Sentences with phrase «as tumor growth»

An inactive rhomboid protease, iRhom2, is normally a short - lived protein that controls a cascade of events involved in wound healing as well as tumor growth.

Not exact matches

As a cancer researcher, do you think the mechanisms of tumor growth are somehow changing to come into line with your perceptions, or is it possible that the process of our learning more about DNA mutations and cell architecture and nutrient exchange and epigenetic effects make it possible for us to inch ever closer to understanding that which is already going on under our noses?

In an article posted on MD Anderson's blog, professor in the Department of Experimental Therapeutics, Dr. Bharat Aggarwal, Ph.D., points out that, «Symptoms common in cancer patients, such as depression, fatigue, neuropathic pain, metastases and tumor growth, are due to inflammation.

Similar to capsaicin, tumor necrosis factor is suspected to both induce and reduce cancer cell growth, and was shown to commit cells to survival when stimulating EGFR transactivation mechanisms, indicating that EGFR could act as a molecular switch determining the antiapoptotic effect of tumor necrosis factor (50).

Radiographs are useful for ruling out abnormalities such as fractures, growth plate irregularities, tumors and infections.

When you are pregnant, you might experience growths on your gums that have a raspberry - like appearance known as «pregnancy tumors.»

«We also confirmed a role in PDAC tumor maintenance as inhibition of PRMT1 in patient - derived mouse models significantly inhibited tumor growth and extended survival,» said Giuliani.

Types 6 and 11 account for about 90 percent of genital warts as well as non-cancerous tumor growths in the respiratory tract.

«Our work strongly supports that cancer stem cells are the main source of growth in these tumors and, as such, should be considered promising targets for treatment,» says Mario Suvà, MD, PhD, of the MGH Department of Pathology, co-senior author of the Nature paper.

Excess expression of the sugar is caused by the same mutation that drives the growth of most DIPG tumors, known as the H3K27M mutation, the team found.

«These changes are often referred to as tumor drivers but these are not the only deviations that impact cancer growth.

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).

Dr. Massagué is particularly interested in the ability of tumor cells to hug blood vessels, as he suspects this behavior may be essential for the survival of metastatic cancer cells not only in the brain but also in other parts of the body where metastatic tumor growth can occur.

These findings also have implications for treatment of cancer and other disorders, such as obesity, in which M2 macrophage cells play a regulatory role in tumor growth and fat deposition.

Researchers found that a combination of drugs — one targeting epidermal growth factor receptor (EGFR) and one targeting tumor necrosis factor (TNF)-- effectively blocks the cancer from using TNF as an escape route.

Kuang is also involved in efforts to model various aspects of tumor growth and management as part of ASU's efforts on cancer research.

Dr. Joaquín Espinosa is enthusiastic about the results of his study, «The constant activation of the Interferon response could explain many aspects of Down syndrome, such as cognitive deficit, stunted growth, increased prevalence of autoimmune disorders, high risk of Alzheimer's disease, and protection against solid tumors.»

Women with the KRAS - variant are also more susceptible to triple - negative breast cancer, tumors whose growth is not fueled by the hormones estrogen and progesterone, or by the presence of a particular genetic mutation known as HER2, which promotes cancer cell growth.

In cancer, these switches inappropriately activate or silence important genes, such as those that regulate cell growth and life cycle, ultimately leading to tumors.

«It's being given to patients as a way of stopping the growth of tumors.

They found that NF - κB, a protein complex known to promote tumor growth, may also have the ability to boost the immune system to eliminate cancerous cells before they harm, as well as promote antitumor responses.

Trebananib (formally known as AMG 386; Amgen) is a first - in - class peptide - Fc fusion protein (or peptibody) that targets angiogenesis (the growth of new blood vessels into cancerous tumors) by inhibiting the binding of both angiopoietin 1 and 2 to the Tie2 receptor.

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.

In particular, drugs that inhibit production of prostaglandin E2 may curb inflammation and tumor growth, while avoiding the cardiovascular side effects of drugs such as Vioxx and the gastrointestinal problems of the earlier class of NSAIDs.

But he found that the lab rats» diets had to be very rich in casein, at least 20 percent, to produce significantly more tumor growth, as opposed to Campbell's results of 10 percent.

