Is there any research on the synthesis of a virus targeted at cancer cells (what I'd call oncothropic)?
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Yes!  There is documented proof on this subject!  Scientists have re-worked the Measles virus so that it will attack cancer cells.  Oh, I wish I could give you a link, but I heard about this months ago.  Try searching the archives at this site:\n\nwww.advanceweb.com\n\nI'm pretty sure that's where I read about it.  Isn't that exciting.  It's one of those things that makes me happy for all of these technological marvels.
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Try Invitrogen (IVGN).  They make products for life science research.
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Melanoma is a cancer...it is not viral or bacterial.  It is found in pigmented skin cells such as moles.  These cells become abnormal, grow uncontrollably and aggressively invade surrounding tissues.  This particular skin cancer metatasizes and can be very lethal.
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Uhmm... no... hmmm... it is really almost impossible for a virus to be made... we still dont have the capability to produce life and what comes with it... THe only thing I can think of is genetical mutation of virus... but its really hard to mutate something... especially a tiny virus....\n\nI heard stories that HIV came from a doctor and a monkey... who copulated.. but i'm not really certain with the credibility of this... but if this is true... it could have mutated a virus, that is now what we call HIV... O.o\n\nBut... nonetheless... I believe that no person is stupid enough to MAKE a virus... that CAN be a threat to his very life... ^^
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I don't know about all know diseases but they can't get cancer. We don't know why but for a couple of years scientist are studing shark to find a cure for cancer in humans.
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CANCER - Yes I can give lot of information but without knowing details from you it is difficult. I can only give general inforamtion. read -\n\nCancer 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 tends to increase with age, due to the fact that DNA damage becomes more apparent in aging DNA. It is one of the principal 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, and may be passed down from one generation to the next as a result of mutations within germ lines.\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 risk factors can be avoided or reduced, there is no known way to entirely avoid the disease.\n\nif you require any specific information please post your question accoringly and there are persons like me to answer your qurries in details-.
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From the ERC (www.endocenter.org), posted to their listserv at http://groups.yahoo.com/group/erc:\n\n\nEndometriosis-ovarian cancer link 'underestimated'\nSource: Human Reproduction 2006; 21: 1237-42\n\nResearchers assess the relative risks of individual cancers over a long period of follow-up among women with endometriosis. \n\nWomen with endometriosis appear to be up to twice as likely as the general population to develop ovarian cancer, say researchers. \n\nCo-existence of endometriosis and cancer has been reported several times. One study showed an overall relative risk of 1.2 in women with endometriosis compared with those without it, and risks for ovarian cancer and non-Hodgkin's lymphoma of 1.9 and 1.8, respectively. \n\nAnna Melin (Karolinska University Hospital, Stockholm, Sweden) and colleagues evaluated whether these risk ratios stood in an extended study. They identified women (n = 64,492) who were discharged from a Swedish hospital with a diagnosis of endometriosis between 1969 and 2000, and assessed their incidence of cancer, using the National Swedish Cancer Register. \n\nExcluding the first year of follow-up, there were 3349 cases of cancer. The overall risk of cancer was no higher than that expected on the basis of the female Swedish population, but ovarian cancer (standardized incidence ratio [SIR] = 1.43), endocrine tumors (SIR = 1.36), non-Hodgkin's lymphoma (SIR = 1.24), and brain tumors (SIR = 1.22) were all more prevalent.\n\nAn even higher risk of ovarian cancer was seen in women with early diagnosed (SIR = 2.01) and long-standing (SIR = 2.23) endometriosis, respectively. \n\n"This study has shown an increased risk of some types of malignancy, above all ovarian cancer, in women with endometriosis," the researchers conclude.\n\n"The material indicates that the risk might have been underestimated."\n\n19 April 2006\n\n------------------\n\nEndometriosis & Malignancies\n\nWe know that Endometriosis can impact every aspect of our lives, from our interpersonal relationships to our careers; from our ability to have children to our ability to get out of bed in the morning.  It can change our views on life and how we think about ourselves - and how we think about others.  The consequences of Endometriosis touch every part of us, inside and out, prompting some women to refer to their disease as a "benign cancer."  Can Endometriosis go one step further and actually turn malignant?  Can it even place us at risk for certain cancers and other illnesses?  Unfortunately, research shows that for some women, it may. \n\nMalignant transformation of Endometriosis can and does occur.  Some researchers even estimate that approximately 0.7-1.0% of patients with Endometriosis have lesions that will ultimately undergo malignant transformation, and urge consideration of performing bilateral oophorectomy at the time of abdominal surgery in patients with significant disease.