D, the same primary breast
cancer cells infected with KLF4 or control lentivirus were cultured in low - attachment plates and the number of mammospheres was counted after 10 days.
That was the first report of such contagious
cancer cells infecting a new species.
Not exact matches
An analysis of the HPV16 genome from 5,570 human
cell and tissue samples revealed that the virus actually consists of thousands of unique genomes, such that
infected women living in the same region often have different HPV16 sequences and variable risks to
cancer.
These don't normally integrate into the genome of
cells that they
infect and therefore present little risk of
cancer.
To address this gap in knowledge, Mirabello and Schiffman teamed up with co-senior author Robert Burk of Albert Einstein College of Medicine to sequence the whole genomes of 5,570 HPV16 -
infected cell and tissue samples from women around the world and to identify associations between HPV16 genetic variants and the risk of cervical precancer and
cancer.
They lack the ability to
infect cancer cells and therefore can not inject the genetic blueprints for the therapeutic molecules to fight the disease.
But this ability to
infect brain stem
cells may prove useful for fighting deadly brain
cancers, many of which are caused by mutated stem
cells.
Developed by Amgen, it uses a modified version of the herpes virus that can't
infect healthy tissue but attacks
cancer cells.
The scientists identified several, including the investigational
cancer drug BEZ235, which blocked a key metabolic pathway in flu -
infected human lung epithelial
cells.
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.
The second challenge to researching viral therapies for childhood
cancers is the fact that mouse
cells don't get
infected with human viruses as easily as human
cells.
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.
Epigenetic therapies are thought to work in two ways to fix these errors in
cancer cells — by correcting the «position» of the gene switches and by making the
cell appear as though it's
infected by a virus, triggering the immune system.
Many clinical trials combine virotherapy with chemotherapy or other immunosuppressive agents to try to allow the virus to survive and
infect as many
cancer cells as possible.
But
infected cells can reach such high numbers that the progression to
cancer is not terminated by the many mutations that kill the
cells or make them nonfunctional.
He is using the virus to cure a rare form of blood
cancer called EBV lymphoma, caused when B lymphocyte immune
cells get
infected with the Epstein - Barr virus (EBV).
The company says the reovirus selectively
infects cancer cells over healthy ones because once a
cell turns malignant it stops making an antiviral factor called protein kinase R.
Next, T
cells — the immune system's foot soldiers — are harvested from the patient's blood and
infected with the virus, which rewrites their genetic code to recognize and destroy
cancer cells.
«They are paralyzed and don't have the fire - power to destroy
cancer or virally -
infected cells.
These
cells are highly specialized guardians of the immune system and their role is to kill
cells infected by a virus, damaged
cells, or
cancer cells.
«How the virus
infects and replicates has a direct influence on how the
cell becomes a
cancer cell,» Gao said, adding that you can not cure
cancer without some kind of roadmap.
But while researchers have previously been able to
infect cultures of human hepatocytes with HBV, the
cells» limited lifespan has made it difficult to study the virus, says Bhatia, who is also a Howard Hughes Medical Institute investigator and a member of MIT's Koch Institute for Integrative
Cancer Research and Institute for Medical Engineering and Science.
«
Infected Tasmanian devils reveal how
cancer cells evolve in response to humans.»
«In people chronically
infected with hepatitis B or C, human papillomaviruses or other viruses known to cause
cancer, radioimmunotherapy could potentially eliminate virus -
infected cells before they're able to transform into
cancer cells.»
In a letter published in the
cancer journal Annals of Oncology, researchers led by Professor Jean - Philippe Spano, head of the medical oncology department at Pitie - Salpetriere Hospital AP - HP in Paris, France, report that while treating an HIV -
infected lung
cancer patient with the
cancer drug nivolumab, they observed a «drastic and persistent decrease» in the reservoirs of
cells in the body where the human immunodeficiency virus (HIV) is able to hide away from attack by anti-retroviral therapy.
«New research helps explain why a deadly blood
cancer often affects children with malaria: Immune responses to malaria -
infected red blood
cells appear to sometimes lead to
cancer - promoting changes.»
First, the viruses
infect and kill
cancer cells.
Doctors in France have found the first evidence that a
cancer drug may be able to eradicate HIV -
infected cells in humans.
Viral agents then burst out of the stem
cells,
infecting the
cancer tissue — but leaving healthy brain tissue alone.
Both strains spread through the tumors,
infecting and killing the
cancer stem
cells while largely avoiding other tumor
cells.
Genome studies show that several such viruses, including one that
infects mouse mammary
cells and has been linked to
cancer, have something in common — a sequence of DNA similar to that found in immune system
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.
But the barrier also prevents treatments — like
cancer drugs — from reaching
infected cells, limiting options for patients.
«It gives credence to the concept that like
cancer cells, HIV -
infected cells can be targeted and eliminated by a drug.»
«Since MCR works by targeting specific DNA sequences, in cases where diseased
cells have altered DNA as in HIV -
infected individuals or some types of
cancer, MCR - based methods should be able to distinguish diseased from healthy
cells and then be used to selectively either destroy or modify the diseased
cells.»
C, primary breast
cancer cells isolated from patients with advanced
cancer were directly
infected with KLF4 or control lentivirus, and the CSC population (CD24 − CD44 + ESA +) was measured by FACS after culturing the
cells for 72 hours in low - attachment plates.
CTLs can destroy
cancer cells and
cells infected with viruses, fungi, or certain bacteria.
In addition, consistent with past studies, AAV2 -
infected cancer cells produced more Ki - 67, an immunity system activating protein and c - Myc, a protein that helps both to increase
cell growth and induce apoptosis.
The body, in return, produces an immune response that attacks virally
infected cervical
cancer cells.
It's not a germ that
infects them but a sickening
cell — a
cancer cell — from a member of their own species.
One of its key
cells is known as the Natural Killer (NK)
cells, which identify and eliminate those
cells that are
infected with viruses or transformed by
cancer.
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.
To sidestep the shortcomings of currently used
cancer models, the Salk team harnessed the power of lentiviral vectors to
infect nondividing as well as dividing
cells and ferry activated oncogenes into a small number of
cells in adult, fully immunocompetent mice.
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.
This protects the normal, healthy
cells from being
infected, while still allowing the virus to work against
cancer cells.
These observations lent additional support for the premise of prostate
cancer tissue contamination by XMRV -
infected LNCaP, and not 22Rv1,
cells.
In 2011, Paprotka, et al. reported that XMRV likely originated through recombination between 2 endogenous murine retroviruses, PreXMRV - 1 and PreXMRV - 2, during in vivo passaging of the human prostate
cancer xenograft CWR - R1, resulting in establishment of the XMRV -
infected 22Rv1
cell line [38].
To prove the hypothesis that an XMRV -
infected cell line had contaminated the prostate
cancer samples in the 2006 Urisman, et al. study, we analyzed available RNA extracts using a novel technique referred to as mitochondrial RNA (mtRNA) profiling.
Natural Killer
cells patrol the body and detect characteristic alterations on the surface of
cancer cells or virus -
infected cells.