Sentences with phrase «of tumor activity»

By contrast, a signal of tumor activity increased sixty-fold in mice treated with the widely used chemotherapy drug gemcitabine.

Not exact matches

The stock popped 55 percent Thursday after management announced a «breakthrough» discovery of a molecule capable of shutting down tumor activity and treating cancer.

Goji's are reported to have anti-aging properties and show anti-tumor activities against various types of skin cancer cells by inhibiting tumor growth and inducing apoptosis.

By comparing the results to cells from paired normal tissue, researchers get a detailed molecular picture of the tumor environment, including the types and activity levels of T cells that are critical to the immunotherapy response.

In this special section of Science, expert contributors retrace the long and tortuous path leading to the mapping and identification of the BRCA1 gene; discuss the ways in which BRCA mutation status has been integrated into the clinical management of patients in high - risk families; and highlight the role of the BRCA proteins in preserving the structural and numerical integrity of chromosomes throughout the cell cycle, a function that may explain their tumor suppressor activity.

The tumor - derived peptide is identical in biological activity and similar in physiochemical properties to the still uncharacterized growth hormone - releasing factor present in extracts of hypothalamic tissues.

«These results also provide a rationale to explore the clinical activity of an OX40 agonist antibody in combination with GSK2636771 in cancer patients with PTEN loss tumors.»

They are working together to mesh her identification of compounds that target tumors with runaway Ras activity and tumor data (analyzed by machine learning) to find patients who could benefit from these potential cancer drugs.

A 44 amino acid peptide with growth hormone - releasing activity has been isolated from a human tumor of the pancreas that had caused acromegaly.

The activity of four transcription factors — proteins that regulate the expression of other genes — appears to distinguish the small proportion of glioblastoma cells responsible for the aggressiveness and treatment resistance of the deadly brain tumor.

For this study, Guttridge, first author David J. Wang, who developed many of the study's concepts, and their colleagues monitored NF - kB activity during tumor development using mouse embryonic fibroblasts and two mouse models.

So scientists choose the lymphocytes with the greatest tumor - fighting activity, grow a large population of them in the lab, then infuse them back into the patient.

When researchers screened a library of more than 200 drugs and related compounds for activity against embryonal subtype tumor cells from three patients, the most promising results involved drugs that increased oxidative stress in tumor cells.

The Leuven - based VIB researchers have revealed a mechanism that explains why the anti-tumor activity of specific immune cells called macrophages is suppressed during tumor growth.

However, tumors produce high amounts of a protein called Transforming Growth Factor - Beta (TGF - β) that suppresses the activity of NK cells.

Nearly one - third of the tumors exhibited high levels of Lin28 activity.

They report that the test can detect significant drops in the metabolic activity levels of all three types of tumors within 72 hours when exposed to an effective drug whereas tumors that were resistant to a drug show no change.

The protein sits on the surface of T cells and helps dampen the activity of the cells after an immune response, but tumors have found ways to hide from T cell attack by flipping on the PD - 1 switch themselves.

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 researchers further found that miR - 486 is itself regulated by the tumor - suppressor gene p53, the most frequently altered gene in human cancers, and that activity of miR - 486 is partially dependent upon functional p53.

«Interestingly, we found that activity of pembrolizumab was seen in both PD - L1 - positive and - negative tumors.

«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.

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 cancer.

For most available T cell immunotherapies, T cells (which play a central role in defending the body against illness) are engineered to recognize and eliminate tumors, but their activity is not specifically controlled, leading to toxicity and unwanted side effects in patients as a result of inflammation or in some cases suboptimal response to treatment.

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.

These studies showed that inhibiting the activity of the signaling protein MEK was essential for these tumors to grow.

More activity of the neuroligin - 3 gene in high - grade gliomas was linked to shorter survival among patients with these tumors.

Investigating how organs far from tumors contribute to cancer progression should lead us to ways of manipulating those systemic activities in therapy.

The converse action — increasing the activity of the microRNAs — could reduce tumors.

Crews noted that RNA splicing - targeted agents have been shown to have activity in a variety of solid tumors so the findings may be relevant to a variety of cancers, such as breast and drug - resistant melanoma.

Both the number and activity of osteoblasts — cells that produce and reshape bone tissue — were increased within the bone marrow of mice with lung tumors compared with cancer - free animals; and reducing the number of osteoblasts in mice not only limited neutrophil infiltration of tumors but also interrupted tumor progression.

Deadly brain tumors called high - grade gliomas grow with the help of nerve activity in the cerebral cortex, according to a new study by researchers at the Stanford University School of Medicine.

A better approach, Monje said, would be to develop drugs that specifically block the tumor - stimulating activities of neuroligin - 3, such as a drug that stops the protein from being secreted into the area around the cancer cells.

This method measures the activity of protein - cutting enzymes called endoproteases, which are made by tumors to help recruit blood vessels and invade surrounding tissues so the cancer can grow and spread.

Images taken with a fluorescent microscope show the activity of a kinase (green) in tumor cells (bottom) compared to normal cells (top).

The two most widely used drugs to treat colorectal cancer act to either inhibit enzyme activity of cancer cells or arrest tumor cell growth.

A new study shows coibamide A has potent anti-cancer activity in mice and cell cultures that model brain tumors and triple negative breast cancer, two of the most aggressive and difficult - to - treat types of cancer.

These new findings suggest that a drug that brings well - being gene activities further down could significantly boost the killer activity of Myc in tumor cells.»

«We found polyploidy in liver cells did not strongly affect the activity of some oncogenes, but it did protect against the loss of tumor suppressor genes.

«When we compared the gene signature activity of glioblastoma cells from around 60 patients we found that a large number of patients could be divided into subgroups that showed a correlation between gene activity, tumor cell characteristics and cell of origin similar to the one we had seen in the mouse study.

McDonnell said is lab is continuing the research, including finding ways to induce cells to eject cholesterol, reverse the inhibition of CYP27A1 activity, or introduce compounds that interfere with cholesterol - production in the tumor.

This approach resulted in the persistent clonal repopulation of T cells in those cancer patients, with the transferred cells proliferating in vivo, displaying functional activity, and trafficking to tumor sites.

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.

Recently, researchers led by Pier Paolo Pandolfi at Harvard Medical School found that PTEN's tumor suppressing activity becomes elevated when two copies of the protein bind together, forming a dimeric protein.

The researchers had previously built a mathematical model that simulates the activity of a blood - vessel - growth - promoting protein called VEGF in a mouse tumor.

The activation of this signaling pathway progressively increased in different types of gliomas, with the highest activity seen in patients with glioblastoma, a particularly difficult - to - treat form of brain cancer that represents approximately 15 percent of all brain tumors.

Hashimoto et al.'s data suggest that future efforts might focus on breast cancer patients whose tumors express high levels of Arf6 signaling proteins, and which could therefore be susceptible to drugs that reduce the activity of Rab11b.

Tumor cells metastasized to bone modify the activity of these cells and, depending on the type of cancer, cause osteoblastic or osteolytic changes.

In a series of studies led by Dr. Arun Sharma, associate professor of pharmacology and Dr. Shantu Amin, professor of pharmacology, both of Penn State College of Medicine, researchers designed and synthesized a compound called napthalamide - isoselenocyanate — NISC - 6 — to inhibit both the Akt1 pathway and human topoisomerase IIα — topo IIα — activity, which contribute to melanoma tumor growth.

Of note, several proteins involved in the tumor necrosis factor, or TNF, pathway increased in activity during the induction and execution phases.