer because they inherited mutations in certain genes (Cancer research UK 2014). Mutation are classified into two, inherited and acquired types of mutation, widely discussed below (ASCO 2017)
Cancer is the development of faulty cells and is caused by mutations in the DNA of the cell which make it defective. Normal cells have methods to prevent cancer cells from forming, such as tumor suppressor genes but sometimes cancer can bypass these methods and grow out of control, forming tumors. If the cancer cells come into contact with the lymphatic system or circulatory system, it can travel to other parts of the body through them and cause cancer in those areas of the body too. Once the cancer has spread throughout the body it leads to death within a few years as the cancer takes over the healthy cells. Mutations in proto-oncogenes and tumor suppressor genes can cause liver cancer, which can be slowed down with treatments
Have you ever wondered how cancer forms? Well, cancer starts when a cell 's DNA becomes
Genomic instability is a trademark of increased risk of cancers with age. This instability arises from several problems, with one of the main ones being double strand breakage (DSB). HRR, one of the DSB repair, is a tightly
Throughout the years, humans, especially scientists, noticed the similar characteristics different living organisms inherit from their parents. How those traits were inherited from one generation to the other left the scientists and researchers in confusion. Later in the 20th century, scientists and researchers found out that the reason behind this heredity lays behind genes, which are made up of deoxyribonucleic acid (DNA)
In human cells, a combination of normal metabolic activities, errors in DNA replication, and external mutagens like radiation can lead to 1 million individual molecular lesions per cell per day. Therefore, DNA repair mechanisms are constantly active to help ensure that these molecular lesions do not lead to various diseases.
There are many types of cancer but they all start the same way. Breast cancer is mostly common among women. The body is made up of millions of cells. When one cell dies the body creates a new cell to replace it. These cells will normally grow, multiply,and die according to a schedule that keeps your body functioning. Inside every cell there is deoxyribonucleic acid, also known as DNA. This is genetic material that determines the cell's growth and reproduction.
The beginning of cancer begins with defects in the cells DNA. When cancer starts, the cell goes through the p53 gene, a gene
Are the commandments absolute pronouncements of right and wrong in all situations or are they more “guidelines” that may need to be adjusted according to circumstance? If we want to be righteous then the answer is yes. These are the guidelines we must use to govern our lives.
One gene that cause an increased risk for cancer is the p53 gene. This gene functions by controlling the cell cycle. It causes and increased risk for cancer by being mutated to many times and is usually the cause of over 50% of all human cancers. Another cell that causes an increased risk for cancer is the BRCA1 gene. This gene functions to stop tumor formations and growths. If the gene has a mutation then a tumor will begin. This is one of the genes that will cause breast cancer. The two types of tumors are benign and malignant. Benign tumors remain at the original site of formation and can be removed by surgery or radiation. Malignant tumors send out a signal to start a blood vessel line at the tumor to spread the cancerous cells around the
Modification of damaged DNA seems to be an understudied subject, there is much to understand on the restoration of DNA damage, repair and DNA methylation. Genomic DNA can be modified by methylation but much of it is affected on a gene when silenced. When epigenetic modification has been implicated with cancer and aging it causes DNA methylation to also have an impact on the double strand of DNA analysis. Modification as such provoke deteriorating changes like aging found in multicellular organisms and DNA damage may magnify biochemical pathways that regulate a cells growth or control DNA replication with DNA repair. In the article “DNA Damage, Homology-Directed Repair, and DNA Methylation” written by Concetta Cuozzo, Antonio Porcellini, Tiziana Angrisano, et al. they hypothesize how DNA damage and gene silencing may induce a DNA double-strand break within a genome as well as when DNA methylation is induced by homologous recombination that it may somewhat mark its reparation through a DNA segment and protect its cells against any unregulated gene expression that may be followed by DNA damage. The experiments used to demonstration how gene conversion can modify methylation pattern of repaired DNA and when that occurs methylation is able to silence the recombined gene. When exploring the molecular mechanisms that link DNA damage and the silencing gene then there is an induced double strand break that can be found at a specific location or DNA sequence in where the
Effects of Mutations on the Human Body If the mutation affects the control processes of a cell, then it can lead to a cell dividing