Sentences with phrase «tumor cells develop»

CU docs had the opportunity to watch how tumor cells develop resistance in real time.

CU docs had the opportunity to watch how tumor cells develop resistance in real time.

Tumor cells develop mechanisms to evade detection by the immune system by expressing a protein called PD - L1.

Researchers found no evidence that mouse tumor cells develop resistance to the drugs.

Unfortunately, in most patients the melanoma recurs within a year because the tumor cells develop drug resistance.

Lead author Dean Ho, a biomedical engineer at Northwestern University in Evanston, Illinois, says that one of the major challenges in chemotherapy is when tumor cells develop mechanisms to pump drugs right back out.

Not exact matches

Today his company is developing a new cancer vaccine technology that teaches immune cells how to recognize and remove tumor cells.

CAR - T cell therapy is a form of immunotherapy, a rapidly developing cancer treatment that uses patients» own immune cells to attack tumors.

The Company focuses on discovering and developing small molecule drugs directed against tumor and immune cell targets that control key metabolic pathways in the tumor microenvironment.

While many researchers are still developing affinity - based techniques for isolating circulating tumor cells, others are exploiting the physical differences between normal and tumor cells.

CCG is also developing cell lines that are cultured to represent tumor behavior in vivo, and computational methods that will help researchers understand tumor behavior and apply the resulting data to diagnoses, treatments, and cures.

The ability for cancer cells to develop resistance to chemotherapy drugs — known as multi-drug resistance — remains a leading cause for tumor recurrence and cancer metastasis, but recent findings offer hope that oncologists could one day direct cancer cells to «turn off» their resistance capabilities.

Shah and his team loaded the herpes virus into human MSCs and injected the cells into glioblastoma tumors developed in mice.

When injected with cancer cells, animals housed there developed tumors 80 % smaller than those in control mice, or no tumors at all.

By releasing the brakes that tumor cells place on the immune system, researchers are developing a new generation of more powerful treatments against malignancy

The stem - cell - derived bone tissue helped repair cranial bone defects in mice without developing tumors or causing infection.

In the last few years, a bulk of data pointing to a small population of cells in tumors that maintain tumor growth, are particularly resistant to chemotherapy, are responsible for relapses, and develop metastases.

Another challenge is producing stem - cell - derived tissues or organs that don't develop teratomas — tumors that contain a variety of tissues found in different organs — when transplanted.

Hence, a major goal of cancer scientists has been to develop drugs that prevent Mdm2 from binding to p53, and to thereby activate p53 to kill the tumor cell.

The scientists have shown that, in all cancers, a sort of «identity crisis» is observed in cancerous cells: in the organs or tissues in which a tumor develops, genes specific to other tissues or to other stages of the development of the organism express themselves in an aberrant manner.

Most cancer vaccines developed to date have been designed to recognize and attack a specific known molecule — such as a cell - surface receptor — that is likely to be found on cancerous cells in any patient with that type of tumor.

Until recently, Ain was renowned for a highly prized repository of 18 immortal cancer cell lines, which he developed by harvesting tissue from his patients» tumors after removal, carefully culturing them to everlasting life in vials.

Interphone compared surveyed cell phone use in 6,420 people with brain tumors to that of 7,658 healthy people in 13 developed countries — Australia, Canada, Denmark, Finland, France, Germany, Israel, Italy, Japan, New Zealand, Norway, Sweden and the U.K. — to try to determine whether people with brain tumors had used their cell phones more than healthy people, an association that might suggest that cell phones caused the tumors.

Now a team of researchers in China has developed a new microfluidic chip that can quickly and efficiently segregate and capture live circulating tumor cells (CTCs) from a patient's blood, with potential applications for cancer screenings and treatment assessments.

There is plenty of anecdotal evidence out there claiming a link between cell phone use and cancer: Keith Black, chairman of neurosurgery at Cedars - Sinai Medical Center in Los Angeles, says that the brain cancer (malignant glioma) that killed O. J. Simpson's attorney, Johnnie Cochran, was the result of frequent cell phone use, based on the fact that the tumor developed on the side of the head against which he held his phone.