(1) \n\nWe have also begun learning of the elevated risks women with the disease have for certain cancers, including non-Hodgkin’s lymphoma.  The reasons why remain unclear; however, women with Endometriosis are more likely take certain drugs, such as Progestagens, and are more likely to have had their ovaries or uterus removed, another factor that influences hormone levels and possibly increases cancer risk.  One patient undergoing Tamoxifen therapy was discovered to have malignant endometrioid neoplasia arising within her Endometriosis, suggesting to her physicians that the Tamoxifen, as a result of its estrogenic effects, caused proliferative and malignant changes in her disease.(2)   \n\nIn a similar study targeting women who had undergone hysterectomy with oophorectomy because of Endometriosis, authors noted that "Endometriosis can undergo estrogen-dependent changes similar to the endometrium and may carry a risk of developing hyperplasia and carcinoma during unopposed estrogen stimulation."  The r
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Try checking out http://nci.nih.gov/, or perhaps contact the American Cancer Society at www.cancer.org
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We may be able to. There is a noval process known as RNAi.\n\nUsing RNAi in mice we have been able to destroy the genome of HIV and Hepatitus C viruses. This is amazing. Once we figured out a way to get it into a persons infected cells, we may well be able to cure a virus infection. It'll take many yearsn though, but watch this space.\n\nThe futures bright, the futures RNAi
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Introduction. This is a brief outline of the steps necessary to produce mice with a mutation targeted to a specific gene. These animals are referred to as "knock-out" mice or "gene targeted" mice. The broad outline of the experiment includes: 1) the investigator constructs a gene targeting vector containing a mutation in the target gene; 2) the targeting vector is introduced into ES cells; 3) ES cell clones which undergo homologous recombination with the targeting vector are identified; 4) ES cell-mouse chimeras are produced; 5) the chimeras breed and transmit the chromosome with the targeted gene to their offspring; 6) homozygous animals are produced from the mating of hemizygous chimera offspring; and 7) the phenotype resulting from the genetic mutation is characterized. Core personnel are available for consultation on all aspects of gene targeting research. Contact Thom Saunders with any questions or Meet the Staff.  The Transgenic Core prioritizes all requests for service on a "first-come, first-serve" basis. Your requests for electroporation, clone expansion, and blastocyst microinjection will be added to the Transgenic Core work queue in the order that they are received. \n2. Plan the experiment. What is the purpose of your experiment? Do you want to completely ablate gene expression in all tissues? Do you want to analyze tissue specific regulatory sequences? Do you want to produce a model for tissue-specific gene deletions? You will need to obtain or clone the structural gene that you want to mutate. The source of the DNA is important since published studies demonstrate genomic DNA isogenic to the embryonic stem cell line give higher gene targeting efficiencies in ES cells (see Key Gene Targeting Papers). While complete sequence information is not necessary, a detailed restriction map of the gene is an irreplaceable tool. During the planning stages the material transfer agreements for R1 ES cells and other reagents should be initiated so that they are ready in time. Once a genomic clone of the gene is in hand and restriction mapped, then it is time to... \n\n3. Clone and the Verify the Targeting Vector. The Core has cloning vectors for investigators to use in gene targeting research. They include pPNT, a basic targeting vector, pNZTK2, designed to insert the lacZ gene behind the promoter of the targeted gene, and pflox, which is designed to introduce loxP sites into the gene. A complete materials transfer agreement is required before they can be distributed. You will need to determine which 5' and 3' fragments of the gene will be used to construct the targeting vector. Generally speaking, a couple of Kb on either end should give a reasonable gene targeting frequency. You will also need to consider the methods and probes that you will use to identify ES cell clones that have undergone homologous recombination with the targeting vector. This means a Southern blot approach with probes outside of the targeting vector or a PCR based assay with primers outside of the targeting vector. Once the orientation of the fragments in the targeting vector are confirmed and the probes are tested then it is time to... \n\n4. Electroporate ES Cells and Select Recombinants. ES cells are a very sensitive reagent, and most often the weakest link in the process of producing gene targeted mice. Fastidious tissue culture technique is necessary to maintain the totipotent state of the cells during electroporation, selection, and expansion. In order to maximize successful outcomes, the Transgenic Core maintains ES cells and companion reagents that are quality tested by producing ES cell-mouse chimeras that transmit the ES cell genome to offspring. Investigators may choose to use the Core's Gene Targeting Service (we do all of the tissue culture work, you do all of the molecular biology), or to use space in the Core lab (rent space in our completely equipped laboratory for ES cell culture work), or to do th
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http://www.cellsalive.com/cell_cycle.htm\n\nThis is a neat interactive website! Check it out and let me know how it works for you!
