Wednesday, October 21, 2009

Is cancer a hereditary disease?

Cancer is not strictly hereditary, but genetics does play a part, and the size of the part it plays varies from one kind of cancer to another.
Cancer is in fact body cells growing out of control, which is triggered when enough mutations of the cells have accumulated. Mutations may be caused by carcinogens, which are various things that can lead to cancer, for example tobacco, radioactive substances, hepatitis B virus. Mutations occur in our bodies every day, and that is why our body cells die every day to lower the possibility that they accumulate enough mutations to become cancerous.
However mutations in germ cells (the reproductive cells like ova and sperms) may be given to offsprings. This means that offsprings now have more mutations to start with, and so easier to accumulate enough mutations to have cancer. Hence, we can see clustering of various types of cancers in families, such as colorectal cancer, cervical cancer, lung cancer. (but lung cancer may also be due to second hand smoke from one family member that smokes)
Even though cancer is not classified as a hereditary disease (contrary to cystic fibrosis, colour blindness etc), genetics does play a part in the development of cancer.
No, it's not.
(m)BIOLOGISTS are agog at a remarkable connection between hereditary diseases and cancer that came to light last week. The connection is that cancer, like some hereditary diseases, can be caused by a strange stuttering in the individual's DNA, the effect of which is that small segments of the hereditary material are copied many times over. The multiple copying, first discovered about two years ago, startled geneticists because it was a novel form of mutation. Three-unit segments of DNA were present in as many as 200 copies, strung together as if the cell's copying mechanism had jammed at that point and turned out the same triplet of bases over and over instead of continuing up the DNA strand. These cascades of multiple triplets lengthened with each generation, and the longer they were, the more severe the disease. Genes with repeated triplets have been found to underlie four genetic diseases so far: Huntington's disease, myotonic dystrophy, fragile X syndrome and spinal and bulbar muscle atrophy. In at least two of these diseases, Huntington's disease and myotonic dystrophy, people who developed the disease earlier in life had longer strings of multiple triplets. Search for Mechanism The origin of these miscopied DNA triplets in hereditary disease is unknown, and scientists are still trying to determine the exact mechanisms by which they cause illness. The new cancer gene reported last week considerably broadened that mystery because it showed that a very similar miscopying occurs in the tumor cells of individuals who inherit the gene. The gene's existence and approximate location were discovered by teams led by Dr. Bert Vogelstein of the Johns Hopkins University School of Medicine and Dr. Albert de la Chapelle of the University of Helsinki in Finland. Dr. Vogelstein said the chances were 90 to 100 percent that people who inherited the gene would develop colon cancer or one cancer of the stomach, small intestine, gall bladder, urethra, pancreas, ovaries, uterus or kidney. But the hallmark of the gene is its effects on tumor cells. The cells have hundreds of thousands of regions where triplets or sometimes shorter units of DNA are copied over and over again. Dr. Vogelstein likened the problem to the chaos caused by a copying machine that is supposed to produce 10 copies and instead prints 20. How the inherited gene causes the miscopying is unknown. It differs from all other known cancer genes. Those are mutations of normal genes, which function by putting brakes on cell proliferation. The mutations release those brakes, allowing cells to divide wildly. As researchers try to understand the new discoveries, they are asking whether the occurrence of repeated triplet genes in both cancer and hereditary diseases is a coincidence or whether there is a deeper meaning yet to be uncovered. Some scientists suspect that the similarities are significant and believe the apparent connection is too fascinating to dismiss. Others caution that the two discoveries might have nothing to do with each other. "At the time that expanding genes were first found, the notion was that they could have an impact on cancer, because they represented a possible way for cells to lose normal controls of growth and development," said Dr. David Housman, a molecular genetecist at the Massachusetts Institute of Technology. Now, he added, that hunch has proved correct. 'More Than Just Chance' The same view is held by Dr. Stephen Thibodeau of the Mayo Clinic in Rochester, Minn., who has studied gene expansions in fragile X syndrome and in colon cancer. He reported last week that 17 percent of the patients he studied had these expanded genes and added that there was likely to be a relationship between expanding genes in hereditary diseases and cancer. "There really are a lot of similarities," Dr. Thibodeau said. "I really do think that this is more than just chance." But Dr. Eric Lander, a molecular biologist at the Massachusetts Institute of Technology, cautioned that the connection between cancer and the hereditary diseases could be spurious. The cancer gene, he said, may lead more generally to all sorts of mutations and not be at all specific for repeated triplets. That could happen, for example, if the cancer gene destroyed a cell's ability to faithfully copy its DNA when it divides. The cell, he said, may be deranged, "left, right and center." Dr. David Ledbetter, a cell biologist at Baylor University College of Medicine in Houston, said that although the cancer results were "very novel, surprising and exciting, I don't know what they mean." He noted that in fragile X syndrome, which he studied, the relevant gene is a constant size in normal people; in those with the disease, the gene is huge but also varies in size from cell to cell in the same person. In colon cancer, however, the gene's length varies enormously from cell to cell, even within the normal size range, Dr. Ledbetter added. That