Sentences with phrase «with tumor proteins»

The technology, developed by MIT professor and Howard Hughes Medical Institute investigator Sangeeta Bhatia, relies on nanoparticles that interact with tumor proteins called proteases, each of which can trigger release of hundreds of biomarkers that are then easily detectable in a patient's urine.

Not exact matches

And so early efforts centered on making sure the gas tank was filled — priming the immune system with cytokines (such as the interleukins) or with immune - signaling proteins like interferon to rev up the tumor - fighting response.

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 cancer.

According to one study, however, cysteine supplementation with whey protein actually lowered levels of glutathione in some tumors, making them more susceptible to chemotherapy.

Both TRPV1 / WT and KO mice treated with capsaicin and TPA together exhibited higher COX - 2 protein levels than groups treated with TPA alone (Fig. 2A), and tumors from TRPV1 / KO mice expressed the highest level of COX - 2 as a result of treatment with capsaicin and TPA together (Fig. 2A).

Unfortunately, the high background of normal proteins, along with the presence of circulating phosphatases and other degradation enzymes, consistently stump researchers searching for these rare tumor biomarkers.

«The minimum sample volume required is only 1 µL for analysis of 92 proteins, which has been proven to be a great advantage for applications with limited sample volumes, such as pediatric applications, fine - needle biopsies, and tumor microbiopsies,» he says.

To confirm this synergistic effect, the team measured serum levels of signaling proteins in tumor - bearing mice receiving OX40 agonist antibodies alone or in combination with GSK2636771.

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.

«Considering that PDPN is associated with poor prognosis in GBM, CAR T - cell therapy that targets this protein is promising for treatment of patients with relapsed or resistant tumors following first - line chemotherapy,» says Toshihiko Wakabayashi, a coauthor and the chair of Department of Neurosurgery Nagoya University School of Medicine.

That suggests that patient ATC biopsies should be examined before an HDAC inhibitor is used with chemotherapy to see whether p21 or BIM protein are being produced in the tumor during treatment, Dr. Smallridge says.

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.

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.

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.

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 collaboration with the University of Texas Southwestern Medical Center (UTSW) in Dallas, the researchers found that the tumor - suppressive activity of geranylgeraniol was accompanied by down - regulation of HMG CoA reductase, a key enzyme in the mevalonate pathway that provides essential intermediates for the posttranslational modification of growth - related proteins such as Ras, nuclear lamins and insulin - like growth factor receptors.

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.

«The treatment of multiple myeloma has improved significantly in recent years with the introduction of therapies such as proteasome inhibitors [which interfere with tumor cells» protein - disposal system] and potent immuno - modulatory agents,» said the paper's senior author and lead investigator, Paul Richardson, MD, clinical program leader and director of clinical research at Dana - Farber's Jerome Lipper Multiple Myeloma Center, and the R.J. Corman professor at Harvard Medical School.

«Shifting protein networks in breast cancer may alter gene function: Changes in gene function in tumor samples correlate with patient survival.»

That's the nodule type of tumor we saw in the mice with the silenced protein,» said Douglas Kniss, professor of obstetrics and gynecology at Ohio State's Wexner Medical Center and senior author of the study.

«The finding that certain cell signaling lipids change the activity of an oncogenic Ras protein, suggests that we might be able to interfere with tumor progression by inhibiting the enzymes which make the specific cell signaling lipid in cells,» Buck said.

Their results demonstrate that specific rhoptry and dense granule effector proteins that T. gondii secretes before and after host cell invasion, respectively, control the development of an effective host antitumor response, and increase the survival of mice with ovarian tumors.

The researchers hope that a better understanding of how Ras proteins cluster together and interact with other proteins in cells will bring them one step closer to developing therapeutic targets for Ras - driven tumors.

«Understanding the molecular mechanism that leads to CD8 T cell exhaustion brings us a step closer to developing strategies to induce optimal T cell responses that can successfully clear infections and kill tumor cells,» explains postdoctoral researcher and co-lead author Renata M. Pereira, Ph.D. «Conversely, it may allow us to interfere with autoimmune responses that paradoxically depend on the same protein.»

