What is the difference between immortalization and oncogenic transformation?
539921
The difference between immortalization and oncogenic transformation has been largely defined through cell-culture experiments and may not actually exist in human cancer cells. But it's an interesting difference nevertheless.\n\nImmortalization refers to the act of creating cells that can divide indefinitely in culture. Typically, normal cells taken directly from an animal (referred to as primary cells) can only divide a certain number of times; after that, their chromosome ends, or telomeres, shorten too much and the cells can no longer divide further. Human cells in culture without any special treatments will always stop dividing eventually. Rodent cells are a little different from the onset. After dividing several times, almost all the cells will either completely cease division (we call this stage "senescence") or die, but a few cells will recover and start dividing anew. These cells can then grow indefinitely in culture and are referred to as immortal.\n\nThe distinction between immortalization and oncogenic transformation is best seen in experiments where these cells are injected into immunocompromised mice. Immortal cells will not cause tumors in these animals. Furthermore, they will generally only grow as a single layer of cells in a dish, exhibiting what is known as contact inhibition. As soon as all of the cells are in contact with other ones, they cease growth until new space is opened up.\n\nTransformation is essentially loss of this contact inhibition. Transformed cells are capable of growing on top of each other in a seemingly limitless fashion. These cells will form tumors if injected into mice. Transformed cells have a number of other characteristics, including the ability to sometimes grow in the absence of survival factors and the ability to divide without being specifically instructed to do so from outside the cell (normally cells will not divide until they receive these specific signals).\n\nCells can be transformed in a number of ways, many of them involving genes called oncogenes, which allow cells to bypass the normal controls on their growth. Interesting experiments using rodent cells show the link between immortalization and transformation. It has long been known that if you introduce two oncogenes together into primary rodent cells (these oncogenes are also known to cause human cancer), the cells become transformed, but introduction of them singly causes the cells to undergo programmed cell death or stop growing altogether. If, however, you begin the experiment using a cell that has become immortalized (but is not transformed), one of those oncogenes alone is capable of causing transformation.\n\nAs I mentioned before, human cells behave a little differently from rodent cells. In the past, scientists were able to create, through poorly understood means, rare human cell lines that were immortalized but not transformed. Recently, scientists did something that was not possible before: they directly transformed human cells with defined oncogenes in culture. The key seems to be differences between how humans and rodents safeguard an enzyme called telomerase, which lengthens telomeres in cells.
338436
Cancer is uncontrolled cell growth.  Normally the cells in your body grow and divide along a fixed schedule, just enough to replace those that have died.  Sometimes, though, mutations occur within the cell in the pathway that controls growth.  These cells then begin growing and dividing without anything to keep them in check.  This is harmful because is destroys healthy tissue in the surrounding area and wastes valuable resources.
681303
In addition to the above individuals with cancer may have cells with a different DNA sequence due to deletions, mutations, and additions.  \n\nThere is also a possibility that an individual can have mossaicism causing different cells in the body to have a different DNA sequence.  Mossaicism occurs when two embryos merge to form one in the uterus.  In most cases a majority of the cells will have one DNA a sequence, but some tissues will have a different sequence from the embryo that was 'absorbed.'
103912
I disagree with Cobra.  Cloning an old human being will not result in advanced aging in the clone.  Remember dolly, the cloned sheep?  At first, scientists thought that she would age much faster than a regular sheep.  This, however, was not the case.\n\nAnd, since the clipping of telomeres (that change in your genes that Cobra was talking about) is the only change that occurs in the genes during the life of a human (barring radioactive exposure), cloning a 100-year-old human would have the same result as cloning the same human when he or she is an infant.  No difference, no additional mutation.\n\nFor info about dolly's aging, see the below article under "Controversy."
