Sentences with phrase «tumor cell division»

The researchers injected a compound normally used to label tumor cell division into patients who had agreed to have their brains examined after death.

In studies of laboratory - grown human tumor cell lines, the drug disrupted tumor cell division and prevented growth of advanced cancer cells.

Not exact matches

When the scientists inserted human colorectal cancer cells into zebrafish embryos and allowed them to grow for 4 days, the resulting tumors showed three hallmarks of human solid tumors: rapid cell division, formation of blood vessels to supply nutrients, and the ability to spread to other locations in the body.

The research team, led by senior author Timothy P. Cripe, MD, PhD, chief of the Division of Hematology / Oncology / BMT at Nationwide Children's Hospital, found that virotherapy doesn't always require a strong virus infection of cancer cells to cause tumors to shrink or die.

The arithmetic is complex, but the consensus is that, to pose a health threat, cancers have to replicate at least 200 to 300 times, even though a clinically relevant tumor contains «only» a million million cells, which could be achieved by «only» 40 or so divisions if the originating cell had all the necessary mutations from the outset.

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.

How cell division occurs and is coordinated with organismal development is a subject of intense research interest, as is how this process malfunctions in the development of tumors.

Such genes help regulate cell division, and when they are missing or inactivated by mutations, cell division runs amok, resulting in tumors.

In order to identify the cancer stem cells from other cells in the tumor, the research team studied epigenetic mechanisms that distinguish between the least - sorted cells, with endless division properties and a potential to create growth, and the more sorted cells which lack this ability.

It thus seems quite likely that this new signaling path also links the performance of the cellular power plants and cell division in human cells,» says Meisinger, who now plans to analyze these mechanisms in tumor tissues.

«We believe one cell fusion event can both initiate malignancy and fuel evolution of the tumor that ensues,» noted lead author Xiaofeng Zhou, Department of Microbiology and Immunology and Surgery and the Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, at the University of Michigan (Ann Arbor).

Ultimately, their work could have medical implications, since a better understanding of cell division could lead to new cancer therapies to hinder tumor cells» reproduction.

The authors uncover the cellular and molecular mechanisms, as well as the gene network regulated by Sox9 during the early steps of skin tumor initiation and demonstrates that Sox9 controls the long term maintenance and expansion of oncogene expressing cells by promoting self - renewing division and inhibiting differentiation.

«Salmonella strains have a natural preference for infiltrating and replicating within the cancer cells of a tumor, making the bacteria an ideal candidate for bacteriotherapy,» said Robert Kazmierczak, a senior investigator at the Cancer Research Center and a post-doctoral fellow in the Division of Biological Sciences in the MU College of Arts and Science.

«Why premature cell division promotes cancers: Researchers have discovered how genes responsible for cell division, when mutated, disrupt the replication process of the genome and promote tumor formation.»

In early clinical trials of these drugs, we noticed that in some breast cancer patients the tumors didn't just remain the same size — as would be expected with drugs that interfere with cell division — but began to recede, sometimes quite dramatically, said Goel.»

«RNAi therapies are a unique approach to cancer treatment as they have the potential to «turn off» the genes» coding for proteins involved in cancer cell division,» said Ramesh K. Ramanathan, M.D., medical director of the Virginia G. Piper Cancer Center Clinical Trials Program at Scottsdale Healthcare and deputy director of the Clinical Translational Research Division of the Translational Genomics Research Institute (TGen) in Phoenix, Ariz. «Using a lipid nanoparticle, the RNAi drug can be delivered to a cancer cell to block the expression of specific proteins involved in tumor growthdivision,» said Ramesh K. Ramanathan, M.D., medical director of the Virginia G. Piper Cancer Center Clinical Trials Program at Scottsdale Healthcare and deputy director of the Clinical Translational Research Division of the Translational Genomics Research Institute (TGen) in Phoenix, Ariz. «Using a lipid nanoparticle, the RNAi drug can be delivered to a cancer cell to block the expression of specific proteins involved in tumor growthDivision of the Translational Genomics Research Institute (TGen) in Phoenix, Ariz. «Using a lipid nanoparticle, the RNAi drug can be delivered to a cancer cell to block the expression of specific proteins involved in tumor growth.»

