Sentences with phrase «what is tumor»

Not exact matches

The key to this effort is the ability to detect what's known as circulating tumor DNA, or CTDNA.

Our partner physicians use data and analytics to do exactly what you described, which is to determine the best protocol for patient care — disease and tumor - specific — so they don't over-treat or waste resources.

... What we found is that even though you've found the mutation in the tumor, there's no drug to treat it.»

They go around telling everyone that it looks good, and they're glad they have the tumor, and then just go on living with it, instead of seeing it for what it really is and having it fixed.

So, what was the really awful thing that placed my father out of God's protection and put him in a position of vulnerability where Satan could smite him with a brain tumor?

That's like me saying, «I don't mind my cancerous tumor, it's a natural part of my sacred body and I don't want to go against what nature or a devine being has dealt me.»

June 7, 2013 — The first - known definitive case of a benign bone tumor has been discovered in the rib of a young Neandertal who lived about 120,000 years ago in what is now present - day Croatia.

Think about it, these single gene changes are usually what results in tumor formation, right?

Well, they went back to have the tumor removed & guess what — the tumor was gone.

First hand knowledge of mental illness shows you that ill people have the capacity to live good lives, unfortunately for them they have a mental disease like a tumor invading their brain... what you don't seem to understand is anything is a weapon.

«Each one of these tumors is unique and different, and we never know what we are going to face when we get into the operating room.

I nursed until my son was 26 months, and a cancerous breast tumor is what stopped me from nursing longer.

What's the best way to give it to minimize the number of tumor cells for the longest amount of time?»»

What matters is why the tumor started,» says study coauthor Richard Goldberg, an oncologist at West Virginia University Cancer Institute in Morgantown.

«What is particularly encouraging is that we are now able to select, based on features in the tumor, approximately a quarter of advanced lung cancer patients who can receive immunotherapy as their initial treatment.

His team discovered that treatment - resistant melanoma tumors, in what is akin to drug addiction, develop a dependency on MAPK - targeted therapy to retain their fitness.

The first - known definitive case of a benign bone tumor has been discovered in the rib of a young Neandertal who lived about 120,000 years ago in what is now present - day Croatia.

Since the cancer cells in both types of tumors were the same, the researchers compared the noncancerous cells present in the induced and transplanted tumors to explore what might be causing the T cell apoptosis.

It's also not hard to imagine that what binds you and your friends (and your «Friends») has analogs in ant colonies and beehives, tumor cells and the brain, terrorist groups and spam hosts, the Internet and the electrical power grid.

What we do know is that the disease is associated with psychiatric symptoms, memory lapses, seizures and tumors, among other problems.

But it isn't so often that we take a tumor that's established and eradicate it — and that's what you want in the clinic.»

«I think what's interesting about combining whole genome analysis and histopathology is that we can study the tumor at multiple levels,» said co-author Rakopoulos.

«What we may be looking at,» he adds, «is a future way to prevent metastasis to many organs simultaneously» using drugs that make tumor cells let go of the blood vessels they cling to.

«As a cancer immunotherapist, what gets me really excited is when you take an established tumor and you make it disappear,» said Crystal Mackall, MD, professor of pediatrics and of medicine and the study's other senior author.

«What our findings show is that the problems with iPS cells don't just involve one or two or a few abnormal iPS cells escaping into the body and forming tumors, but that the whole population of cells is screwed up,» Lanza says.

When the Johns Hopkins scientists saw that their nanoparticle - encapsulated version of BPTES shrunk mice tumors by half, Le and her colleagues searched for what major metabolic pathway was driving the growth of the remaining half of the tumor.

Instead, Schlom says, «what we're seeing is increases in patient survival, as opposed to tumor shrinkage.»

«Clearer vision of what's inside a tumor and what's going on in there: Researchers combine powerful imaging and metabolic analysis techniques to record disease events in high resolution.»

