JJ Miranda, PhD, reported that certain drugs affect genes in
tumor cells infected with the Epstein - Barr Virus.
Not exact matches
In human
cells and in mice, the virus
infected and killed the stem
cells that become a glioblastoma, an aggressive brain
tumor, but left healthy brain
cells alone.
The immune system depends on molecules called T
cell receptors on the surface of T
cells to recognize and respond to foreign antigens from virus -
infected cells,
tumors and other threats.
The virus, redesigned using sophisticated protein engineering techniques, works: With its shield and its adapter, these viral gene shuttles efficiently
infected tumor cells in laboratory animals.
Researchers led by Andreas Plueckthun, professor at the Department of Biochemistry at the University of Zurich, have now succeeded in rebuilding the viruses so that they effectively recognize and
infect tumor cells.
Although changes in treatment methodology still have to be studied, Dr. Cripe believes it may be that the timing of various treatments is what matters, and that perhaps initially suppressing immunity could allow the virus to
infect a large number of
tumor cells before relieving the immunosuppression to allow the body's own T
cells to fight off the
tumor.
Dr. Cripe and his colleagues at The Ohio State University, the University of Pittsburgh School of Medicine and Cincinnati Children's Hospital Medical Center tested how well the oncolytic viral therapy — a cancer - killing form of the herpes simplex virus, called oHSV —
infected and killed
tumor cells in mice with and without a healthy immune system.
However, some human
tumor cells may also be hard to
infect with viral therapies, Dr. Cripe reasoned, and knowing how
cells respond in those situations could also be important to improving cancer treatments.
Both strains spread through the
tumors,
infecting and killing the cancer stem
cells while largely avoiding other
tumor cells.
Led by Ludwig Lausanne investigator Alexandre Harari and George Coukos, director of the Ludwig Institute for Cancer Research, Lausanne, the study shows that ovarian
tumors harbor highly reactive killer T
cells — which kill
infected and cancerous
cells — and demonstrates how they can be identified and selectively grown for use in personalized,
cell - based immunotherapies.
CSCs were prepared from 231BrM and CN34BrM
cells that were
infected with lentivirus carrying with or without miR -7-2, and they were transplanted into nude mice through intracardiac injection followed by monitoring metastatic
tumor growth in the brain.
The
tumor cells were dissociated and the
cells were
infected with KLF4 lentivirus and cultured in low - attachment plates.
These
cells can find and kill
cells that have viruses
infecting them, and can kill
tumor cells.
Mouse mammary
tumor virus uses mouse but not human transferrin receptor 1 to reach a low pH compartment and
infect cells.
The Pexa - Vec virus was originally developed by Michael Mastrangelo, MD, and Edmund Lattime, PhD, of Thomas Jefferson University in Philadelphia, who engineered the harmless vaccinia virus to
infect only cancer
cells and other rapidly dividing
cells, as well as to stimulate immune activity, in hopes of boosting the immune response to
tumors.
They are important especially for the destruction of
cells infected by a virus or of
tumor cells.
In addition, the CD8 subset primarily function as cytolytic killers for clearing pathogen -
infected cells or for targeting
tumors.
In these experiments, the virus managed to
infect and destroy only a small proportion of
tumor cells directly, the researchers found, but within five days of the initial infection, the rest of the
tumor began to be killed by a powerful immune reaction.
A new UC San Francisco study has shown that a cancer - killing («oncolytic») virus currently in clinical trials may function as a cancer vaccine — in addition to killing some cancer
cells directly, the virus alerts the immune system to the presence of a
tumor, triggering a powerful, widespread immune response that kills cancer
cells far outside the virus -
infected region.
From there they showed that cancer
cells had lost structural polarity, resulting in random distribution of CAR receptors on their surface, thereby allowing the virus to attach to and
infect the
tumor cells.
In a study published in the journal Biochemical and Biophysical Research Communications, a team led by Miranda examined how certain drugs affect genes in EBV -
infected tumor cells.
On the contrary, recent evidence indicates that XMRV is a contaminant originating from the recombination of two mouse endogenous retroviruses during passaging of a prostate
tumor xenograft (CWR22) in mice, generating laboratory - derived
cell lines that are XMRV -
infected.
Effector and target modules together form a novel platform which allows us to engage target
cells (e.g.
tumor cells, virus
infected cells) directly with immune effector
cells.
According to the Federation of American Societies for Experimental Biology, hyperthermia, or the exposure of the body to high temperatures, gives these
cells the ability to destroy virus -
infected cells and
tumor cells.
Basal
cell tumors frequently ulcerate and bleed and the ulcer may become
infected.
M032 kills
tumor cells directly through oncolytic replication and then proceeds to
infect tumor cells in proximity, continuing the process of
tumor destruction.