Sentences with phrase «of cancer cell metabolism»

The researchers are reporting preclinical findings for a potential two - treatment strategy to block multiple mechanisms of cancer cell metabolism in pancreatic cancer at the American Association for Cancer Research Annual...

Not exact matches

It seems to decrease cell growth, increase self - destruction of abnormal cells and shift estrogen metabolism to less cancer - promoting forms.»

Because cancer cells in general are metabolically inflexible, we are able to take advantage of ketone metabolism as a way of placing cancer cells in a weakened state.

Middle - aged people who eat protein - heavy diets are four times as likely to die of cancer as those who eat only a little protein, according to the study, which was published in the journal Cell Metabolism.

The Salford team set out to assess the bioenergetics of cancer stem cells — the processes which allow the cells to live and thrive — with a view to disrupting their metabolism.

Contrary to current research this new study found that LKB1, a molecule that regulates the metabolism of many adult cells, is an important molecule in the cancer's promotion and survival.

Researchers measure the impact on cancer stem cell metabolism of 3 natural substances, 3 experimental pharmaceuticals and 1 clinical drug.

This suggests that «the python intestine may represent a valuable model for studying the interactions of metabolism with the regulation of cell division / death and WNT signaling relevant to cancer,» the researchers said.

«Cancer cell metabolism is a little bit peculiar,» said senior author Julie K. Schwarz, MD, PhD, an associate professor of radiation oncology.

A team led by professor Massimiliano Mazzone has demonstrated that the metabolism of macrophages, a particular type of white blood cell, can be attuned to prevent the spread of cancer.

Frigo and his team demonstrated in this study that androgens take control of the AMPK signaling cascade, a master regulator of metabolism, to increase prostate cancer cell growth.

In a study presented in the featured clinical investigation article of the November issue of The Journal of Nuclear Medicine, they used 18F - fluorodeoxyglucose (FDG) PET / CT imaging to show that the amount of cell - free tumor DNA circulating in the bloodstream correlates with tumor metabolism (linked to cancer aggressiveness), not tumor burden (amount of cancer in the body).

After completing her graduate studies in 2006, she joined the laboratory of Dr. Craig B. Thompson at the University of Pennsylvania for postdoctoral work focusing on cancer cell metabolism.

For instance, researchers used virtual screening to identify compounds that target the gene for PFKFB3, an enzyme that helps regulate the metabolism of cancer cells.

Aware that cancers rewire their metabolism in ways that could change the epigenome and that distant metastases in pancreatic cancer naturally spread to organs fed by a sugar - rich blood supply, the researchers wondered if the tumor cells had altered the way they use the basic form of sugar, glucose.

«Cancer cell metabolism kills: Possible new therapies targeting energy supply of cancer cells?.&Cancer cell metabolism kills: Possible new therapies targeting energy supply of cancer cells?.&cancer cells?.»

In addition, he investigates the role of glucose metabolism in cell proliferation and survival of cancer cells, and how it could be exploited for cancer therapy.

The investigated connections between Myc, energy metabolism and apoptosis will help us to understand the biochemistry of cancer cell apoptosis.

Craig Thompson, president of the Memorial Sloan - Kettering Cancer Center in New York City, yesterday was hit with a second lawsuit alleging that he made an improper business deal to exploit his research on the metabolism of cancer Cancer Center in New York City, yesterday was hit with a second lawsuit alleging that he made an improper business deal to exploit his research on the metabolism of cancer cancer cells.

«Cancer doesn't sleep: MYC oncogene disrupts clock, metabolism in cancer cells: Findings inform time - dependent treatment for reducing side effects, increasing effectiveness of cancer medications.&Cancer doesn't sleep: MYC oncogene disrupts clock, metabolism in cancer cells: Findings inform time - dependent treatment for reducing side effects, increasing effectiveness of cancer medications.&cancer cells: Findings inform time - dependent treatment for reducing side effects, increasing effectiveness of cancer medications.&cancer medications.»

To address these questions, Dang, Altman, and Hsieh collaborated with Penn colleague, Aalim Weljie, PhD, research assistant professor of Pharmacology, using an osteosarcoma cancer cell line to study the interaction of MYC and metabolism in cancer cells.

«This work ties together the study of cell metabolism and cancer chronotherapy — If cells don't have to «rest,» they may replicate all the time, with no breaks at all.»

The findings may help to explain how cancer cells maintain their high levels of metabolism — and could uncover future targets for cancer treatment.

«Metabolism drives growth, division of cancer cells.»

«I would like to point out, however — concludes Alimonti — that our discovery does not imply that cancer patients must undergo a strict dietary regime, which might in fact hurt them: a reduction of fat in cancer cells can only be obtained by blocking the cancer cells metabolism through specific drugs.»

Further research showed that the WWOX gene plays a role in the altered metabolism of cancer cells which are known to use glucose differently to normal cells.

«This difference in metabolism is a key part of how cancer cells have a competitive advantage over normal cells.

Scientists, led by Ottar Rolfssonat the University of Iceland, have built a mathematical model to examine the metabolism of breast epithelium — as the majority of breast cancers originate from these cells.

Researchers have built a model to investigate the metastasis of cancer by examining the metabolism of breast epithelial cells and look at the role of signaling.

