Sentences with phrase «tumor models with»

Another key finding was observing the inhibitor effect on tumor models with a gene PTEN deficiency as a biomarker — of huge interest because PTEN, a tumor suppressor, is known to be defective in as many as half of all advanced solid tumor cancers.

Not exact matches

In December 2017, writing in Computer Methods in Applied Mechanics and Engineering, Yankeelov and collaborators at UT Austin and Technical University of Munich, showed that they can predict how brain tumors (gliomas) will grow and respond to X-ray radiation therapy with much greater accuracy than previous models.

«Indeed, in a second tumor model of metastatic breast cancer, we demonstrated that mice treated with the EphA2 - targeting paclitaxel conjugate presented nearly no lung metastases, while a large numbers of lesions were observed in both untreated mice and in mice treated with just paclitaxel.»

«Particularly in such patients with underlying CKD, our modeling results support the integration of renal tumor anatomic features at cross-sectional imaging into decision making for treatment of small renal masses and may be used to provide a patient - centered framework for selection of optimal candidates for ablative therapy,» Kang said.

«This model was trained on genetic data from human tumors in The Cancer Genome Atlas and was able to predict response to certain inhibitors that affect cancers with overactive Ras signaling in an encyclopedia of cancer cell lines,» Greene said.

Traditional genetic approaches together with the new wealth of genomic information for both human and model organisms open up strategies by which drugs can be profiled for their ability to selectively kill cells in a molecular context that matches those found in tumors.

In the Cell study, Dr. Massagué, with Fellow Manuel Valiente, PhD, and other team members, found that in mouse models of breast and lung cancer — two tumor types that often spread to the brain — many cancer cells that enter the brain are killed by astrocytes.

«It's very difficult to produce a mouse model of a solid tumor of the type we see in most women who are diagnosed with cervical cancer.

By hitting breast cancer cells with a targeted therapeutic immediately after chemotherapy, researchers from Brigham and Women's Hospital (BWH) were able to target cancer cells during a transitional stage when they were most vulnerable, killing cells and shrinking tumors in the lab and in pre-clinical models.

The researchers confirmed these findings in a mammary carcinoma mouse model — treatment with dasatinib just a few days after administering two high doses of chemotherapy prevented tumor growth and increased survival rates.

Weeraratna's team used an artificial skin reconstruct model to recreate the interactions of melanoma cells with either a young or aged tumor microenvironment.

Importantly, while using rosiglitazone in conjunction with targeted therapy reduced tumor growth in both young and aged pre-clinical models, using rosiglitazone alone accelerated tumor growth in young models, while inhibiting it in aged ones.

«Despite the low infection levels of mouse cells with oHSV, we were able to cause a delay in tumor growth in one of the cancer models and even cure many of the mice in a second model,» said first author Jennifer Leddon, who conducted much of the laboratory work during a research experience in the Center for Childhood Cancer and Blood Diseases.

The common pathway found in mouse models was also found in human tumors, suggesting that resistance could indeed be blocked in patients with the same drug as in mice.

In collaboration with the group of Valerian Kagan, Ph.D., D.Sc., at the University of Pittsburgh, Gabrilovich and colleagues analyzed in great detail the events that take place in the DCs from tumor - bearing mice models and found that impaired cross-presentation, which occurred in the presence of tumor - derived factors, was associated with defective trafficking of the antigen - MHC complex to the cell surface.

In a mouse model of triple - negative breast cancer, mice injected with cancer cells that over-express ZMYND11 had tumor volumes of less than 50 cubic millimeters while control mice and those injected with cells expressing ZMYND11 deficient for binding to the methyl group had tumor volumes ranging from 150 to 400 cubic millimeters at eight weeks.

Desgrosellier said the team will follow up with mouse models containing tumor fragments from patients to better reflect the diversity of cell types present in human disease.

A study combining tumor cells from patients with breast cancer with a laboratory model of blood vessel lining provides the most compelling evidence so far that a specific trio of cells is required for the spread of breast cancer.

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.

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.

The researchers showed in mouse models that chronic skin inflammation caused by continuous skin contact with allergens contributes to tumor development.

The size difference between tumor and healthy circulating DNA was initially discovered in animal tumor models created by inducing tumors with human cancer cells.

In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colors.

Combining their strategy with an existing immunotherapy treatment that works by releasing the «brakes» on immune cells, they found they could shrink melanoma tumors, and prolong survival in preclinical models for melanoma.

We created a mouse xenograft model in which SiHa cervical cancer cells were injected into mice subcutaneously, and the resultant tumors were treated with PAL three times a week for 6 weeks.

Efforts aimed at finding better drug regimens would therefore greatly benefit from a mouse model with an intrinsic marker that can indicate different stages of pancreatic tumor formation leading to cancer and reflect the effects exerted by novel drug candidates.

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.

