How do P53 Mutations arise?
353863
Like any other mutation.  DNA damage usually, or chromosomal problems such as nondisjunction.  Often p53 will be inactivated by multiple different mechanisms including deletion of the chromosomal region (chr17 in humans I believe), and point mutations of the coding region of the gene.  DNA damage is promoted by loss of repair pathways (due to mutation, etc), but is caused by UV radiation, or IR radiation, or other stress such as chemotherapy drugs, or carcinogens.  DNA damage can occur numerous ways, and there are many different repair pathways.  The damage has to first occur, then be 'missed' by repair pathways, and then the damage has to be at a critical region (ie p53), to promote tumorogenesis.
143311
Mutation not nutation\nIn biology, mutations are changes to the genetic material (usually DNA or RNA). Mutations can be caused by copying errors in the genetic material during cell division and by exposure to radiation, chemicals, or viruses, or can occur deliberately under cellular control during the processes such as meiosis or hypermutation. In multicellular organisms, mutations can be subdivided into germline mutations, which can be passed on to progeny and somatic mutations, which cannot be transmitted to progeny. Mutations, when accidental, often lead to the malfunction or death of a cell and can cause cancer. Mutations are considered the driving force of evolution, where less favorable (or deleterious) mutations are removed from the gene pool by natural selection, while more favorable (beneficial or advantageous) ones tend to accumulate. Neutral mutations are defined as mutations whose effects do not influence the fitness of either the species or the individuals who make up the species. These can accumulate over time. Contrary to tales of science fiction, the overwhelming majority of mutations have no significant effect, since DNA repair is able to revert most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells.\n\nBy effect on structure\nThe DNA sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health, depending on where they occur and whether they alter the function of essential proteins. Structurally, mutations can be classified as:\n\nSmall-scale mutations affecting one or a few nucleotides, including: \nPoint mutations, often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another. Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mispairing, or mutagenic base analogs such as 5-bromo-2-deoxyuridine (BrdU). Less common is a transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔ A/G). A point mutation can be reversed by another point mutation, in which the nucleotide is changed back to its original state (true reversion) or by second-site reversion (a complementary mutation elsewhere that results in regained gene functionality). These changes are classified as transitions or transversions. An example of a transversion is adenine being converted into a cytosine. There are also many other examples that can be found. Point mutations that occur within the protein coding region of a gene may be classified into three kinds, depending upon what the erroneous codon codes for: \nsilent mutations: codes for the same amino acid \nmissense mutations: codes for a different amino acid \nnonsense mutations: codes for a stop, which can truncate the protein \nInsertions add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements (e.g. AT repeats). Insertions in the coding region a gene may alter splicing of the mRNA, or cause a shift in the reading frame (frameshift), both of which can significantly alter the gene product. Insertions can be reverted by excision of the transposable element. \nDeletions remove one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. They are irreversible. \nLarge-scale mutations in chromosomal structure, including: \nAmplifications (or gene duplications) leading to multiple copies of chromosomal regions, increasing the dosage of the genes located within them. \nDeletions of large chromosomal regions, leading to loss of the genes within those regions. \nMutations whose effect is to juxtapose previously separate pieces of DNA, potentially bringing together separate genes to form functionally distinct fusion genes (e.g. bcr-abl). These
277848
No clue yet on this one. But leading research is showing that this may be a random event because of chromosome breakage. I would look into telomerase extension if I were you. Most of the time this is bad (Double stranded DNA breaks), but it happens all of the time (but luckily we have a good DNA repair system, I believe there are well over 1000 breaks a day and all we need is 1 for some bad genetic disease)
182301
Alleles. Mutations are just general changes in the DNA, they do not necessarily have to be in a gene, therefore, not all mutations cause the creation of new alleles (ie if a mutation occurred in an area that did not code for anything)
995002
Mutations occur frequently, not like in the cartoons, but small changes happen in chromosomes that are not inherited from the mother or the father.  Some of them cause terrible diseases, others may not cause problems at all.
18875
Both are required. Variation in the population provides something for natural selection to act on. Mutation is one way to generate variation. Recombination  during meiosis is another. This sounds like a trick question. The correct answer is not one or the other--you would have to explain variation. One part of the process generates choices, the other part of the process "chooses" among the available options.
596217
A mutation in a lung cell is present in that cell only and the cells that will come from its division. This doesn't affect the genetic composition of all your cells and specially not from the germ line cells (spermatozoides or oocyte).\n\nAny cell that is not a germline cell is called somatic cell. Any mutation in a somatic cell will never be passed on to offspring.
539312
Proto-oncogenes are genes that are involved in normal cell developpement. We all have those genes in our cells and they are crucial for our survival. There are 5 classes of oncogenes. The genes that regulate the cell cycle, genes that code for transcription factors, second messengers, growth factors and cell surface receptors. The mutation of any of these "proto-oncogenes" turns on the "oncogene".\n\nThe problem is that when they get mutated, their normal function is affected and they cannot continue protecting the cell integrity/function. Without them, we would die anyway.\n\nDon't forget that cancer developpement is a multi-step process that is extremely complicated. It's not just one gene being mutated... it's a serie of events that lead to cell survival (blocking of cell apoptosis) and chaotic developpement.