«Our original hypothesis was that cancer cells were modifying their metabolism based on communications they were receiving from cells in the microenvironment near the tumor,» said Nagrath, assistant professor of chemical and biomolecular engineering at Rice and co-author of a new study describing the research in the open - access journal eLife.

Cancer cells are well - known as voracious energy consumers, but even veteran cancer - metabolism researcher Deepak Nagrath was surprised by their latest exploit: Experiments in his lab at Rice University show that some cancer cells get 30 - 60 percent of their fuel from eating their neighbors» «words.&Cancer cells are well - known as voracious energy consumers, but even veteran cancer - metabolism researcher Deepak Nagrath was surprised by their latest exploit: Experiments in his lab at Rice University show that some cancer cells get 30 - 60 percent of their fuel from eating their neighbors» «words.&cancer - metabolism researcher Deepak Nagrath was surprised by their latest exploit: Experiments in his lab at Rice University show that some cancer cells get 30 - 60 percent of their fuel from eating their neighbors» «words.&cancer cells get 30 - 60 percent of their fuel from eating their neighbors» «words.»

When stromal signaling molecules — isolated from patients or generated in the lab — were present, the metabolism of pancreatic cancer cells changed, the researchers found.

Zinc finger nuclease mediated knockout of ADP - dependent glucokinase in cancer cell lines: effects on cell survival and mitochondrial oxidative metabolism.

Further, they present two new hallmarks — reprogramming of energy metabolism and evasion of immune destruction — that have emerged as critical capabilities of cancer cells.

Analogous to nicotine, arecoline was identified as an inhibitor of the enzyme ACAT1, which contributes to the metabolism - distorting Warburg effect in cancer cells.

Anna Huttenlocher, University of Wisconsin, USA Neutrophils in the Tumor Microenvironment Neutrophils, Wounds, and Cancer Progression Stefan Kaufmann, Max Planck Institute, Germany Pathology and immune reactivity: understanding multidimensionality in pulmonary tuberculosis Constitutive BAK activation as a determinant of drug sensitivity in malignant lymphohematopoietic cells Kathryn Moore, New York University, USA MicroRNA -33-dependent regulation of macrophage metabolism directs immune cell polarization in atherosclerosis Lalita Ramakrishnan, University of Cambridge, UK Myeloid Growth Factors Promote Resistance to Mycobacterial Infection by Curtailing Granuloma Necrosis through Macrophage Replenishment Beth Stevens, Harvard University, USA Microglia: Dynamic Mediators of Synapse Development and Plasticity Do glia drive synaptic and cognitive impairment in disease?

Understanding these pathways, and the identification of the key proteins that control the ability of cancer cells to reprogram their metabolism through biochemical, and epigenetic or genetic alterations that make them resistant to therapies, is of paramount importance for the design of more targeted and therefore less toxic therapies.

One hallmark of cancer is the accelerated metabolism, high energy requirements, and increased glucose uptake by the tumor cells, the latter being the first and rate - limiting step for glucose metabolism [2,3].

Advances in research into the immunological evasion, metabolism and latency of metastatic cancer cells allow the identification of potential targets to test therapies.

While investigating one of the most commonly mutated genes in lung cancer, Shaw discovered an energy - sensing pathway that shuts down cell growth and reprograms metabolism when nutrients are scarce.

Yet its contribution to tumor cell proliferation only increases the evidence that changes in metabolism are a cause of cancer and not just a consequence, according to Leif Ellisen, a cancer genetics researcher and oncologist who directs the MGH Translational Research Laboratory.

Autophagy eventually kills cells, so new therapies that deprive cells of nutrients or otherwise thwart metabolism will likely cause more harm to cancer cells than to normal cells.

A transcriptome research of its organs revealed its gene signature is highly evolved and adapted for extreme longevity (slow metabolism, improved insulin gene signaling and glucose homeostasis, thus reduced blood glucose, improved cancer genes, improved endothelial function by eNOS (endothelial Nitric Oxide Synthase) meaning improved vascular coronary blood flow, improved microvasculature arterial and heart endothelium function) but more importantly, to answer your question, some whales display low blood glucose hypoglycemia, this affects the quantity and period of proteins / DNA / cell exposure to glucose glycation, glycosylation and glycoxydation reactions.

IDH is mutated early in the development of those cancers, supporting the theory that cancer cells evolve toward altered metabolism, «selecting» mutated genes as they develop.

Jared Mayers (Brigham and Women's Hospital Boston, USA), winner of the prize category Translational Medicine, kicked the event off with his research on differences in how cancer cells and normal cells utilize of nutrients and how this has been linked to genetic changes in cancer, opening up an opportunity for drugs targeting metabolism.

Thus, it is not unreasonable to suspect that stromal fibroblasts could influence the metabolism of adjacent cancer cells, and visa versa.

Cancer cells alter their metabolism in the interest of sustaining rapid growth, and high levels of PHGDH appear to drive such metabolic change.

The research, published in Cell Metabolism, identified the role of a particular protein, IL - 6, released by cancer cells even before cachexia manifests.

In TNBC cells, Poldip2's absence appears to be part of the warped cancer cell metabolism known as the Warburg effect.

the metabolism of cancer cells, the responses of cancer cells to stress, and mechanisms involved in control of the cell cycle