i'm confused,there are more than 30000 genes in our body and how it is possible to find the related gene for a specific disease
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In general, a gene cannot be directly inserted into a person’s cell. It must be delivered to the cell using a carrier, or “vector.” The vectors most commonly used in gene therapy are viruses.\n\nIn one form of therapy cells from the patient’s blood or bone marrow are removed and grown in the laboratory. The cells are exposed to the virus that is carrying the desired gene. The virus enters the cells and inserts the desired gene into the cells’ DNA. The cells grow in the laboratory and are then returned to the patient by injection into a vein. This is called ex vivo because the cells are grown outside the body.\n\nIn another form of therapy, vectors (again viruses) or liposomes (fatty particles) are used to deliver the desired gene to cells in the patient’s body. This form of gene therapy is called in vivo, because the gene is transferred to cells inside the patient’s body.\n\nUsing these approaches researchers are trying a variety of theraputic options, namely:\n\n1) Replacing a mutated gene that causes disease with a healthy copy of the gene.\n2) Inactivating a mutated gene that is functioning improperly.\n3) Introducing a new gene into the body to help fight a disease.
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click here:http://rds.yahoo.com/_ylt=A0geuuCMJFdFWDsB6.FXNyoA;_ylu=X3oDMTE2NXZmaDBwBGNvbG8DZQRsA1dTMQRwb3MDOQRzZWMDc3IEdnRpZANERlg1XzMw/SIG=122s68rjs/EXP=1163425292/**http%3a//www.wellcome.ac.uk/en/fourplus/DNA.html
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there are databases with which you can do homology searches. best to know what genes you are looking for though as genome wide homology may be difficult to search for\ntry the ensemble database:\nhttp://www.ensembl.org/index.html\notherwise a broad literature search might be better suited. odds are someone else has already done a similar comparison.\n\nfound this old review\n\nhttp://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6VS0-45765F9-2J-1&_cdi=6248&_user=911953&_orig=search&_coverDate=06%2F30%2F1997&_qd=1&_sk=999929996&view=c&wchp=dGLbVtz-zSkWA&md5=03f894feac6d92afb553850237f34bcf&ie=/sdarticle.pdf\n\nmight be of some help. if the link doesnt work, can be found using a Pubmed search.
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UPDATE: I've just read your comment so I'm leaving the difficult stuff below. \nFirst things first:\nProbably you know (but it's worth repeating) that the genetic information in each cell is kept as DNA. This DNA is able to copy parts of itself as RNA. RNA in turn builds proteins. Our bodies are not made only of proteins, but proteins are the ultimate regulators of what our body looks like and how it works. So, if a gene in your DNA synthesizes a specific RNA, and this in turn can make a particular protein, this protein will have to do with the way you look and function. Another person with a somewhat different "variety" of the same gene, will have a different appearance and/or function. Each gene codes for one protein, so it takes a really large amount of genes to code for all of them (and this is VERY simplified, the interactions are much more complex).\n\nNow for the second part: the fact that you have several really long DNA strands in each cell (these DNA strands are what can be visualized as chromosomes under special circumstances) does not mean that every single little gene in your DNA will generate RNA and ultimately produce a protein. Only a part of the DNA is actually active (and it's a small proportion), the rest is just "there" and doesn't code. And the expression of the gene (=when the gene's information becomes visible) depends on the interaction with other genes, with other substances that are cellular regulators, and many environmental factors. \n\nExample: you know Siamese cats? they have a genetic constitution such that the dark color proteins are formed especially at the body parts that are colder. So usually you get a sand-colored cat with black legs, tail, and ears. But for this pattern to show, there has to be interaction with the right temperatures. If the cat is not exposed to these colder temperatures, the dark parts don't develop. Or maybe other proteins or regulators "got in the way" of the process. And you get a cat with no dark parts (or the opposite, a very dark animal from excess cold). \nAnother example: suppose a baby is born from tall parents; they in turn had tall parents, so it's highly probable that the baby has the "tall" potential. But if this baby is not well nourished during his/her development, he/she will not reach the height that he "potentially should" have had. \nCan you see the difference? The genotype is ALL the genetic information that you have, and the phenotype is the result of the combination of this genetic information with other factors: the person/animal/plant as it is realized. \nI hope this helps you, I'll be around :-)\n\nCheck