Although changes in treatment methodology still have to be studied, Dr. Cripe believes it may be that the timing of various treatments is what matters, and that perhaps initially suppressing immunity could allow the virus to infect a large number of tumor cells before relieving the immunosuppression to allow the body's own T cells to fight off the tumor.

Researchers studying the devil tumor hope to learn what cancer does when the inconvenient obstacle of its host's death isn't enough to stop it.

«The effective immune response didn't happen in every tumor model we tested, so we still need to figure out exactly what triggered the tumor shrinkage and how to predict which tumors will shrink in response to virotherapy,» said Leddon, who is also working toward her medical and doctoral degrees at the University of Cincinnati.

The tumors» recruitment of these inflammatory cells thus enabled them to resist what would otherwise have been a deadly dose of radiation, so that their growth slowed only modestly compared to control mice that had received no radiation.

«Our study sought to understand what happens to make those growth - plate cartilage cells remain, and this work will ultimately be used to determine what causes those benign tumors to become malignant.»

Scientists now know that what matters most in determining the behavior of a particular cancer (and its response to specific therapy) are the molecular pathways that drive malignant cell growth instead of where the tumor begins in the body.

«By understanding what causes malignant transformation we can determine what can be done for patients with benign tumors to suppress them before they reach the malignant stage,» Alman said.

By linking these layers and others to expand from genomics to multi-omics, scientists might be able to meet the goals of personalized medicine: to figure out, for example, what treatment a particular cancer patient will best respond to, based on the network dynamics responsible for a tumor.

Allison wondered what would happen if he injected mice with tumors after they were cured.

«What he showed us is turning the immune system on isn't enough; the crucial step is to make sure it doesn't turn itself off,» says Antoni Ribas, director of the tumor immunology program at UCLA's Jonsson Comprehensive Cancer Center.

Spinhenge@home What it is: The group researches nanomagnetic molecules, which may eventually be targeted for local tumor chemotherapy and the development of tiny memory modules.

«Being able to understand what came from the original tumor and what happened only in the metastases is key to improving treatment.

Metastasis, or cancer spread by the formation of tumors at new sites, is generally what makes cancers deadly because surgery and other treatments are unlikely to find and destroy every cancer cell.

«The model allowed us to ask what would have been the right drug in each case, how could we have known from the tumor's genetics, and what difference it made,» says Jennifer R. Diamond, MD, CU Cancer Center investigator and medical oncologist at the University of Colorado Hospital.

Another is that the transplanted bits of tumor act nothing like cancers in actual human brains, Fine and colleagues reported in 2006: Real - life glioblastomas grow and spread and resist treatment because they contain what are called tumor stem cells, but tumor stem cells don't grow well in the lab, so they don't get transplanted into those mouse brains.

When COXEN looked back through this registry of advanced ovarian cancer, it first sorted tumors into those that had responded and those that had not responded to each drug («what would have been the right drug in each case»).

Now he and his team are putting cells from human brain tumors into the organoids, which have reached the level of development and complexity of a 20 - week - old human fetus's, to see whether they reprise what happens in patients.

«The macrophage is migrating into a site and doing what we want it to do rather than driving tumor development in a normal way,» Lewis says.

«The recent discovery of tumor - promoting milieus, referred to as metastatic niches, that are established at distant sites prior to or upon the arrival of disseminated tumor cells could explain cancer cells that relapse early, but in late relapsing populations, what tumor cells do from the time of dissemination to the time they become clinically detectable has been a big question.»

Although other tumor suppressors exist, what makes Par - 4 so special is that it is not mutated as frequently as other known suppressors, and it's «selective» in its actions in that Par - 4 will only kill cancer cells and not normal cells.

These are two pathways that are very commonly mutated in human tumors, and we try to understand where those pathways are mutated, which type of tumors, what are the mutations that co-occur with mutations in those pathways; and try to understand, if we try to inhibit those pathways, what can we expect in patients.

Delivery of XL184 directly to the tumor site produced these promising results at a dosage level less than one thousandth of what is used in oral therapy, with little or no toxicity.