means that in cancer, genes do not have to become gigantic before their sizes are unstable. He concluded that hereditary diseases and cancer could use very different mechanisms to create the expanded genes. For example, Dr. Thibodeau said, people with fragile X syndrome have more than 200 repetitions of a three-unit segment in the fragile X gene, but in normal individuals the unit is repeated only 6 to 60 times. Patients with myotonic dystrophy have more than 50 repetitions of a unit in their gene, compared with the normal quotient of 5 to 27. In cancer, different cells of the tumor seem to have different numbers of repetitions, and segments that are expanded in one cell may be of normal size in a nearby tumor cell. Lack of Information Scientists have no idea what these repeated units do. "Our information is really pretty sketchy," Dr. Thibodeau said. Researchers have speculated that they might be sites for recombination, the breaking and rejoining of DNA during cell division. Another possibility is that they somehow enhance the copying of DNA. But whatever they do, Dr. Vogelstein said, there is something about them that makes them hard to copy accurately when cells are dividing. In studying the cancer gene mutation, Dr. Vogelstein and Dr. de la Chapelle have begun addressing Dr. Lander's question, asking whether cancer cells arising from the gene are generally aberrant, with all sorts of genetic errors throughout their DNA, or whether the errors are confined to expanded genes. So far, Dr. Vogelstein said, they have not found any mutations other than the expanded genes. He cautioned that he and Dr. de la Chapelle had examined only a few indicator genes to look for mutations and that it still could be that the cancer gene induced a variety of nonspecific DNA copying errors. "To me, the common thread is instability," Dr. Vogelstein said. Even in people who have neither cancer nor a hereditary disease, the repeated units of DNA are of varied lengths, although the lengths of each person's repeated units remain constant in the absence of disease. Still, Dr. Vogelstein said, "you have to wonder what makes cells tolerate such liquidity?" He speculated that the expanding segments might speed genetic changes that allow organisms to evolve and that in cancer, that mechanism goes awry. "One way to think about tumors is as an evolutionary process in which evolution occurs fanatically," Dr. Vogelstein explained. Dr. Housman said that a full understanding of the phenomenon would come when researchers actually isolated the cancer gene that caused the mutations. He said researchers were finding that the DNA replication apparatus was functioning less precisely in cancers caused by the gene. "What remains to be seen is where the crucial mistakes might be made that lead to cancer," he said. "If there is an intersection between the DNA replication apparatus and the length of the repeat, we'd like to have all the pieces of that puzzle worked out."
We don't have all the answers to that yet. There is evidence of a heritary connection in who gets it but only for a few types so far. Certain genes seem to make it easier for cancer to occur. Beyond that, the facts aren't all in yet.
Not necessarily.
cancer is uncontrolled cells reproduction due to to such disturbance in the controll system for the cell (RNA) , THIS COULD BE hereditary disease , which is transfer via the chromosomes in side the cell , who are responsible for transferring hereditary diseases .
Some types of cancer have a HUGE heritable component. If you have the gene that predisposes you to that tumour, you are likely to develop multiple tumours of the same type; not spread, but separate bits that become cancerous.Examples:Wilm's tumour of the kidney
some types of breast cancers run in families
So do some tumours / polyps of bowel and nose
Gorlin Syndrome; this is also called Basal Cell Naevus Syndrome, and similar terms.
I have Gorlin Syndrome; I develop Basal Cell Carcinomas all the time. We GS people also have increased risk of brain tumours, and tumours in bones (keratocysts). {Fortunately, I did not get the brain tumours, but I had multiple keratocysts.} Some sites on GS say is is due to an unstable genome; ie less stable than other people.AFAIK, I have one copy of the gene missing; one of my chromosomes has that gene deleted. If any of my cells then lose the other copy, they can start a tumour.BTW, I helped them find the gene; my deletion was in just the right place to save the researchers a lot of work.Because the problem is a chromosome that lacks a gene, the GS characteristic acts as if it is a "dominant gene". You can pass GS to your kids, even if your partner is normal. Fortunately, I had no kids.
Some cancers do have a hereditary link(a disposition) but it is only a small part of what makes a person get cancer.
CYTOGENETIC TECHNOLOGISTYes some Cancers are genetically linked (Li-Fraumeni syndrome, a problem with the TP53 gene, these cancers can range from breast, colon, soft tissue and brain) meaning that there is a higher rate of incidence in family members than other cancers. Also some leukemia's (CML,AML for example) hold trisomy 8's for example or trans location between 2 chromosomes. If it's a balanced trans location (getting one from each parent) it's generally alright but if its a de novo (new mutation) within that specimen then it's a bad thing
if some types of cancer have been in your family then you tend to stand a higher chance of getting that cancer too. e.g. if your mother or grandmother had breast caner. you hear of some ladies who choose to have mastectomies even though they do not have breast cancer.
If I may interpret your question, I think what you are looking for is a way to estimate your chances of acquiring the disease. We are currently working on a new diagnostic tool that will provide an answer to your question (important note: the tool is not yet marketable!). The diagnostic tool is based on a recent discovery of the cause of many cancers made by Dr. Hanan Polansky. If you would like to read a description of this discovery go to (there are many other websites which describe the discovery).

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