what are tumor-associated antigens and what exactly do they do?
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THEY R PROTEINS IN BLOOD FOUND WHEN 1 IS AFFECTED BY THE RESPECTED CANCER.THEY R USED TO DETECT AND ALSO TO FIND THE PROGNOSIS AND THE RESPONSE OF CANCERS TO THERAPY
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It's complex.  Basically the virus infects cells, and the viral protein is present on the cell surface by MHC molecules.  The circulating T cells then can latch on to and identify the virus-infected cell as foreign.  That specific T-cell then proliferates, and starts hunting down infected cells.  There is alot more going on, including antibody production and release by B cells.\n\nWell described in this book chapter.
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As far as I know... mAbs are engineered for specific antigens.  Find out what the antigen is and research it.
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The dendritic/cancer cell fusion technology combines a patient's dendritic cells-powerful immune stimulators-with their inactivated tumor cells in a chemical fusion procedure. The fused cells are injected back into the patient in order to stimulate an immune response against the patient's cancer.\n``Cell fusion technology eliminates the need to identify specific antigens for these vaccines because it incorporates the entire menu of antigens found on the original tumor to provide targets to the immune system,'' said Dr. Kufe. ``This novel process allows us to develop a potentially life-saving cancer treatment that could be used in a broad range of cancers,'' said Dr. Avigan. \n\nMark Goldberg, senior vice president medical affairs, Genzyme, said, ``We are very excited about starting the new fusion cell trials and proud of our growing clinical program in immunotherapy. We now have three ongoing trials utilizing this promising technology -- one each in breast cancer, melanoma, and kidney cancer -- in addition to our two melanoma gene therapy cancer vaccine trials currently underway. Fusion technology complements our antigen specific vaccines and allows us to address cancers where antigens are not yet known or well understood.'' \nthe ability of the dendritic cell fusion technology to be used in a broad range of cancers, plans for initiating additional cancer vaccine trials, the data the trials are expected to provide, and the incidence and mortality rates for melanoma and kidney cancer
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An epitope is the part of a macromolecule that is recognized by the immune system, specifically by antibodies, B cells, or cytotoxic T cells. Although usually epitopes are thought to be derived from nonself proteins, sequences derived from the host that can be recognized are also classified as epitopes.\n\nMost epitopes can be thought of as three-dimensional surface features of an antigen molecule; these features fit precisely and thus bind to antibodies. The part of an antibody that recognizes the epitope is called a paratope. Exceptions are linear epitopes, which are determined by the amino acid sequence (the primary structure) rather than by the tertiary structure of a protein.\n\nEpitopes can be mapped using protein microarrays, and with the ELISPOT or ELISA techniques.\n\nGenetic sequences coding for epitopes that are recognised by common antibodies can be fused to genes, thus aiding further molecular characterization of the gene product. Common epitopes used for this purpose are c-myc, HA, FLAG, V5.\n\nInterestingly, epitopes are sometimes cross-reactive. This property is exploited by the immune system in regulation by Anti-idiotypic antibodies (originally proposed by Nobel laureate Niels Kaj Jerne). If an antibody binds to an antigen's epitope, the paratope could become the epitope for another antibody that will then bind to it. If this second antibody is of IgM class, its binding can upregulate the immune response; if the second antibody is of IgG class, its binding can downregulate the immune response.\n\nIntensive research is currently taking place to design reliable tools that will predict epitopes on proteins.
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One is a simple binding assay, in which the ligand (usually radiolabeled) is added to a hemogenate of the tissue-a number of washes are done, in the presence of cold ligand, in order to retain only that ligand that has bound with high affinity.\nThe others are all protein-based.  Western blotting with specific antibodies, immunohistochemistry to determine the presence and cellular localization.  RT-PCR or Northern blotting will tell you if the mRNA is present, but not if the receptor protein itself it there.
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Cytotoxic  or killer T cells (CD8+) do their work by releasing lymphotoxins, which cause cell lysis. Helper T cells (CD4+) serve as managers, directing the immune response. They secrete chemicals called lymphokines that stimulate cytotoxic T cells and B cells to grow and divide, attract neutrophils, and enhance the ability of macrophages to engulf and destroy microbes. Suppressor T cells  inhibit the production of cytotoxic T cells once they are unneeded, lest they cause more damage than necessary. Memory T cells  are programmed to recognize and respond to a pathogen once it has invaded and been repelled.
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alright i got this one for you right off the top of my head...\n\nfirst off i think you are talking about a receptor tyrosine kinase (RTK).  \n\nthings to know about an RTK: 1. a kinase is an enzyme that adds a phosphate to something else. 2. a receptor binds a ligand and leads to a signal activation.  3.  tyrosine is an amino acid that is found in the intracellular portion of a receptor tyrosine kinase.  4.  a membrane bound receptor is something that is encased inside the cell membrane. aka part of it is outside the cell and part of it is insdie the cell.\n\nso an RTK is a membrane bound receptor which receives an extracellular ligand and when the ligand binds the receptor a cross phosphorlyation event occurs in the intracellular portion of the receptor tyrosine kinase.  if you dont know what i'm talking about view the diagram below:\n\nextracellar space (outside of cell)\n+  <--Ligand aka extracellular signal\n&#92;/ <--- receptor portion of Receptor tyrosine kinase\n{}=====   <-- cell membrane  wraps around in a circle\n[]  <--kinase portion of receptor tyronsine kinase\nPxP <--- cross phosphorylation \n\n\nintracellular space (inside the cell)\n============ <-- more cell membrane that connects with the other cell memebrane\nextracellular space\n\n\nwhen the ligand (the + in the diagram) binds the receptor the cross phosphorylation occurs and then the signal proceeds via other chemical reactions into the nucleus where the DNA is housed.  \n\nWHY is this such a big deal?????  because this is the mechanism for how a cell is told to divide!  so basically when there is ligand present outside the cell and it hits the receptor then the cell divides.   the big point is that when the receptor does not work properly and the cross phosphorylation occurs IN THE ABSENCE of LIGAND then the tyrosine kinases is degregulated and this LEADS TO CANCER. \n\nwhy and how does it become deregulated and cross phosphorylate with out having to bind ligand?  mainly b/c the tyrosine kinase is defective when it is made by the cell.  This can happen because the DNA which is the blueprint or directions on how to make the tyrosine kinase is altered so that it shows the cell how to make a faulty or mutant tyrosine kinase.  Then it sticks this tyrosine kinase on the membrane but instead of waiting for ligand it just cross phosphorylates on its own and this leads to cancer.  \n\nI wrote sooo much i dont know if this helps.  but i doubt you will get a more complete answer to your question.  if you want a short quick answer. then it would be mutation in the DNA makes a bad tyrosine kinases which tells the cell to divide with out control.