1166019
Cancer is a class of diseases or disorders characterized by uncontrolled division of cells and the ability of these cells to invade other tissues, either by direct growth into adjacent tissue through invasion or by implantation into distant sites by metastasis. Metastasis is defined as the stage in which cancer cells are transported through the bloodstream or lymphatic system. Cancer may affect people at all ages, but risk increases with age. It is one of the leading causes of death in developed countries.\n\nThere are many types of cancer. Severity of symptoms depends on the site and character of the malignancy and whether there is metastasis. A definitive diagnosis usually requires the histologic examination of tissue by a pathologist. This tissue is obtained by biopsy or surgery. Most cancers can be treated and some cured, depending on the specific type, location, and stage. Once diagnosed, cancer is usually treated with a combination of surgery, chemotherapy and radiotherapy. As research develops, treatments are becoming more specific for the type of cancer pathology. Drugs that target specific cancers already exist for several cancers. If untreated, cancers may eventually cause illness and death, though this is not always the case.\n\nThe unregulated growth that characterizes cancer is caused by damage to DNA, resulting in mutations to genes that encode for proteins controlling cell division. Many mutation events may be required to transform a normal cell into a malignant cell. These mutations can be caused by chemicals or physical agents called carcinogens, by close exposure to radioactive materials, or by certain viruses that can insert their DNA into the human genome. Mutations occur spontaneously, or are passed down generations as a result of germ line mutations.\n\nMany forms of cancer are associated with exposure to environmental factors such as tobacco smoke, radiation, alcohol and certain viruses. While some of these can be avoided, there is no known way to entirely avoid the disease, and public health and vaccination programs are also important on a global scale.\n\n\nI hope you find what your looking for.\n\nGood Luck!\n\n=)
448144
Neither is true.  In a broad sense #1 is true, but every time a cell divides errors accumulate.  So every cell has a unique signature, but it may only be one base pair difference in 3 billion.  #2 is not true either, error accumulation leads to diseases like cancer (mostly cancer).  Aging is thought to occur by telomere shortening. Every time a cell replicates, the telomere shortens.  It can be repaired by telomerase, but in some cases telomerase is not active.  When it gets too short the chromosome can stick to another chromosome, leading to aneuplody.  Once the telomere gets short, the cell enters crisis.  Two things can happen; one is that the cell dies.  Two is that the cell becomes immortalized, which is the next step on the road to cancer.\n\nPS DNA damage does not cause AIDS!
556440
Cancer is a class of diseases or disorders characterized by uncontrolled division of cells and the ability of these cells to invade other tissues, either by direct growth into adjacent tissue through invasion or by implantation into distant sites by metastasis (in which cancer cells are transported through the blood or lymphatic system). Cancer may affect people at all ages, but risk increases with age. It is one of the leading causes of death in developed countries.\n\nThere are many types of cancer. Severity of symptoms depends on the site and character of the malignancy and whether there is metastasis. A definitive diagnosis usually requires the histologic examination of tissue by a pathologist. This tissue is obtained by biopsy or surgery. Most cancers can be treated and some cured, depending on the specific type, location, and stage. Once diagnosed, cancer is usually treated with a combination of surgery, chemotherapy and radiotherapy. As research develops, treatments are becoming more specific for the type of cancer pathology. Drugs that target specific cancers already exist for many cancers. If untreated, cancers may eventually cause illness and death, though this is not always the case.\n\nThe unregulated growth that characterizes cancer is caused by damage to DNA, resulting in mutations to genes that encode for proteins controlling cell division. Many mutation events may be required to transform a normal cell into a malignant cell. These mutations can be caused by chemicals or physical agents called carcinogens, by close exposure to radioactive materials, or by certain viruses that can insert their DNA into the human genome. Mutations occur spontaneously, or are passed down generations as a result of germ line mutations.\n\nMany forms of cancer are associated with exposure to environmental factors such as tobacco smoke, radiation, alcohol and certain viruses. While some of these can be avoided, there is no known way to entirely avoid the disease, and public health and vaccination programs are also important on a global scale.\n\nLeukemia or leukaemia (see spelling differences) is a cancer of the blood or bone marrow characterized by an abnormal proliferation of blood cells, usually white blood cells (leukocytes). It is part of the broad group of diseases called hematological neoplasms.