If they can be used in living tissue, they might eventually track cells in developing embryos, the immune system, or cancerous tumors.

However, tumor cells are smart and have developed ways to avoid immune detection.

To overcome these problems, Min and his team developed a new modality to visualize glucose uptake activity inside single cells based on stimulated Raman scattering (SRS) imaging, and demonstrated its use in live cancer cells, tumor xenograft tissues, primary neurons and mouse brain tissues.

The regrowth of cancer stem cells is responsible for the drug resistance that develops in many breast tumors and the reason that for many patients, the benefits of chemo are short - lived.

Now, thanks to the new mouse model, it will be possible to study how renal tumors are able to develop in an environment with a normal immune system, and how cancer cells manage to evade the immune system's attacks.

«This model supported cancer development so strongly that some mice developed invasive squamous cell skin cancers similar to the patient's tumor,» said lead author Shadmehr Demehri, MD, PhD, a dermatologist and postdoctoral fellow.

In a bid to progress beyond the shotgun approach to fighting cancer — blasting malignant cells with toxic chemicals or radiation, which kills surrounding healthy cells in the process — researchers at the Harvard - MIT Division of Health Sciences and Technology (HST) are using nanotechnology to develop seek - and - destroy models to zero in on and dismantle tumors without damaging nearby normal tissue.

But it's much harder to develop therapies that restore malfunctioning genes that should be triggering cell death in abnormal cells, known as tumor - suppressor genes.

Researchers have identified a group of immune system genes that may play a role in how long people can live after developing a common type of brain cancer called glioblastoma multiforme, a tumor of the glial cells in the brain.

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 authors said their results, which they have made publicly available, constitute an invaluable resource to help clinicians predict which chemotherapies will be most effective against tumor cells with particular genetic mutations, and how to rationally combine therapies to prevent cancers from developing resistance.

Understanding how cancer cells are able to metastasize — migrate from the primary tumor to distant sites in the body — and developing therapies to inhibit this process are the focus of many laboratories around the country.

Researchers used IL - 15 to develop a whole tumor cell vaccine to target breast (TS / A) and prostate (TRAMP - C2) cancer cells in animal models; results showed that tumor cells stopped growing after the vaccine was introduced and that beneficial effects were enhanced further when IL - 15Rα was co-produced by the vaccine cells.

Shah next plans to rationally combine the toxin - secreting stem cells with a number of different therapeutic stem cells developed by his team to further enhance their positive results in mouse models of glioblastoma, the most common brain tumor in human adults.

In addition, cancer cells» susceptibility to these agents varies widely, and tumors often develop resistance to drugs that initially seem effective.

They propose that normal tissue becomes primed for cancer when oncogenes are activated and tumor suppressor genes are silenced or lost, but that cancer develops only when a cell in the tissue reverts to a more primitive, embryonic state and starts dividing.

When mice bearing pancreatic tumors were injected with an antibody that prevents galectin - 9 from docking into dectin - 1, they developed M1 macrophages, which sent signals that dramatically increased the number of T cells capable of attacking the cancer cells.

As tumors grow and develop, they shed micro-metastases, clusters of a few cells that take up residence in far - flung organs such as the brain, liver and bone.

By tracking and understanding which host cell pathways are manipulated by these T. gondii proteins, scientists can identify potential new targets to develop more effective therapies against highly aggressive solid tumors.

«Dormant disseminated tumors can be ticking time bombs, but now that we know some of the triggers, it may be possible to develop therapies to ensure that disseminated cancer cells remain in a dormant state, or other therapies that eradicate these cells before they form full - blown metastases.»

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.»

By contrast, 16 out of 17 mice that produced annexin A2 in their cells developed metastatic tumors in the liver, lungs or abdominal cavity.

A new optogenetic technology developed by scientists at the University of Massachusetts Medical School and Texas A&M Health Science Center Institute of Biosciences & Technology, called optogenetic immunomodulation, is capable of turning on immune cells to attack melanoma tumors in mice.

There's a need for ways to find these cells and to study them, and importantly, to develop drugs that target them, because these cancer stem cells are resistant to chemotherapy drugs that target the main tumor.