development process of cancer, from DNA mutation, to tumor formation, to angiogenesis, to metastasis?
469268
Just follow the link to find out all you need to know about cancer.
282086
The causative factors in the developemnt of breast cancers  are still not much known as other cancers in the body.  Any how it is assumed  by experiments that the following factors influence in the developemnt of breast cancer: 1.Genetic factors. 2. Harmones. 3. Viruses. and 4. Environmental factors which is  not yet proved.
1112155
the process would be mutation of the genes
427400
Cancer cells originate among the normal cells of the tissue or organ in which the cancer arises.  Some combination of external factors, e.g. carcinogenic chemical exposure, and a cell's response to those factors produces a cell that is genetically different from its normal neighbors.  It has become a mutant, containing altered DNA.  The most important result of this mutation is that the transformed cell escapes from the controls that regulate the growth, maturation, and rate of replication of its normal neighbors.  The transformed cell begins to grow more rapidly and divide at more and more frequent and irregular intervals.  The developing cancer becomes a cluster of deviant cells that consume more and more metabolic resources (nutrients and oxygen), depriving surrounding cells of these resources.\n\nAs this is happening, the malignant cells come to resemble their original cell type less and less.  Among other things, they will begin to produce plasma membrane proteins that differ from those of their normal precursors.  Often this occurs early enough in the course of the cancer development that the malignant cells can be recognized as foreign by the body's immune system and destroyed before they have a chance to develop into an actual tumor.  Many cell biologists believe that this process, the emergence, detection, and destruction of early incipient malignancies, begins to occur very early in life.  Part of the reason that clinically significant cancer becomes so much more frequent as we age is probably that this immune surveillance for abnormal cell development loses its effectiveness with age.\n\nCancers arising in different tissue types, and even in the same tissue types, vary widely in how much their cells are altered morphologically and phsyiologically from the original precursor cell type.  They also vary widely in how fast they grow, how early in their development they begin to invade and damage surrounding tissue, and how readily they colonize other tissues/organs via the bloodstream or the lymphatic circulation (metastasis).  Cancers in which the cells more closely resemble their precursors, which grow relatively slowly, and metastasize rarely or not at all, are usually easier to treat medicallly or surgically once they have been detected.  Cancers whose cells have been radically altered from the original cell type, which grow rapidly, and metastasize early, are much more difficult to treat and are more likely to be lethal.  This is especially true of cancers that grow to large size and metastasize before they even begin to produce symptoms noticeable by the patient.  Examples are most lung cancers, pancreatic cancers, and stomach cancers.\n\nIn any case, cancer cells differ greatly from their normal neighbors, most critically in the structure of their DNA and in the ways that the genetic information contained in their DNA is expressed.  The key result, again, is the abililty of these cells to grow and reproduce more rapidly and uncontrollably than their normal precursor cells.
823822
Not sure, but new treatments are comming....\n\nUS scientists crack entire genetic code of breast and colon cancers\n\nResearch on cancer and the genetic code looks like it may at long last  produce real breakthroughs\n\nFor more info, visit:\nhttp://www.librarynews.info/\nhttp://www.medical-research-study-directory.info/medical-research-study-directory/\nhttp://www.medical-research-study-directory.info/\nhttp://www.lasik-surgery-san-diego.info/\nhttp://www.san-diego-dentist.us\nhttp://www.san-diego-plastic-surgery-cosmetic-surgery-doctors.us/\nhttp://www.acne-treatment-medicine-1.info/
493151
its proto-oncogene, read here\n\nhttp://en.wikipedia.org/wiki/Tumour_suppressor_gene\n\nhttp://en.wikipedia.org/wiki/Proto-oncogene
154571
1) G1 growth of the cell and replication of organelles\n2) S replication of DNA\n3)G2 growth of cell and replication of oraganelles
739274
You will learn a great deal by reading this\n\nhttp://dgwa1.fortunecity.com/body/cancer.html
1104927
read here\n\nhttp://en.wikipedia.org/wiki/Mutation
937352
Check out "mitosis" in a suitable source (Wikipedia, for example).  The process is a bit long to describe here.
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.
697543
development of drugs using biochemistry\nunderstanding of organic processes\nenergy production\nmany others
904760
the list of activities is endless:\n\nDNA replication, mitosis, protein synthesis, lipid synthesis, protein and lipid metabolism, oxidative phosphorylation, cholesterol synthesis, and on and on and on the list goes . . . . of course it all depends on the type of cell.
195299
Ok I hope this is not a waste of your time. Not all cancers are genetic. Some people have the genetic marker for some cancers or other diseases. The occurance of these markers increases if a parent or grandparent had the disease or a marker for it. It is like a lottery, the more decendents that had the disease the more likely you are to get it. A larger part of cancers depend on a Myriad of other factors though. -Risk factors.\n Here is a link for you.\nhttp://www.cancer.gov/cancerinformation
310214
That's a rather broad question...  You would probably have to specify it a little more to get the answer you are looking for.  But that said, there are numerous reasons as to why animal cells may develop an "abnormal" morphology.  Basically, there are perhaps two categories that can roughly be differentiated, even though - again - you have to be careful there.  One would be genetic reasons, another would be environmental reasons.  Genetic causes could be numerous as well, but take certain cancers for example, that have a genetic predisposition.  Certain environmental toxins can likewise lead to malformation of cells.  Please note that I was talking of a genetic "predisposition".  Often in case of cancer ebnvironmental and genetic effects are both responsible for the adverse effects observed.  So, the two categories are not ontological absolutes.  \n\nPerhaps what would help you to envision the problem is the basics.  First, cells divide mitotically in unicellular organisms.  consequently, a central question would be the default state of the cell.  There are three possibilities: (a) quiescence (i.e., the cell does not divide and needs an initiation of the mitotic process), (b) proliferation (i.e., cells default state is division and it needs particular factors to asure quiesence as needed in many multicellular organs), and (c) neither, since cell division is contextual.  The most common assumption in biology (and cancer biology, for that matter) is (a).  (b) has been suggested by  Carlos Sonnenschein and Ana Soto ("The Society of Cells. Cancer and Control of Cell Proliferation." New York: Springer, 1999).  Personally, I tend towards (c).  \n\nSecond, cells that proliferate during organogenesis have to further differentiate into the morphology and functionality they are to have in a specific organ.  \n\nThird, certain organs have cells that proliferate, whereas other organs don't.  Consequently, once everything goes well intially in organs of the second type, malformation may not occur as easily.  However, that said there are of course cancers of organs that normally do not have proliferating cells.  \n\nThese three basics may help you to ask your question a little more specifically and then seek out the literature that could give you answers accordingly.\n\nFinally, just remember that what is considered normal in science is the mean of a population.  But what determines this mean is often unclear.  I am thinking here for example of norms of reaction where cells may be shaped quite differently in response to environmental factors, and yet function wonderfully - in fact just exactly as they should given the particular environment.  Now, what is "deformed" would have to be probably understood functionally (i.e., a morphology associated with a functional break down).  And it seems to me that this is what you are looking for anyway.\n\nHope this helps.
170448
p53 is one of the most important tumor suppressor genes. There is never one specific thing that CAUSES cancer, it is really chain reactions through different pathways in the cell that lead to it becomeing cancerous, or dying. Go to cell signal.com to get an idea of how much is actually involved in cancer development. Keep in mind that cancer is just a cell with a mutation that cannot kill itself and keeps growing, and sometimes travels throughout the body and continues to grow in other places. (I am just starting out in cancer research, please dont think one cigarette will cause generations of hideous and deathly tumors in all of your offspring.)
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.