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It's pretty well established that the apoptotic machinery gets deprogrammed by cells progessing through tumorogenesis.  One way is the well understood p53/Mdm2 pathway.  P53 is a tumor supressor and, upon DNA damage, can either halt cells to repair the damage (at the G1/S checkpoint) or trigger apoptosis.  It does this by promoting gene expression.  \n\nAnother mechanism is to inhibit t-cell induced apoptosis, by deregulation of FasL and other proteins.\n\nThere's a whole bunch of info in the Cancer Medicine book online at NCBI (below).
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unfortunately, it is possible for cancer cells to mutate and evade chemo drugs.\n\nthe principle here is to hit the cancer hard (hence the side effects on the rest of the body) and take out all the uncontrollably-dividing cells with strong treatment, and not give them a chance to evade. your doctor had to choose the dosage to give you based on this principle.\n\nthe problem is that once cells reach the cancer state, they tend to just start mutating like crazy. some of them won't live, but some will be even more out of whack than their predecessors. mutations are the enemy in cancer. hopefully the drug will do its thing before this happens.\n\n*best of luck to you* in this fight! keep your spirits up. my mom got through a very rough battle with ovarian cancer almost 20 years ago now and while she never forgets all she went through, she is alive and doing pretty well. i wish you all the best.
492627
Cancer is a defect in DNA.  Don't know what causes the defect, but in order for you to develop cancer, this has to be triggered by something.  It could be anything.  With any look, if we have this defective DNA, we will never encounter the trigger which causes the cancer to develop.   My little girl is a leukemia survivor, so I don't wish cancer on anyone.
521716
It can be right because resonance can occur and cause that the hydrogen bonds link to another base ( that will cause a mutation). However there will be enzymes to correct that error. And some U residues are methylated so they cannot join to adenine.
785504
Generally, high energy radiation causes cell deaths.  With extremely high doses, enough of your bodies cells die that you die.  With sub-fatal doses, you can still have large numbers of cells die in  your body, or sometimes the radiation will knock atoms off of molecules in your cell's nucleus, specifically in the DNA.  If this happens, than any type of mutation is possible, since DNA is highly specific.  The most common mutation will be that the cell is unable to divide, and so it will not pass on the mutation.  The second most common mutation is that the cell overproduces, which we call cancer.
1128686
Genetic mutation occures on average every 100,000 cell division, which given the number of cell in a multi-cellular organizm or the number of single cell organizm in a population is quite often.\nNot all mutation has a measurable effect, and it isn't always passed on (in multi-cellular organizms). It is more likely to have a negative effect, and many genetic diseases originate in gene mutation. If by chance a mutation has a positive effect it is likely to be preserved and spread through evolution. \nBut it certainly cannot give a human (or any other organizm) any ability that contradicts the laws of physics, like many of those shown in movies.
240849
Cancer is the result of a change in the DNA of a cell that make sthe cell reproduce uncontrollably and to the detriment of other cells. Chnages in DNA are called mutations, and can occur through the influence of chemicals called mutagens.\n\n By lowering the number of mutagens in the environment of an organisms, the chance of any of the cells undergoing a cancerous mutation drops to a lower level. Therefore, finding mutagens is the first step to getting rid of them and thus preventing cancer developing for a longer period of time.
613105
let's define a few terms first... ;p\n\nan oncogene is a modified gene that increases the malignancy of a tumor cell. some oncogenes usually involved in cancer development increase the chance that a normal cell develops into a tumor cell, possibly resulting in cancer.\n\na proto-oncogene is a normal gene that can become an oncogene, either after mutation or increased expression. proto-oncogenes code for proteins that help to regulate cell growth and differentiation. proto-oncogenes are also often involved in signal transduction and execution of mitogenic signals, usually through its protein product. upon activation, it or its product becomes a tumor inducing agent, an oncogene.\n\nthus... since the activation of the proto-oncogenes either by mutation or increased expression could both occur naturally, then i guess inducing or manipulating these proto-oncogenes to become oncogenes in laboratories is done solely for further studies and research purposes. i think these endeavors more or less aim to equip us with the knowledge and means to better understand how to deal, treat and maybe even prevent it as well as its effects... and definitely not with the intent of killing people...
324305
To fix the second response, I must just say that an individual can have any type of mutation; it does not have to be cancer. A carcinogen (cancer-causing substance) is a type of mutagen (a substance that causes mutations in individuals), and there are many chemicals that are not carcinogenic, but are indeed mutagens (exempli gratia, certain base-manipulating mutagens).\n      Now that this is cleared up, I will say that changes in genetic makeup in an individual is a mutation, and in a population, is evolution.\n      In truth, your question is one that can be taught over the period of months. Basically (and I know that my fellow biologists will be mad at me for trying to simplify such a complex subject), over time, the usage and presence of of introns and exons changes. Introns are "intervening" parts of the gene (and are not expressed), and the "exons" are the expressed portions. Introns are the "junk" in an individual's genes, yet over time, a population may realize that this "junk" can actually be useful in adapting to the organism's environment. This results in evolution. I do advise that you read more about the intron-exon system. Evolution is, put simply, changes in an organism's genome, OVER TIME, caused by the reproduction of the fittest of the species.