872183
You have 10 to 100 Trillion cells in your body.  Every cell has the same genetic code.  How would you change that code in so many cells?\n\nAdditionally, the genome is turning out to be much more complicated than was thought just a few years ago.  Much of a gene's 'performance' is determined by 'epigenetic' regulation of the gene's expression.  You can have 'normal' genes, but if they are not being expressed properly, that is the same as having defective genes.\n\nThis is a very, very complex issue.
558764
Cancer, in laymans's terms, is the unregulated growth of a cell.  Now cell growth, and activities in general, are typically regulated through cell receptors which, in response to a stimulus, activate or release a kinase.  These kinases transfers phosphates to other proteins or phosphorylates them making them active to stimulate DNA replication and transcription (growth).  Cancer is commonly characterized by high levels of (active) kinase due to suppressed phosphotase activity (opposite of a kinase) or defective oncoreceptors stuck in the "ON" position.
546065
Not a stupid question at all. Mutation (as mentioned above) does occur, though of course it will only affect individual cells and their descendents, not all cells in the individual. There is also a process that is being increasingly studied called genomic imprinting or epigenetic inheritance. These are not DNA sequence changes, like you asked about, but seem to be related to your question. The wikipedia article is a decent introduction but there are other summaries available.
551447
Cell division or Mitosis is how your body replaces worn out cells.  All cells degrade over time, and if your body could not replace them, then you wouldn't live very long.  Partial cell division, or Meiosis(sp) is necessary for reproduction
967758
It is called Phosphorylation\n\nIn eukaryotes, protein phosphorylation is probably the most important regulatory event. Many enzymes and receptors are switched "on" or "off" by phosphorylation and dephosphorylation. Phosphorylation is catalyzed by various specific protein kinases, whereas phosphatases dephosphorylate.\n\nA protein kinase is an enzyme that modifies other proteins by chemically adding phosphate groups to them (phosphorylation). This usually results in a functional change of the target protein (substrate) by changing enzyme activity, cellular location, or association with other proteins. Up to 30% of all proteins may be modified by kinase activity, and kinases are known to regulate the majority of cellular pathways, especially those involved in signal transduction, the transmission of signals within the cell. The human genome contains about 500 protein kinase genes; they constitute about 2% of all eukaryotic genes.\n\nAdding a phosphoryl (PO3) to a polar R group of an amino acid might not seem like it would do much to a protein, but it can actually turn a nonpolar hydrophobic protein into a polar and extremely hydrophilic molecule. Phosphorylation is observed on serine, threonine, tyrosine and histidine residues.\n\nAn example of the important role that phosphorylation plays is the p53 tumor suppressor gene, which—when active—stimulates transcription of genes that suppress the cell cycle, even to the extent that it undergoes apoptosis. However, this activity should be limited to situations where the cell is damaged or physiology is disturbed. To this end, the p53 protein is extensively regulated. In fact, p53 contains more than 18 different phosphorylation sites.
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...
252256
Well, i'm a cell and molecular biology student so my answer is more to do with cancer and differentiation\ndifferentiation is the proliferation of cells, EG/ you start with 1 cell in humans, then meiosis results in 4 daughter cells and then these cells keep dividing until you get a foetus and then a human (3 X 10-14 cells). Cancer is a disease of differentiation. stem cells are pluripotent, undifferentiated but determined. the different stages of differentiation are: 1. TOTIPOTENT, 2. PLURIPOTENT, 3. MULTIPOTENT, 4. UNIPOTENT. hope that helped
507551
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.
1184816
Are you asking about chromosome transformations such as rearrangements and translocations?
33392
Precancerous cells are cells that may, or are likely to, become cancer.\n\nPrecancerous cells have little capacity to repair their DNA and so are more likely to become cancerous.