Sentences with phrase «cancer tumor development»

Moreover, experiments on an ovarian cancer murine model that investigated the effects of orally administered ONA resulted in longer lifespans and inhibited ovarian cancer tumor development.

Not exact matches

Her discovery of radium lead to the development of using X-rays in medicine, and Curie was at the forefront for cancer research, directing the first studies that used radiation to treat tumors.

Teixeira and his team also found that a malfunctioning tumor - suppressing gene that's associated with certain cancers, such as colon and pancreatic, and is known as Stk11, additionally influenced the development of BPH.

A research team at the University of California, Riverside has discovered a way for chemotherapy drug paclitaxel to target migrating, or circulating, cancer cells, which are responsible for the development of tumor metastases.

«Our study identified miR - 182 as a glioblastoma tumor suppressor that reduces the expression of several oncogenes that promote cancer development,» said senior author of the study Alexander Stegh, an assistant professor in the Ken and Ruth Davee department of neurology and of medicine at Northwestern University Feinberg School of Medicine.

An experimental drug in early development for aggressive brain tumors can cross the blood - brain tumor barrier, kill tumor cells and block the growth of tumor blood vessels, according to a study led by researchers at the Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James).

Looking to target a key pathway in order to interfere with the processes that lead to tumor spread, a research team led by Irwin H. Gelman, Ph.D., of Roswell Park Cancer Institute (RPCI) has identified a new suppressor of cancer metastasis that may point the way toward development of more effective treatments for prostate cancers and other malignant solid tCancer Institute (RPCI) has identified a new suppressor of cancer metastasis that may point the way toward development of more effective treatments for prostate cancers and other malignant solid tcancer metastasis that may point the way toward development of more effective treatments for prostate cancers and other malignant solid tumors.

Although proteasome inhibitors are very efficient in selective killing of cancer tumor cells grown in a dish (in - vitro), their success in the clinic has largely been undermined by the development of resistance — mechanisms of which are poorly understood.

EMD Serono, Kirschbaum says, «focuses on the development of targeted cancer therapies on three therapeutic platforms: targeting the tumor cell, the tumor environment, and the immune system.»

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.

Along with finding that the tumor suppressor protein SIRT6 is inactive in around 30 percent of cases of pancreatic ductal adenocarcinoma (PDAC), the team identified the precise pathway by which SIRT6 suppresses PDAC development, a mechanism different from the way it suppresses colorectal cancer.

When cancer cells start dividing rapidly to form tumors, these cells are actually reverting to an earlier time in their development when they were supposed to divide rapidly.

The study, «The nuclear transport receptor Importin - 11 is a tumor suppressor that maintains PTEN protein,» which will be published online February 13 in The Journal of Cell Biology, suggests that the loss of Importin - 11 may destabilize PTEN, leading to the development of lung, prostate, and other cancers.

This is why findings by Cincinnati Cancer Center researchers, showing that a tumor suppressive microRNA, when activated by an anti-estrogen drug, could contribute to development of future targeted therapies, are important.

Investigators found that NPTX2 was expressed in all stages of kidney cancer, especially metastasis, which suggests it plays an important role in tumor development and progression.

«We also found that the tumors developed quickly, at the time in early development that corresponds to when such tumors develop in children with the cancer.»

«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 fact, associations of cancer cells with the normal peritumoral microenvironment can profoundly impact tumor growth and development.

This demonstrated that non-small-cell lung cancer selectively requires autophagy for tumor development and that therapeutically targeting autophagy may be an alternative to targeting Ras.

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.

She is investigating the role of glycosylated molecules in tumor progression and metastasis, tissue - and species - specific expression of lectin receptors that play a role in regulating host innate immune responses and inflammation, and the immunological mechanisms underlying chronic inflammation and cancer development.

miR - 184 is known to suppress tumor development by regulating a variety of genes involved in cancer growth, while SND1 has been shown to play a significant role in the development of breast, colon, prostate and liver cancers.

Other studies have found that nutrients in dark, leafy greens may inhibit the growth of tumor cells in breast, skin, lung and stomach cancers and that green tea may thwart cancer development in colon, liver, breast and prostate cells.

Dr. Gnjatic's research focuses on human antigen - specific immune responses to tumor antigens, in an attempt to define new targets for the development of cancer immunotherapies, assess the efficacy of these immunotherapies, and learn why they may fail.

Researchers developed models to examine the influence of driver mutations — mutations that promote cancer development — on the initiation and development of gliomas, and how tumor genomic profiles evolve as the cancer progresses.