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Cancer causing viruses insert genetic material into infected cells that leads to uncontrolled growth which leads to cancer (such as the case with HPV - human papilloma virus).\n\nOther viruses can cause infections leading to chronic inflammation of an organ, which leads to mutations occuring in that organ (such as Hepatitis B Virus and Hepatitis C Virus, both of which can lead to a higher incidence of Hepatocellular Carcinoma).\n\nLastly, some viruses can cause immunesuppression of the T- and B-cells which mediate cellular immune response, and inhibit their ability to attack abnormal cells (Kaposi's Sarcoma and some lymphomas with HIV infection).
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i think yea, i have seen commericals about HPV Human Pampollina Virus( u get the idea however that is spelt)being linked to certain (cervical) cancers but if ur talking about colds or flus i doubt it
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Apoptosis is characterized by maintenance of intact cell membranes during the suicide process so as to allow adjacent cells to engulf the dying cell so that it does not release its contents and trigger a local inflammatory reaction. Cells undergoing apoptosis usually exhibit a characteristic morphology, including fragmentation of the cell into membrane-bound apoptotic bodies, nuclear and cytoplasmic condensation and endolytic cleavage of the DNA into small oligonucleosomal fragments (Steller, 1995). The cells or fragments are then phagocytosed by macrophages.\n\nSignals that can trigger apoptosis can include\n\nlineage information \ndamage due to ionizing radiation or viral infection \nextracellular signals. \nExtrinsic signals may either suppress or promote apoptosis, and the same signals may promote survival in one cell type and invoke the suicide program in others (Steller, 1995). For example, death receptors that are members of the tumour necrosis factor receptor (TNFR) family sit in cell membranes, but their intracellular domains have direct access to the cell death machinery that lies ready and waiting within the cell (Ashkenazi and Dixit, 1998). When members of the TNF ligand family bind to their receptors some of the pathways activated can include those that bring about cell death. Conversely, there are other factors, such as the neurotrophins, that bind to cell surface receptors and which act to prevent cell death!\n\nInvocation of the suicide program involves the synthesis of specific messenger RNA molecules and their translation. PCD can sometimes be suppressed by inhibiting transcription or translation (Steller, 1995), which provides evidence that cell death is mediated by intrinsic cellular mechanisms.\n\nI'm interested in life! Why do I want to think about death?\nCell death is currently the subject of considerable research activity. This interest stems, in part, from the potential for understanding oncogenesis and the possibility of exploiting the cell death program for therapeutic purposes. For example, inhibition of cell death might contribute to oncogenesis by promoting cell survival instead of death. Likewise, triggering cell death might provide the means for eliminating unwanted cells (e.g., tumor cells).\n\nWhat on Earth has death got to do with development?\nRecognition of PCD as a developmental mechanism dates back well over 100 years (Clark and Clark, 1996; this is an excellent account of old descriptions of "apoptosis" before there was "apoptosis"). Developmental processes that involve PCD include:\n\nElimination of transitory organs and tissues. Examples include phylogenetic vestiges (pronephros and mesonephros in higher vertebrates), anuran tails and gills and larval organs of holometabolous insects. \n\nTissue remodeling. Vertebrate limb bud development (Fig. 11.42, Saunders, 1982; Fig. 1, Saunders, 1966) is an example. If PCD fails, in formation of the digits, digits remain joined by soft tissue. Compare, for example, the situation in the chick and duck hind limbs. If chick limb mesoderm is combined with duck ectoderm, PCD fails and the digits remain joined (Saunders, 1966). This observation implicates the ectoderm in providing the signal to trigger PCD. Another example is formation of heart loops during vertebrate development. Depletion of cells in spinal ganglia occurs during development of the chick embryo. As shown in Table 11.1 (Saunders, 1982), there is precise chronological and spatial control over this process. Interestingly, injections of nerve growth factor reduce the frequency of cell death in the spinal ganglia. This observation provides a link between growth control and PCD.
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The SV40 virus has been implicated in the Glioblastoma multiforme Grade III type of brain malignancy. Many of the early 'Salk' polio vaccines were allegedly contaminated with this virus when the vaccine components were prepared using the harvested kidneys of monkeys as a culture medium. Some of the kidneys were believed to have been infected. Need I say more?
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Basically, it is tagging the substance to be delivered to an incredibly tiny particle of gold; usually, there is an antibody (or other targeting substance) attached to the gold particle as well, to target a specific cell type or cellular structure.  It is the antibody that does the targeting; the gold nanoparticle is but the (essentially passive) tool used to carry the targeting molecule and the drug molecule.\n\nIt's one of the developing technologies--it's far from being routine, yet, last I heard.
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Not with current freezing techniques. Too much cell damage. In the future I think that a process will be possible. Will it be ethical or moral in a rapidly overpopulating world will be the ultimate question.