Sentences with phrase «cancer cells change»

Also like bacteria, cancer cells change their own environment.

We have to find out how cancer cells change as they do this, and how they become resistant to our treatments.

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

Not exact matches

The wrong set of changes to a single cell's genetic code, combined with other system breakdowns, can lead to cancer.

Most large scale studies looking at cancer rates don't show changes related to cell phone use.

As a cancer researcher, do you think the mechanisms of tumor growth are somehow changing to come into line with your perceptions, or is it possible that the process of our learning more about DNA mutations and cell architecture and nutrient exchange and epigenetic effects make it possible for us to inch ever closer to understanding that which is already going on under our noses?

The specimen is sent to a lab to check for abnormal cell changes and cervical cancer.

«By studying the ways different proteins like keratin dynamically change within a cell, we can better understand the progression of cancers and other diseases,» they say.

«Our study suggests that epigenetic changes to cells treated with cigarette smoke sensitize airway cells to genetic mutations known to cause lung cancers,» says Stephen Baylin, M.D., the Virginia and D.K. Ludwig Professor for Cancer Research and professor of oncology at the Johns Hopkins Kimmel Cancer Center.

Baylin and Johns Hopkins scientist Michelle Vaz, Ph.D., first author on the study, suspected that the interplay of epigenetic and genetic changes may occur when normal lung cells develop into cancer, but, Baylin says, the timing of such changes was unknown.

She demonstrated that early experience leads to lasting changes in the molecular structure of the brain and discovered a gene involved in the spread of brain cancer cells into healthy brain tissue.

Vaz and Baylin say the results suggest that early epigenetic changes triggered by chronic cigarette smoke exposure can build up over time and make the airway cells increasingly sensitive to responding to mutations that initiate cancer.

Scientists at the Johns Hopkins Kimmel Cancer Center say they have preliminary evidence in laboratory - grown, human airway cells that a condensed form of cigarette smoke triggers so - called «epigenetic» changes in the cells consistent with the earliest steps toward lung cancer develoCancer Center say they have preliminary evidence in laboratory - grown, human airway cells that a condensed form of cigarette smoke triggers so - called «epigenetic» changes in the cells consistent with the earliest steps toward lung cancer develocancer development.

Now classified as an assistant scientist and paid by Keely's grants, Ponik continues to conduct her own research identifying cell - signaling changes in cancer metastasis.

Changes in the normal function of Ras proteins — mutations which are responsible for 30 percent of all cancers — can power cancer cells to grow and spread.

«In addition, changes in how the genes are expressed (turned on or off) could be used in the future to predict how and when the cancer cells will spread to other parts of the body and how fast they will grow.»

It also sought to match epigenetic changes and genetic differences to the physical characteristics of each cell type and use this knowledge to understand how these can lead to blood disorders, cancer and other complex diseases.

Now Bruce Spiegelman at the Dana - Farber Cancer Institute in Boston and colleagues have shown that foreskin cells from mice can be changed into brown fat cells.

«Current therapies in clinical trials are focused on targeting genetic changes in tumors and helping to boost one's immune system to fight the cancer cells.

Recent evidence also shows that nicotine can cause cancer cells to change their shape, increase their motility and become metastatic.

The bacteria Helicobacter, believed to be a cause of stomach cancer, has been shown to trigger potentially cancer - inducing epigenetic changes in gut cells.

The new discoveries show that bacteria toxins in some patients enable cancer cells to send off signals that obstruct and change the immune defence mechanism, which would otherwise fight the cancer cells.

Previous work from Shenoy's group has shown that the relationship between cancer cells and the extracellular matrix is dynamic, containing feedback mechanisms that can change the ECM's properties, including overall stiffness.

Dr Claudia Wellbrock, study author and Cancer Research UK scientist at The University of Manchester and a member of the Manchester Cancer Research Centre, said: «We used to think that cancer cells spread by first specialising in invading other parts of the body and then change in order to grow raCancer Research UK scientist at The University of Manchester and a member of the Manchester Cancer Research Centre, said: «We used to think that cancer cells spread by first specialising in invading other parts of the body and then change in order to grow raCancer Research Centre, said: «We used to think that cancer cells spread by first specialising in invading other parts of the body and then change in order to grow racancer cells spread by first specialising in invading other parts of the body and then change in order to grow rapidly.

Bowel cancer, also called colorectal cancer, results from a series of genetic changes (mutations) that cause healthy cells to become progressively cancerous, first forming early tumors called polyps that can eventually become malignant.

In cancer cells, the protein networks that control the behavior are changed in such a way as to cause the cells to lose control and break away — a mutated skin cell, for instance, might then migrate into the bloodstream.

In these canine cells we induced a morphological change similar to what happens in cancer progression and we have seen displayed significant alterations in the modulation of genes, called epigenetic lesions,» says Manel Esteller.