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.

Unlike other solid tumors, there has been limited progress in understanding the contribution of genetic risk factors to the development of uveal melanoma, researchers say, primarily due to the absence of comprehensive genetic data from patients as the large sample cohorts for this rare cancer type have not been available for research.

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.

The discovery, published in the journal Nature Communications, marks the first time this little - known protein has been characterized in relation to cancer development and tumor growth.

This webinar is the third in a series focusing on the cancer pathways that support tumor development, the emerging research in identifying and targeting these pathways, and innovations in the development of increasingly effective cancer therapy options.

This webinar is the second in a series (see Part 1 here) focusing on the cancer pathways that support tumor development, the emerging research in identifying and targeting these pathways, and innovations in the development of increasingly effective cancer therapy options.

When cancer develops, the generated cells are not uniform in their biological properties and contribute differently to tumor development.

«We have indications that our discovery constitutes a fundamental principle in the development of tumors and plays an essential role in other cancers.

This phenomenon could result in breakage in the human genome, and when a breakage impacts important genes, such as tumor suppressors, it could lead to cancer development.

This led to development of newer technology, called single cell sequencing (SCS), that has had a major impact in many areas of biology, including cancer research, neurobiology, microbiology, and immunology, and has greatly improved understanding of certain tumor characteristics in cancer.

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

In the absence of this and other defense mechanisms, Weinberg says, «cancer development would be inevitable, and we would be covered by tumors by the time we're several years old.»

«To answer these questions, one has to divide cancers into two groups: solid tumors that require the development of a blood supply to metastasize and enlarge, and soft tumors that may have circulating cells, as in leukemias.

Answering important clinical questions — such as whether genetic diversity is a risk factor for aggressive tumor development or how it relates to treatment resistance — requires analyzing samples from many patients with different types of cancer.

In a development that could lead to a new generation of drugs to precisely treat a range of diseases, scientists from the Florida campus of The Scripps Research Institute (TSRI) have for the first time designed a drug candidate that decreases the growth of tumor cells in animal models in one of the hardest to treat cancers — triple negative breast cancer.

They further investigated this phenotype in a skin tumor model system, provided by Maria Sibilia from the Institute for Cancer Research of the Medical University of Vienna, and found that deactivating HDAC1 actually accelerates tumor development, while HDAC2 deactivation has no effect.

And with non-melanoma skin cancers being the most frequent human tumors, there is clearly a tremendous need to understand the underlying molecular mechanisms, to allow the development of drugs to treat these types of cancer.

By matching normal and cancer cells from a patient, we can now study the differences — what molecules are key to tumor development and growth, and, ultimately, match treatments that might disable this cancer,» says the study's senior investigator, associate professor of pathology, Xuefeng Liu, MD, a member of the Center for Cell Reprogramming (CCR) at Georgetown University Medical Center.

This innovative approach — using high - intensity sequencing to detect cancer from circulating tumor DNA in the bloodstream — heralds the development of future tests for early cancer detection.

While circulating tumor DNA tests targeting a smaller set of cancer genes are already available for use in routine practice to guide care, by covering a much larger number of cancer genes, this high - intensity sequencing approach may enable development of future tests for early detection of cancer.

In a previous study, investigators at the Cancer Institute showed that using a vaccine treatment for bladder and breast cancer tumors in laboratory models resulted in a reversal of the traditional immune blockade, as well as the development of tumor specific immunity throughout theCancer Institute showed that using a vaccine treatment for bladder and breast cancer tumors in laboratory models resulted in a reversal of the traditional immune blockade, as well as the development of tumor specific immunity throughout thecancer tumors in laboratory models resulted in a reversal of the traditional immune blockade, as well as the development of tumor specific immunity throughout the body.

The findings, published in the journal Cancer Research, show regular consumption of dietary emulsifiers in mice exacerbated tumor development.

«If our findings are confirmed by additional studies, they may open doors to the development of targeted therapies against the tumor subtypes more likely to affect African Americans and potentially help reduce racial disparities in breast cancer.»

He received the 2014 William B. Coley Award for Distinguished Research in Tumor Immunology and the 2017 Warren Alpert Foundation award for this work, which led to development of the PD - 1 pathway blockade for cancer immunotherapy.

«We suggest to sequence the healthy DNA and that of the tumor of each patient to really know which genes are responsible for the development of cancer,» explains Nikolaev.