Not exact matches
Immunotherapy differs from more traditional
cancer treatments, such as surgery (cutting malignant cells out of the body), chemotherapy and radiation (poisoning the deadly mutants), and even the newer, more precise molecular drugs that attempt to jam the
protein signals that tell
tumor cells to keep dividing and conquering.
Chicago, GenomeWeb — A new study by researchers from Memorial Sloan Kettering
Cancer Center has demonstrated the predictive power of an AR - V7 protein expression test using Epic Sciences» non-EPCAM-based circulating tumor cell detection platform, which could help guide treatment decisions for men with metastatic castration - resistant prostate c
Cancer Center has demonstrated the predictive power of an AR - V7
protein expression test using Epic Sciences» non-EPCAM-based circulating
tumor cell detection platform, which could help guide treatment decisions for men with metastatic castration - resistant prostate
cancercancer.
One of his many discoveries was that casein, the
protein found in milk products, promotes
cancer tumor growth.
Even before treatment,
cancer patients in the study had a small number of infection - and
tumor - fighting T cells that target these unusual
proteins, the researchers found.
Recent advances in the understanding of
cancer have led to more personalized therapies, such as drugs that target particular
proteins and tests that analyze gene expression patterns in
tumors to predict a patient's response to therapy.
Another possible application for the new machine is generating peptides that could be used as personalized
cancer vaccines targeting unique
proteins found in individual patients»
tumors.
Conventional, high - dose chemotherapy treatments can cause the fibroblast cells surrounding
tumors to secrete
proteins that promote the
tumors» recurrence in more aggressive forms, researchers at Taipei Medical University and the National Institute of
Cancer Research in Taiwan and University of California, San Francisco, have discovered.
In demonstrating that FOXO4 works to prevent the spread of cancerous
tumors by binding to and inhibiting the
protein RUNX2, the team identified a circuit that controls metastatic progression in prostate
cancer.
Nagoya University - led research team shows in mice the potential of a special immune cell that targets a key
protein in
tumor growth that helps stop brain
cancer.
About 15 to 20 % of breast
cancers are classified as «triple negative,» so called because these
tumors do not express three key
proteins that are biomarkers and / or drug targets for breast
cancer: the estrogen receptor, the progesterone receptor, and HER2 (a member of the epidermal growth factor receptor family).
Researchers at the Bellvitge Biomedical Research Institute of Bellvitge, the Catalan Institute of Oncology and the University Hospital of Bellvitge have participated in an international study published in the journal
Cancer Cell that describes how exosomes secreted by
tumor cells contain
protein and microRNA molecules capable of transform neighboring cells into tumoral cells promoting
tumor growth.
Instead of displaying the full complement of incriminating
proteins on the
tumor cell's surface, the dog
cancer displays just a few, obfuscating the invasion underway.
Along with finding that the
tumor suppressor
protein SIRT6 is inactive in around 30 percent of cases of pancreatic ductal adenocarcinoma (PDAC), the team identified the precise pathway by which SIRT6 suppresses PDAC development, a mechanism different from the way it suppresses colorectal
cancer.
The approach is already routine for some
cancer patients, such as women and men with breast
cancer tumors that have high levels of a
protein called HER2, or lung
cancer tumors with mutations in the EGFR gene.
Moderna is also doing animal safety tests of a personalized
cancer vaccine that would code for immune - activating
proteins unique to a person's
cancer cells, based on genetic sequencing of their
tumor.
PTEN prevents
tumor cells from growing uncontrollably, and mutations in the gene encoding this
protein are commonly found in many different types of
cancer.
An analysis of ZMYND11 levels in the
tumors of 120 triple - negative breast
cancer patients showed that those with high levels of the
protein had an 80 percent probability of surviving for 10 years while those with low levels had a 50 percent probability.
In a study published in the journal Nature Medicine, the researchers reported that the
tumor - suppressing
protein AIM2, or Absent in Melanoma 2, helps prevent colon
cancer by restricting a signaling molecule called Akt.
UC San Francisco researchers have found a way to knock down
cancers caused by a
tumor - driving
protein called «myc,» paving the way for patients with myc - driven
cancers to enroll in clinical trials for experimental treatments.
But mutated or dysfunctional Rb is associated with several major
cancers and Cyclin D has long been described as an oncogene that promotes
cancer because it was believed to inactivate the Rb
tumor suppressor function through a process called phosphorylation, which involves phosphate molecules being added to
proteins, essentially turning them on or off.
RNA sequencing of both single and clustered CTCs from breast
cancer patients identified several genes expressed at elevated levels in CTC clusters, one of which — a
protein called plakoglobin — also was overexpressed in the primary
tumors of patients with reduced survival.
«These findings reveal a unique fulvestrant signaling process involving the increased regulation of hsa - miR - 765 that suppresses the HMGA1
protein as part of the mechanism underlying the
tumor suppressor action in prostate
cancer.
The study, «The nuclear transport receptor Importin - 11 is a
tumor suppressor that maintains PTEN
protein,» which will be published online February 13 in The Journal of Cell Biology, suggests that the loss of Importin - 11 may destabilize PTEN, leading to the development of lung, prostate, and other
cancers.
«
Tumor - suppressing
protein actually promotes
cancer.»
To make the vaccine,
cancer cells are harvested from a
tumor after surgery and stripped of their
proteins; then those
proteins are cultured with dendritic cells, a subclass of white blood cells, drawn from the patient's blood.
In earlier studies involving animal models and human
cancer cell lines, researchers found that breast
cancer spreads when three specific cells are in direct contact: an endothelial cell (a type of cell that lines the blood vessels), a perivascular macrophage (a type of immune cell found near blood vessels), and a
tumor cell that produces high levels of Mena, a
protein that enhances a
cancer cell's ability to spread.