Loeb points out that much of the concern over cancer risk is that, as part of standard therapy for advanced prostate cancer, tumor growth is decreased by drugs that drastically reduce rather than increase male hormones.

Some types of innate immune cells, such as natural killer cells, can actually protect against tumor growth.

Because those organoids include stroma, a scaffold of connective tissue essential for tumor growth, they may prove better for studying therapies that target the stroma, such as cancer immunotherapy.

However, if both genes are deleted, tumor growth slows — a phenomenon referred to as a synthetic growth defect.

Inhibition of transcription (blockade of water) on tumor suppressor genes, such as p21, leads to cell transformation (growth of the cactus - like eremophytes instead of normal plants from the drought).

One adaptation to this fortunate reality is that rather than using overall survival (OS) as the measure of a drug's success, many clinical trials now use a kind of midpoint, namely progression - free survival (PFS)-- the time that it takes for a tumor controlled by the trial's medicine to restart its growth.

As a result of their quicker growth, however, many tumors have a high oxygen consumption.

As proof - of - principle of the potential efficacy, Zhang's team grew human ovarian tumors in immunocompromised mice, then injected short - interfering RNAs to block the tumors» growth using RNA interference against FAL1.

By performing a genome - wide screen in breast cancer cells, Dr. Oesterreich and her colleagues identified a gene called HOXC10 as one that the cancer seems to modify to allow continued tumor growth in patients whose cancer becomes resistant to traditional therapies.

If the targeted RNA encodes a tumor suppressor protein, as scientists have found for some, the ultimate effect of the microRNA could be to promote cell — and tumor — growth.

About 20 percent of breast cancer patients have overexpressed growth receptors, known as Her2 + receptors, on the cancer cells, which cause uncontrolled tumor growth.

Joining forces with dermatologists and oncologists from the University Hospital in Zurich and backed by the University Research Priority Program «Translational Cancer Research,» Sommer's team was able to demonstrate that, in melanoma cells, the epigenetic factor EZH2 controls genes that govern tumor growth as well as genes that are important for the formation of metastases.

But in diseases such as breast cancer, the breakdown of this order has been associated with the rapid growth and spread of tumors.

Their study, published in the ACS journal Chemical Research in Toxicology, found that triclosan, as well as another commercial substance called octylphenol, promoted the growth of human breast cancer cells in lab dishes and breast cancer tumors in mice.

The expected outcome, if MYC was the sole driver of the cancer, was tumor growth on the MYC line as well as the paired line.

Researchers from the Vetmeduni Vienna have now discovered that NK cells can switch and promote tumor growth, with STAT5 acting as the key regulator.

They confirmed this by showing that tumor growth was reduced in mice treated with an antibody drug that targets TIM - 3 and the chemotherapy agent paclitaxel, as compared to treatment with paclitaxel alone.

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.

Blood vessel development is critical for the growth of any solid tumor, such as breast, colon or lung cancer.

But a new study published April 12 in The Journal of Clinical Investigation shows that stress hormones, such as adrenaline, can directly support tumor growth and spread.

As detailed in a recent study by Dr. Margulis in The Journal of Urology, «Patients with the disease who undergo surgery have a mortality rate that can be as high as 10 percent, depending on the location of the tumor and its growth into the venous systeAs detailed in a recent study by Dr. Margulis in The Journal of Urology, «Patients with the disease who undergo surgery have a mortality rate that can be as high as 10 percent, depending on the location of the tumor and its growth into the venous systeas high as 10 percent, depending on the location of the tumor and its growth into the venous systeas 10 percent, depending on the location of the tumor and its growth into the venous system.

«Thus, we have proven that Tie2 on pericytes serves as a growth brake for vessels and, hence, also for tumors,» said Laura Milde, who is one of the first authors of the publication.

«The fact that turning off Tie2 in pericytes accelerates tumor growth so much came as a real surprise to us.»

«Proof - of - principle» for synthetic biologists opens doors to myriad applications — such as monitoring the environment or the growth of tumors

At the same time, other switches get flipped throughout the body, modifying everything from metabolism to cell growth, via other cytokines, such as IL - 6 and tumor necrosis factor — a, and things like CRP, which mark bacteria for destruction.