this site, it's great:\nhttp://evolution.berkeley.edu/evosite/evo101/IIIA1Genotypevsphenotype.shtml\n-------------------------------\nThe genotype is the genetic information that the said individual carries in each of his/her body cells. Much of that information is never expressed (=becomes "visible" or translates into actual characteristics), and much genetic information can yield different characteristics depending on the interaction with many environmental factors (which occur both inside and outside the cell or organism in question). Thus, the final fully developed individual is the result of the genotype ("raw" genetic information) PLUS environmental/developmental factors; the characteristics of this final product, the real individual, constitute the Phenotype. \nFor instance, an individual with a perfectly "normal" genotype may develop many types of abnormalities due to problems during pregnancy, including drugs, lack of oxygen, etc. Identical twins have the same genotype (they come from a single cell) but are never completely identical; and of course they have different personalities. This is because of all the epigenetic phenomena that influence development. And it's also the reason why reductionist approaches that s
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This should keep you busy for hours.....\nhttp://en.wikipedia.org/wiki/List_of_genetic_disorders
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I don't like your teacher.  I think he/she is looking for B. genes, but then he/she should not have put chromosomes as an alternative choice.  Mendel's theory of independent assortment was only true because the genes he studied were on separate chromosomes.  It could be argued that what he was actually studying was chromosomal inheritance.
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There are many alternative cures, the best way to find out about what is out there is to keep searching. I found a great web site just follow the link there is loads of info.
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It is amazing how prevalent a disease can be, and yet so unknown. Neurofibromatosis (NF) is the most common neurological disease caused by a single gene. Both forms, NF1 and NF2, affect more than 100,000 Americans. The Children’s Tumor Foundation Web site (www.ctf.org) says “this makes NF more prevalent than Cystic Fibrosis, hereditary Muscular Dystrophy, Huntington's Disease and Tay Sachs combined.” While there is no known cure for NF, and it’s various forms, research is working toward an effective treatment.\n\nThe goal of this site is to create a local communication center for people with NF, as well as medical providers. Soon new features will be added, such as chat rooms and forums to encourage communication between the people involved. please check back often and help us grow.
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This could be linked, but Im not a doctor so I cant say.  it may be worth looking at and reading.\n\nPS I hope it helps.
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A lot of the tests depend on the type of cancer in your family history.  A lot of people believe it is hereditary.
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chromosomes are what makes you they carry your genetic information eg hair colour eye colour, you have 46 chromosomes in each cell or 23 pairs, but in sex cells the egg and the sperm u have only 23 as they join up with the opposite sex cell to make 46. thats meitosis, miosis is the development of ordinary body cells, this is done so if for example you cut your self you body is able to repair itself, hope you understand this and it was useful for you :)
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The genotype is the specific genetic makeup (the specific genome) of an individual, in the form of DNA. Together with the environmental variation that influences the individual, it codes for the phenotype of that individual. Non-hereditary mutations are not classically understood as representing the individuals' genotype. Hence, scientists and doctors sometimes talk for example about the (geno)type of a particular cancer, thus separating the disease from the diseased. While codons for different amino acids may change in a random mutation (changing the sequence coding a gene), this doesn't necessarily alter the phenotype.