BRCA1 and 2, genes whose
proteins are supposed to work as
tumor suppressors and also repair DNA damage, were the first known risk factor genes for familial breast
cancer as well as ovarian and other
cancers.
For
tumors to grow and spread,
cancer cells must make larger than normal amounts of nucleic acids and
protein, so they can replicate themselves.
The research suggests that a cytokine produced by inflammatory cells near a prostate
tumor induces
cancer cells to decrease production of a
protein that blocks metastasis.
The team of medical and engineering researchers at The Ohio State University previously determined that modifying a single gene to reduce this
protein's level in breast
cancer cells lowered the cells» ability to migrate away from the
tumor site.
«
Cancer overrides the circadian clock to survive: Misfolded
proteins cause disruptions in circadian rhythm that contribute to
tumor growth.»
The study showed that mice implanted with breast
cancer cells lacking the
protein developed small, self - contained
tumors consisting of cells that didn't leave the
tumor.
«Shifting
protein networks in breast
cancer may alter gene function: Changes in gene function in
tumor samples correlate with patient survival.»
But the cells also changed shape and other properties in the absence of the
protein in ways that reduced the likelihood that they would travel away from the
tumor — a sign that myoferlin not only changes genes in
cancer cells, but also alters the cells» mechanical properties.
Tumor cells use the unfolded protein response to alter circadian rhythm, which contributes to more tumor growth, Hollings Cancer Center researchers at the Medical University of South Carolina (MUSC)
Tumor cells use the unfolded
protein response to alter circadian rhythm, which contributes to more
tumor growth, Hollings Cancer Center researchers at the Medical University of South Carolina (MUSC)
tumor growth, Hollings
Cancer Center researchers at the Medical University of South Carolina (MUSC) find.
The study, conducted in mice and including analyses of human
cancers, found very high levels of two
proteins — dectin - 1 and galectin - 9 — in pancreatic
tumors.
Moffitt
Cancer Center, a leader in molecular cancer research, and a research team led by Jia Fang, Ph.D., assistant member of the Tumor Biology Department, has discovered a new way to control the activity of SETDB1, a protein that is often upregulated in c
Cancer Center, a leader in molecular
cancer research, and a research team led by Jia Fang, Ph.D., assistant member of the Tumor Biology Department, has discovered a new way to control the activity of SETDB1, a protein that is often upregulated in c
cancer research, and a research team led by Jia Fang, Ph.D., assistant member of the
Tumor Biology Department, has discovered a new way to control the activity of SETDB1, a
protein that is often upregulated in
cancercancer.
Curious about the possibility of circular RNAs contributing to
cancer, Pandolfi and his colleagues set out to see if they could detect relevant changes in
tumors known to harbor distinct fusion
proteins, which result when different chromosomes abnormally join together, melding two separate genes into a new centaur - like gene.
«Can
protein 14 -3-3 sigma prevent or kill breast
cancer tumors?
Further research could test these
cancer stem cell gene expression at the RNA and
protein level in circulating
tumor cells and biopsies from patients on trial.
A new study led by University of Kentucky researchers suggests that activating the
tumor suppressor p53 in normal cells causes them to secrete Par - 4, another potent
tumor suppressor
protein that induces cell death in
cancer cells.
Cincinnati
Cancer Center (CCC) and UC Cancer Institute researchers have found that a vaccine, targeting tumors that produce a certain protein and receptor responsible for communication between cells and the body's immune system, could initiate the immune response to fight c
Cancer Center (CCC) and UC
Cancer Institute researchers have found that a vaccine, targeting tumors that produce a certain protein and receptor responsible for communication between cells and the body's immune system, could initiate the immune response to fight c
Cancer Institute researchers have found that a vaccine, targeting
tumors that produce a certain
protein and receptor responsible for communication between cells and the body's immune system, could initiate the immune response to fight
cancercancer.
A relatively new biomarker called prostate - specific membrane antigen (PSMA) is the bullseye for three new magnetic resonance imaging (MRI) agents that bind to the
protein in not only prostate
cancer, but a range of
tumor types, according to research unveiled at the 2015 annual meeting of the Society of Nuclear Medicine and Molecular Imaging (SNMMI).
P53 is a
tumor suppressor gene, a
protein that regulates cell growth, and it is the most frequently mutated suppressor gene in
cancer.
The discovery, published in the journal Nature Communications, marks the first time this little - known
protein has been characterized in relation to
cancer development and
tumor growth.
Scientists from the Crick Institute, London and the Hebrew University, Jerusalem, discover a
protein that plays a key role in turning
cancer tumor cells into
cancer stem cells that are able to renew outbreaks of the disease
The
protein seems to help
cancers spread in people too: 50 % of colon
cancer patients with high amounts of L1CAM
protein in their
tumors had the
cancer spread within 5 years of treatment, compared to only 14 % of individuals with low amounts, the researchers reported here 13 December at a meeting of the American Society for Cell Biology.
In humans, a similar
protein complex called CSN and its subunit CSN6 is now believed to be a
cancer - causing gene that impacts activity of another gene (Myc) tied to
tumor growth.
Now, results of a new study by Johns Hopkins Kimmel
Cancer Center scientists suggests a powerful role for the
protein in normal breast cells, acting as a
tumor suppressor that halts abnormal cell growth.
Rather than simply identifying a
cancer by location or tissue type, researchers now use advanced molecular profiling tests to characterize
tumors, the
proteins they express and the novel mutations they develop — known as neoantigens.