Recently, teaming up with co-investigator Associate Professor Dr. Rolf A. Brekken, they looked into its possible involvement in Pancreatic Ductal Adenocarcinoma (PDA), the most common form of pancreatic cancer, in a mouse model with an early onset aggressive form of tumor development.

Morris says vaccination with modified tumor cells producing IL - 15 and IL - 15Rα slowed tumor growth and led to increased survival for animal models.

In their report that has received advance online publication in Nature Nanotechnology, a research team based at the Wellman Center for Photomedicine at Massachusetts General Hospital (MGH) describes how a nanomedicine that combines photodynamic therapy — the use of light to trigger a chemical reaction — with a molecular therapy drug targeted against common treatment resistance pathways reduced a thousand-fold the dosage of the molecular therapy drug required to suppress tumor progression and metastatic outgrowth in an animal model.

Both Tsigelny and Kurzrock agreed that this finding is an excellent example of the power of collaboration between SDSC and the Moores Cancer Center, and that such modeling needed to be studied across tumors and with multiple different genes involved in cancer.

In two mouse models of pancreatic cancer, a single treatment consisting of intravenous delivery of the PMILs followed by localized delivery of near - infrared light to the tumor site via optical fibers resulted in significantly greater reduction in tumor size than did either treatment with XL184 or PDT with BPD alone.

With the help of various mouse models for pancreatic cancer, they have succeeded in elucidating the molecular pathways of tumor development in detail and have gained a better understanding of how various characteristics of the disease arise.

In experiments with cancer cell lines, the PIM1 inhibitors killed cells in a MYC - dependent manner, and in two different mouse models — one in which mice were implanted with patient tumors and the other in which a genetic alteration of MYC predisposes the mice to tumor development — the administration of PIM1 inhibitors resulted in significant tumor regression.

Meng and Nel also collaborated with Dr. Timothy Donahue, chief of gastrointestinal and pancreatic surgery and a Jonsson Comprehensive Cancer Center member, to demonstrate that treatment with the iRGD peptide can enhance tumor cell killing for patient - derived pancreatic cancers, growing subcutaneously in a mouse model.

«We demonstrated that the co-administration of the iRGD peptide with the particles can enhance the effectiveness of pancreatic cancer treatment in the tumor model, leading to increased tumor shrinkage, disappearance of metastases and enhanced animal survival» said Meng, an adjunct assistant professor of nanomedicine.

Using all the existing data that was available, Andrechek, along with MSU doctoral student Daniel Hollern, analyzed 1,172 mouse mammary tumor samples from 26 different preclinical models and was able to compile one of the largest databases to show which strains of mice were best suited to study a particular type of human breast cancer.

«Having these personalized laboratory models, which we can make in a matter of weeks, will let us test multiple different drugs on the tumor and help us bring precision medicine to individuals with bladder cancer.»

Their recent study, which appears as the cover article in the May issue of Cancer Research, shows that mathematical models can be used to predict how different tumor cell populations interact with each other and respond to a changing environment.

Ongoing studies from the Discher lab are focused on finding that sweet spot with additional tumor models, as well as on how to engineer macrophages for longer - lasting effect.

In their research, scientists at Rutgers created animal models that closely resemble the cancerous tumors found in women with ovarian cancer by injecting tumor tissues obtained from gynecological cancer patients treated at the Cancer Institute into laboratory mice.

Injections of antibody molecules that block CD47 from interacting with SIRPA are already being tried in the clinic based on observations of some reduction in the sizes of tumors in mouse models.

When using a well established model of colorectal cancer, the researchers observed that dietary emulsifier consumption was sufficient to make the animals more susceptible to developing colonic tumors because this created and maintained a pro-inflammatory environment associated with an altered proliferation / apoptosis (cell death) balance.

«BMI1 plays a substantial role in many solid tumors, including one of the most aggressive models of lung cancer, and its expression is linked with tumor growth, invasion, metastasis, prognosis and recurrence,» Levantini said.

«The current study investigated the impact of dietary sugar on mammary gland tumor development in multiple mouse models, along with mechanisms that may be involved,» said co-author Lorenzo Cohen, Ph.D., professor of Palliative, Rehabilitation, and Integrative Medicine.

«By using an animal model to expand tumor cells recently removed from patients, we hoped to re-create more closely what actually happens in patients with pancreatic cancer rather than by using existing artificial cell lines,» said Wei Zhang, Ph.D., an endowed Hanes and Willis Family Professor in cancer at Wake Forest School of Medicine, a part of Wake Forest Baptist, and principal investigator of the study.

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.

After first verifying that stem cells injected to the brain would travel to multiple metastatic sites and not to tumor - free areas in their model, the team injected stem cells loaded with oHSV into the carotid artery of metastasis - bearing mice..

«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.»

Using animal models and cells, Counter and colleagues found that when they experimentally inhibited copper uptake by tumors with the BRAF mutation, they could curb tumor growth.