Fighting-Cancer-With-Viruses.

[D.ap]

Scientists are using viruses to fight cancer. This type of cancer therapy is known as oncolytic virotherapy and uses genetically modified viruses to destroy cancer cells. By studying how viruses infect cells, scientists have devised methods for using altered viruses to target cancer cells, while leaving healthy cells unharmed. The presence of these viruses in cancer cells also kicks the immune system into action and the tumor cells are destroyed.

Oncolytic viruses may also be manipulated to import therapeutic drugs into cancer cells. This provides a more direct delivery system for the drugs to reach targeted cancer cells. Some of the potential cancer fighting viruses being studied include the human reovirus, the vesicular stomatitis virus, and the measles virus.

http://biology.about.com/od/biotechnolo ... iruses.htm

Measles Virus and Cancer
Using a genetically engineered measles virus, researchers from the Mayo Clinic were successful at fighting multiple myeloma (bone marrow cancer) in patients. The virus attacked cancerous blood cells called plasma cells in bone marrow. These cancer cells began to clump together and burst open. The virus also stimulated an immune response which helped to destroy other infected cancer cells.

By studying the mechanisms behind measles virus infection, researchers from the University of Texas Medical Branch and the Mayo Clinic have identified two proteins that help the virus infect cells. One protein helps the virus to attach to the host cell's outer membrane and the other helps the viral envelope to fuse with the cell membrane. Using computer-based molecular modeling, the researchers discovered that the measles virus attachment protein heads cause a twisting motion that allows the virus to infect a cell. This discovery could be used to manipulate the measles virus so that it can infect different types of cancer cells.

"Possibly using the https://en.wikipedia.org/wiki/Human_cytomegalovirus , that seems to be used by the ASPS to begin or utilize to metastasis , could be a possible beginning to investigate for a theroputic delivery of a med to induce destruction on the tumors that are in our loved ones systems ,
systemically ?"


http://www.ncbi.nlm.nih.gov/m/pubmed/26990748/

Which Johannes so gracefully informed us of_

http://cureasps.org/forum/viewtopic.php ... 1232#p9225

Love
Debbie

[D.ap]

My limited understanding of viruses includes this article of a viruse(s )as it (they) can be asymtomic, as ASPS is , and why it becomes so serious for the patient who can house the primary tumor for 2 to 20 years and show no systoms til a twinge of pain causes patient to ask for investigation.
Stage 4 dx

https://en.wikipedia.org/wiki/Virus_latency

[D.ap]

So viruse to metastasis?

https://en.wikipedia.org/wiki/Metastasis

Sure would like to see an answer folks

Night and prayers to all

Love,
Debbie

[D.ap]

Innate Immune Defense Defines Susceptibility of Sarcoma Cells to Measles Vaccine Virus-Based Oncolysis


ABSTRACT

The oncolytic potential of measles vaccine virus (MeV) has been demonstrated in several tumor entities. Here, we investigated the susceptibility of eight sarcoma cell lines to MeV-mediated oncolysis and found five to be susceptible, whereas three proved to be resistant. In the MeV-resistant cell lines, we often observed an inhibition of viral replication along with a strong upregulation of the intracellular virus-sensing molecule RIG-I and of the interferon (IFN)-stimulated gene IFIT1. Not only expression of IFIT1 but also phosphorylation of IFN-stimulated Stat1 took place rapidly and were found to be persistent over time. In contrast, susceptible cell lines showed a much weaker, delayed, or completely missing expression of IFIT1 as well as a delayed or only transient phosphorylation of Stat1, whereas exogenic stimulation with beta interferon (IFN-β) resulted in a comparable profound activation of Stat1 and expression of IFIT1 in all cell lines. Pretreatment with IFN-β rendered three of the susceptible cell lines more resistant to MeV-mediated oncolysis. These data suggest that differences in the innate immune defense often account for different degrees of susceptibility of sarcoma cell lines to MeV-mediated oncolysis. From a therapeutic perspective, we were able to overcome resistance to MeV by increasing the multiplicity of infection (MOI) and by addition of the prodrug 5-fluorocytosine (FC), thereby exploiting the suicide gene function of virotherapeutic vector MeV-SCD armed with the SCD fusion protein, which consists of yeast cytosine deaminase and yeast uracil phosphoribosyltransferase




https://jvi.asm.org/content/87/6/3484

[D.ap]

“Every day we are alive, humans encounter potentially harmful disease causing organisms, or “pathogens”, like bacteria or viruses. Yet most of us are still able to function properly and live life without constantly being sick. That’s because the human body requires a multilayered immune system to keep it running smoothly. The two main classes of the immune system are the innate immune system and the adaptive immune system, or “acquired immunity”. In this article, we’ll discuss the first line of defense: the innate immune system.”


https://www.khanacademy.org/test-prep/m ... e-immunity