Not exact matches
Kite Pharma, one of the companies chasing a new generation of cancer drugs called chimeric antigen
receptor T -
cell (CAR - T) therapies, announced a patient
death in a clinical trial of its experimental KTE - C19.
For some years now, a new class of drugs called antibody - drug conjugates (ADCs) have been used, which work in two ways: they consist of an antibody that binds selectively to the tumor
cell receptor and interrupts the signal to propagate; they also act as a transport vehicle for a chemical substance that enters the cancer
cells with the antibody and triggers their
death.
IGFBP3 binds to a
receptor protein on colonic stem
cells causing their
death and, in turn, damaging the intestinal lining.»
Akassoglou and her colleagues thought they had a good candidate in the gene for the p75 neurotrophin
receptor (p75NTR), a regulator of
cell death in the brain that also switches on soon after liver injuries.
PD - 1 (programmed
cell death protein 1) is a
receptor on the surface of T
cells (the white blood
cells that are part of the immune system), while PD - L1 (programmed
death - ligand 1) is a molecule that binds to PD - 1 and is often over-expressed on the surface of cancer
cells, enabling them to evade the immune system and allow cancer to grow and spread.
The Max Planck researchers then showed that less necroptosis of endothelial
cells and less metastasis occur in genetically modified animals in which
Death Receptor 6 is disabled.
The scientists also found that endothelial
cells themselves give the signal for their own
death: To do this, the vascular wall cells have a receptor molecule called Death Receptor 6 (DR6) on their sur
death: To do this, the vascular wall
cells have a
receptor molecule called Death Receptor 6 (DR6) on their
receptor molecule called
Death Receptor 6 (DR6) on their sur
Death Receptor 6 (DR6) on their
Receptor 6 (DR6) on their surface.
Under normal circumstances,
cells must have some way of preventing the
death domains of neighbouring
receptors from coming together.
In the process, the plasma membrane
receptor Fas (CD95) is key; this
cell receptor occurs in almost all human
cells and is involved in programmed
cell death (apoptosis).
But the Israeli researchers have shown that the
receptors can trigger
cell death simply by binding to one another.
Across multiple triple - negative breast cancer subtypes, inhibiting the androgen
receptor greatly increased apoptosis (programmed
cell death), inhibited growth and increased necrosis by 60 percent in animal models.
Syndax Pharmaceuticals, Inc. («Syndax,» the «Company» or «we»)(Nasdaq: SNDX), a clinical stage biopharmaceutical company developing entinostat and SNDX - 6352 in multiple cancer indications, in collaboration with The Wistar Institute and Indiana University Melvin and Bren Simon Cancer Center, today announced the publication of a preclinical report demonstrating that entinostat, Syndax's oral, Class - I histone deacetylase inhibitor, enhances the antitumor effect of PD - 1 (programmed
death receptor - 1) blockade through the inhibition of myeloid derived suppressor
cells (MDSCs).
HIPK2 - Mediated Transcriptional Control of NMDA
Receptor Subunit Expression Regulates Neuronal Survival and
Cell Death
In cancer
cells, IL - 13 binds to the
receptor IL13Rα2 and, through a series of steps, prevents cancer
cells from undergoing normal
cell death.
To devise a potential new therapy, the investigators engineered a population of neural stem
cells to express a potent version of a gene called TRAIL, which codes for a molecule that activates
cell -
death - inducing
receptors found only on the surface of cancer
cells.
PHILADELPHIA --(July 11, 2017)-- Researchers at The Wistar Institute, an international leader in biomedical research in the fields of cancer, immunology and infectious diseases, with collaborators at Indiana University Melvin and Bren Simon Cancer Center and Syndax Pharmaceuticals, Inc., (Nasdaq: SNDX) announce the results of a preclinical study demonstrating that entinostat, Syndax's oral, Class - I histone deacetylase inhibitor, enhances the antitumor effect of PD - 1 (programmed
death receptor - 1) blockade through the inhibition of myeloid derived suppressor
cells (MDSCs).
As an initial focus, researchers at Chicago will search for novel ways to take advantage of steroid hormones and their
receptors to detect metastases, define their boundaries and deliver treatments directly to tumor
cells in order to inhibit
cell division or promote
cell death.
Cardiac thromboxane A2
receptor activation does not directly induce cardiomyocyte hypertrophy but does cause
cell death that is prevented with gentamicin and 2 - APB.
In prostate cancer
cells the STAT3 - androgen
receptor (AR) axis was inhibited by niclosamide and
cell death in NSCLC was effected via c - JUN stress kinase and generation of ROS [39, 40].
Cell - surface galectin - 3 confers resistance to TRAIL by impeding trafficking of
death receptors in metastatic colon adenocarcinoma
cells.
The rationale for using CT - 011, an immunotherapy antibody that blocks the programmed
death (PD)-1
receptor, is to boost the function of the immune system by inhibiting PD - 1 whose function, in part, is to inhibit T -
cell response.
Glial
cell line - derived neurotrophic factor (GDNF) was selected based on clear evidence that it increases neuronal sprouting, prevents
cell death [20], [21] and has neuroprotective effects in the brain [11], [22]--[24], spinal cord [12] and retina [25]--[30], and because
receptors for GDNF are expressed within mature retina [26], [31]--[34].
The Lauffenburger research group focuses on elucidating important aspects of
receptor - mediated regulation of mammalian blood and tissue
cell behavioral functions such as proliferation, adhesion, migration, differentiation, and
death.
Response of Varicella Zoster specific T
cells to Programmed
Death Receptor - 1 blockade.
The halogens bromide, chloride, and fluoride compete with iodine for the
receptor binding sites in the thyroid, but instead of activating the
receptors they build up in thyroid tissue and cause thyroid
cell death and inflammation.
The study found that curcumin is able to induce apoptosis (normal programmed
cell death) in the most resistant breast cancer
cells that lack estrogen
receptors.