\n\nTypically, one refers to an individual's genotype with regard to a particular gene of interest and, in polyploid individuals, it refers to what combination of alleles the individual carries (see homozygous, heterozygous). Any given gene will usually cause an observable change in an organism, known as the phenotype. The terms genotype and phenotype are distinct for at least two reasons:\n1. To distinguish the source of an observer's knowledge (one can know about genotype by observing DNA; one can know about phenotype by observing outward appearance of an organism). \n2. Genotype and phenotype are not always directly correlated. Some genes only express a given phenotype in certain environmental conditions. Conversely, some phenotypes could be the result of multiple genotypes. The genotype is commonly mixed up with the Phenotype which refers to the physical appearance\n\nThe distinction between genotype and phenotype is commonly experienced when studying family patterns for certain hereditary diseases or conditions, for example, hemophilia. Sometimes people who do not have hemophilia can have children with the disease, because the parents each "carried" hemophilia genes in their body, even though these genes have no effect on the parents health. The parents in this case are called carriers. Healthy people who are not carriers and healthy people who are carriers of the hemophilia gene have the same outer appearance (ie they do not have the disease), therefore they are said to have the same phenotype. However, the carriers have the gene and the other healthy people do not (they have different genotypes).\n\nWith careful experimental design, one can use statistical methods to correlate differences in the genotypes of populations with differences in their observed phenotype. These association studies can be used to determine the genetic risk factors associated with a disease. They may even be able to differentiate between populations who may or may not respond favorably to a particular drug treatment. Such an approach is known as personalized medicine.\n\nInspired by the biological concept and usefulness of genotypes, computer science employs simulated genotypes in genetic programming and evolutionary algorithms. Such techniques can help evolve mathematical solutions to certain types of otherwise difficult problems.
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positional cloning is finding the location of the disease gene. linkage analysis is used. usually a marker is used to narrow down the location to 10Mb. the marker can be STR, defective enzyme that are always linked to the disease. then more marker are chosen near the site to further narrow down the range. then cloning of the region is done. if DNA can be hydridize to RNA library to see which gene it coded for. from the gene found, there should be one with mutation in and it si possibly your target\nfunctional cloning is used when you know the pathology of the disease so that you know the protein (gene product of your target). the protein can be cleaved. sequenced. and generate cDNA to probe the genome for the gene\npostional candidate is used when you have idea of the pathology. first you find the subchromosomal location of the gene jist as positional do, but you dun need to narrow down the region as it take many works. then from the region you find out if there is any gene that may cause the disease\nfor example, you target rodopsin if you wantto find an eye disease. this method is certainly better than postional\ncandidate is you find the homologue in other species \nby studying the disease that cuse same phenotype \nto give you some clues of the gene
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Knudson's two hit hypothesis works well here.\nSay for example you have a germ-line mutation that makes you heterozygous for the BRCA1 gene.\nif something else happens in your lifetime that creates a mutation in your "good copy" of BRCA1, then the gene will now be mutated, and you will have no functioning BRCA1 (this is often called a "loss of heterozygosity"--which can also occur via translocation, deletion, etc.)...that is step 1.\nthis has to happen multiple times with many different genes (as there has not been discovered merely a single gene that causes cancer)...but IF this were to happen multiple times, perhaps with BRCA1, BRCA2, p53, etc.  then you would develop cancer...\n\nhope this is along the lines of what you were looking for...
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I believe there are known cures of cancers and they are being held back.how can we study a disease for 30 years or more and not have a cure. why because too many people and big corps are making a fortune off of this killing disease.
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Not sure if this will help but try the link below\n\nhttp://www.answers.com/topic/gene
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For any kind of cancer it has to do with the cells, now each cell has a copy of DNA, but it duplicates this in the form of RNA and sends that arround the cell to do the going ons.  However cancer results when a certain part of the RNA is miss duplicated, this dosn;t happen very often respectivley since there is somthing that goes over the RNA to make sure it is correct.  However when that substance has a problem it cannot check the RNA and therefore cancer is much more likley.  Because cancer is the rapid reproduction of cells and when the RNA dosn't tell the cell to stop reproducing it makes more and more cells.  Things like ciggarets destroy the substance making them much more likley to get cancer.  So ya thats just a really breif crash course, i reckon you google it if you have anymore questions.