As these cells change, they can acquire mutations that can result in further progression to pancreatic cancer, says senior author Peter Storz, Ph.D., a biochemist and molecular biologist at Mayo Clinic.

Analyzing tissue specimens from 10 people with stomach cancer, the researchers found evidence that those same mature cells in the stomach also had reverted to a stem cell - like state and had begun to change and divide rapidly.

But that doesn't mean the patient isn't responding — cancer cells are dying, but the size hasn't changed.

The researchers demonstrated that blocking the PGD enzyme genetically or with a pharmacologic inhibitor reversed the epigenetic reprogramming and malignant gene expression changes detected in distant metastases, and also strongly inhibited their tumor - forming capacity, with no effect on normal cells or peritoneal pancreatic cancer controls.

These epigenetic changes are continuous and are at the core of how healthy cells transform into cancer cells.

In addition, the KDM4 inhibitor induces a change of the molecular make - up of the cancer stem cells and drives them out of stemness.

Vogelstein, Kenneth Kinzler, and other colleagues found a minor change in the APC gene, which normally holds cell growth in check and can cause colon cancers when mutated.

He notes that the increase could be misleading; it's possible, for example, that the drug changes the architecture of cancer cells in the prostate, making them only look worse.

My cancer systems biology team at the University of California, Merced, is tackling diagnosis and treatment of therapy - resistant cancers by elucidating the network of changes within cells as a way to identify new drug targets and circumvent cancer resistance.

The researchers said the findings fundamentally change the understanding of G1 cell cycle regulation and the molecular origins of many associated cancers.

The researchers were able to reverse these epigenetic changes with the use of an FDA - approved drug, forcing the cancer cells out of hiding and potentially making them better targets for the same immune therapy that in the past may have failed.

After treatment with AZA, the epigenetic changes were reversed, rendering the cancer cells unable to evade the immune system any longer.

Professor Johann de Bono, Regius Professor of Cancer Research at The Institute of Cancer Research, London, and Consultant Medical Oncologist at The Royal Marsden NHS Foundation Trust, said, «Our study identifies, for the first time, genetic changes that allow prostate cancer cells to become resistant to the precision medicine olaCancer Research at The Institute of Cancer Research, London, and Consultant Medical Oncologist at The Royal Marsden NHS Foundation Trust, said, «Our study identifies, for the first time, genetic changes that allow prostate cancer cells to become resistant to the precision medicine olaCancer Research, London, and Consultant Medical Oncologist at The Royal Marsden NHS Foundation Trust, said, «Our study identifies, for the first time, genetic changes that allow prostate cancer cells to become resistant to the precision medicine olacancer cells to become resistant to the precision medicine olaparib.

The researchers treated 63 cancer cell lines (26 breast, 14 colorectal and 23 ovarian) with low - dose 5 - azacitidine (AZA), an FDA - approved drug for myelodysplastic syndrome, that reverses epigenetic changes by stripping off the methyl group that silences the gene.

They found that cancer cells had acquired new genetic changes that cancelled out the original errors in DNA repair — particularly in the genes BRCA2 and PALB2 — that had made the cancer susceptible to olaparib in the first place.

«Elevated calcium triggers multiple signaling pathways that promote cell doubling, survival and changes in the cell that promote cancer invasion and metastasis,» says Dr. Copland.

Meanwhile Coussens and her colleagues at U.C.S.F. found in a 2005 study, published in Cancer Cell, that the removal of antibody - making B cells from mice engineered to be prone to skin cancer prevented the tissue changes and angiogenesis that are prerequisites for disease progreCancer Cell, that the removal of antibody - making B cells from mice engineered to be prone to skin cancer prevented the tissue changes and angiogenesis that are prerequisites for disease progrecancer prevented the tissue changes and angiogenesis that are prerequisites for disease progression.

Some patients with non-small cell lung cancer (NSCLC) have changes in the anaplastic lymphoma kinase (ALK) gene, which can drive the development of their cancer.

Since protein production is tied to circadian rhythm, Diehl's group asked if misfolded proteins might change circadian rhythm in cancer cells.

Existing experimental evidence showed that mechanical forces were at play in the changes in both fibrosis and cancer and that these forces were important to their development and progression but could not explain the long - ranging changes cells were able to produce to change their environments.

A multicenter team of researchers reports that a full genomic analysis of tumor samples from a small number of people who died of pancreatic cancer suggests that chemical changes to DNA that do not affect the DNA sequence itself yet control how it operates confer survival advantages on subsets of pancreatic cancer cells.

Using in vitro, or test tube, experiments, the researchers applied these chemicals to human cancer cells to measure changes of estrogen receptor - and androgen receptor - target genes and transcriptional activity.

«Breast cancer researchers track changes in normal mammary duct cells leading to disease.»