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TI-2 antigens are able to directly activate B lymphocytes in the absence of T cells, by their ability to extensively cross-link membrane immunoglobulin. Activation of B lymphocytes by TI-2 antigens requires functional expression of Bruton's tyrosine kinase (Btk), a molecule involved in the surface immunoglobulin receptor-mediated signaling cascade.
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Phenotypes (i.e. antigens present): A or AB (postive or negative for both)\n\nAntigens: A for sure, and possibly B\n\nGenotypes: AA, AO, or AB (still don't know positive or negative)
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Although gamma delta T cell receptor-bearing lymphocytes (gamma delta T cells) constitute a significant minority of circulating and tissue-associated T lymphocytes, the mechanism responsible for the activation of these cells is unknown. To address this question, resting gamma delta TCR+, CD3+, CD4-, CD8- cells isolated from the blood of healthy volunteers were cultured with allogeneic dendritic cells (DC) or monocytes, and their proliferative response measured. DC alone induced gamma delta T cells to proliferate, with a peak response on the sixth day of culture. Pretreatment of DC with an anti-HLA-DR mAb, but not anti-HLA class I or anti-CD1 mAbs, inhibited the response of gamma delta T cells. Antibodies to gamma delta T cell receptor, CD2, CD3, or CD11a were also inhibitory, whereas antibodies to alpha beta T cell receptor, CD4, CD5, and CD8 had no effect. Although only 40-60% of freshly isolated gamma delta T cells expressed CD28, mAbs directed against CD28 or its ligand, CD80, were markedly inhibitory. Moreover, removal of CD28+ cells from the gamma delta T cell population nearly abrogated the response to DC. These results demonstrate that resting gamma delta T cells recognize and respond to MHC class II determinants on allogeneic DC in a manner that is highly dependent on the CD28 activation pathway as well as molecules such as CD2 and CD11a that mediate cell-to-cell adhesion.
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HLA are Human Leukocyte Antigens.  HLAs are products of your Major Histocompatibility Complex I (MHC I) genes. HLAs couple with the products of antigen digestion in the cell (peptide fragments of viruses for example) and are required components for the process of antigen presentation to T and B lymphocytes.  T and B  lymphocytes are then 'activated' by the antigen presentation.  So... HLAs participate in antigen presentation to activate T and B lymphocytes.
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What is your question?  Antigenic determinants, also known as epitopes, are the site on an antigen that binds to the complimentary determining region (CDR) of the antibody.  The CDR is determined by the hypervariable regions of the antibody.  An epitope is generally 5-7 amino acids long, which corresponds roughly to the size of the CDR.  Different antigens can share epitopes, which is the basis of cross reactivity.
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proto-oncogenes are genes that normally function in regulating proliferation. Mutations that activate them will usually cause the cell to growth without control (this is when we refer to them as oncogenes).\nTumor suppressor genes are caretakers and gatekeepers. They make sure to control uncontrolled proliferation and give the time to a cell to repair any damage. If necessary, wil cause the cell to die. If these genes get mutated then cells would tend to keep unrepaired DNA damages and turn into tumors.
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B cells produce antibodies when triggered by an antigen.  They also produce memory cells (these "remember" a particular antigen and allow large scale production of antibodies if the antigen enters the system again) \n\nAntibodies are also called immunoglobins, and their job is to combine with specific antigens (such as pollen, dust, etc.).  They may coat the antigens in such a way that they can be absorbed by phagocytic cells, combine with an antigen in order to inhibit its function, or may actually lyse and destroy the antigens.  \n\nCytotoxic, or killer, T cells lyse and destroy foreign cells and material and any cells in the organism infected with foreign material.\n\nHope this is helpful :-)
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Many of the chemotherpeutics are designed to rob the tumor of Oxygen and blood vessels (VEGF blockers is a common group), but the truth is it is more complicated than that. If you rob a cell of oxygen you trigger the HIF (hypoxia inducible factor) set of genes as a first response. These can help a cell cope in anoxic conditions. There are many cases where a tumor is deprived of oxygen and in some cases you get a necortic core, but in other cases nothing happens. Second problem is that to deprive the whole tumor of O2 you will have to remove it from the body (b/c it is attached at the basement membrane and that has a source of O2) so at that point you've successfully removed a tumor anyway so you don't need to "kill" it any further.
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Unfortunately, scientists have yet to be able to locate specific features of malignant and immune cells that would make them uniquely targetable (barring some recent examples, such as the Philadelphia chromosome as targeted by imatinib). This means that other fast dividing cells such as those responsible for hair growth and for replacement of the intestinal epithelium (lining) are also affected.\n\nIn simpler terms, chemotherapy can't target the cancer cells themselves, only any cell in the body that grows quickly like hair, so it dies and falls out...