Researchers found that patients with a higher amount or higher proportion of an inflammatory protein called type 1 interferon beta compared with another inflammatory protein, type 1 interferon alpha, do not respond as well to tumor necrosis factor inhibitors as others.

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.

But mutations, which are found in 96 percent of patients with high - grade serous ovarian tumors, can cause p53 to form clumps, or «aggregates,» which impair the protein's normal function.

Results showed that tumor cells containing the protein carried anywhere from 10 to 17 times fewer breast stem cells, and tumors grown from the injected cells were about three times smaller than those in mice who had received tumor cells with depleted levels of HOXA5.

Filled with tumor - specific proteins and implanted under the skin, the porous plastic disk David Mooney developed reprograms the body's immune system to attack tumors.

Monje's team identified a specific protein, called neuroligin - 3, which is largely responsible for the increase in tumor growth associated with neuronal activity in the cerebral cortex.

Similarly, patients with tumors containing low amounts of HOXA5 protein also had lower cancer relapse - free survival rates.

The scientists also found consistent evidence of increased pro-inflammatory markers, such as C - reactive protein and tumor necrosis factor alpha, associated with PTSD.

This was used in combination with another adenovirus vector carrying an immune stimulatory protein, cytokine, to recruit immune cells into the tumor.

To confirm that the missing mutations were important for generating an immune response, the researchers cultured a subset of the neoantigen protein fragments containing the tumor mutations with immune cells taken from three patients» blood samples.

The tumor becomes differentiated, its cells now cyst - like and filled with fluid that contains, among other things, milk proteins.

Studying mice with breast tumors transplanted from patients, researchers at Washington University School of Medicine in St. Louis, The Broad Institute of MIT and Harvard, and Baylor College of Medicine have analyzed the proteins present in these tumors.

Inflammation is a known feature of heart failure, and it is associated with high levels of inflammatory proteins called cytokines — including one called tumor necrosis factor alpha or TNF - a — that ramp up immune cell responses.

When researchers at Johns Hopkins University in Baltimore, Maryland, examined tumor tissue from the original man with colon cancer who responded to a PD - 1 inhibitor, they found a clue: His tumor had mutations in «mismatch repair» genes, so - called because their encoded proteins fix errors in DNA bases when cells replicate their DNA.

Now, a new approach that tailors a personalized vaccine to the mutated proteins in an individual's tumor appears to have prevented early relapses in 12 people with skin cancer.

VIC - 008 is a fusion protein combining an immune - activating protein from the tuberculosis bacteria with a small antibody fragment targeting mesothelin, a protein expressed in several types of tumor — including mesothelioma, pancreatic and ovarian cancer.

Analysis of genomic, epigenetic, and RNA sequencing data revealed that the combinations of mutations that lowered the levels of functioning BRCA1 and BRCA2 RNA — genes that produce the breast cancer tumor suppressor proteins — were associated with significantly better survival outcomes.

When there is a mutation in one or both of the PTEN genes, it interferes with the protein's enzymatic activity and, as a result inhibits its tumor suppressing ability.

Comparing proteins within the microvesicles with the originating tumors showed that the vesicles also accurately reveal the protein content of the tumors, providing still more information about how tumors might respond to specific therapies, the researchers report.

The researchers designed a modification in the chemistry of the ProCA32 MRI contrast agent so detectable metals form a bond with calcium molecules on proteins specific to liver tumor tissue.

By analyzing a dataset of human immune cells stimulated with interferon — a signaling protein created in response to pathogens or tumor cells — the team could precisely identify which genes were switched on in each of 13 responding cell types.

In the sensitive tumor models, the ability of anti — cytotoxic T lymphocyte — associated protein 4 or anti — programmed cell death 1 therapy to increase vessel perfusion strongly correlated with its antitumor efficacy.

«This model, when combined with a rare genetic disease, revealed for the first time how a protein known to prevent tumor growth in most cases, p53, may instead drive bone cancer when genetic changes cause too much of it to be made in the wrong place.»