«The CDK4 and 6 proteins are critical drivers of the cell - division cycle and are required for the formation and growth of various types of solid tumors,» says Dana - Farber's Shom Goel, MD, PhD, co-first author of the study with Molly DeCristo of the Hematology Divisiondivision cycle and are required for the formation and growth of various types of solid tumors,» says Dana - Farber's Shom Goel, MD, PhD, co-first author of the study with Molly DeCristo of the Hematology DivisionDivision at BWH.

As an initial focus, researchers at Chicago will search for novel ways to take advantage of steroid hormones and their receptors to detect metastases, define their boundaries and deliver treatments directly to tumor cells in order to inhibit cell division or promote cell death.

As a powerful tumor suppressor, p53 turns on genes that either halt cell division to allow time for repair of damaged DNA or, when all rescue attempts prove futile, to prevent cells with genetic defects from dividing, as this would fuel the development of cancer.

The subpopulation that failed to produce Wnt1 contributed to tumor growth with a mutation in a gene called HRas, which regulates cell division.

Researchers have identified a protein that activates the well - known tumor suppressor gene p53 to prevent the division of cells that have damaged DNA.

It affects the division of cancer cells and can slow tumor growth.

Title: Two sides of the Myc - induced DNA damage response: from tumor suppression to tumor maintenance Authors: Campaner S and Amati B Date: 2012 Publication Details: Cell Division 2012; 7 (1): 6

A cancer cell is a cabin that wants to expand (cell growth) and then build a cluster of additional cabins to create a tumor (cell division).

Downregulation of tumor suppressors and upregulation of proto - oncogenes can directly inhibit the ability of a cell to undergo programmed cell death while simultaneously stimulating growth and division.

In addition to a critical role in cell division, it is also clear that survivin has a function in protecting cells from apoptosis and that this pathway is followed in nearly every human tumor.

The efficient compaction of DNA during cellular division ensures equal distribution of DNA into daughter cells and prevents aneuploidy, which has been implicated as a major driver of tumor development.

However, in the present study there is no evidence of untoward donor cell proliferation or tumor formation up to at least 130 days post-transplantation, suggesting that cell division is a regulated or balanced event.

When tumor suppressor genes work properly, they «slow down cell division,» repair broken DNA, and trigger programmed cell death.

Likewise, unregulated growth, abnormal cell division, and defective cell death pathways are hallmark features of tumors.

Tumor Treating Fields (TTFields) are low intensity alternating electric fields tuned to disrupt the division process of cancer cells.

Introducing miR - 24 into proliferating normal and tumor cells also stopped them from further cell division.

In essence, Knudson, far ahead of his time (and ahead of his own hard data) hypothesized that some genes» normal role in life is to behave as anticancer or tumor - suppressor genes that keep cell division under healthy control.

It promotes tumor cell proliferation and resistance to apoptosis (programmed cell death after a certain number of cell divisions, a good thing when it comes to cancer cells).

Cancer information and prevention with ellagic acid Cancer: a malignant neoplastic disease -(any malignant growth or tumor caused by abnormal and uncontrolled cell division; it may spread to other parts of the body through the lymphatic system or the blood stream).

In the journal Nature on Sept. 6, three science teams reported a major link between tumor suppression and stem cell division.

Cells that are undergoing frequent cell divisions (multiplying) are the most sensitive to radiation and this is why tumor cells tend to be more susceptCells that are undergoing frequent cell divisions (multiplying) are the most sensitive to radiation and this is why tumor cells tend to be more susceptcells tend to be more susceptible.

This growth is technically not a tumor but is actually an area of excessive sebaceous cell division.

The mutations may be in genes governing some aspect of the immune system but they might also be in tumor suppressor genes whose job it is to seek out and destroy cancerous cells, genes that control cell division, genes that control normal cell death, and other types as well.

A brain tumor is any intracranial tumor created by abnormal and uncontrolled cell division, normally either found in the brain itself, in the cranial nerves, in the brain envelopes (meninges), skull, or pituitary and pineal gland.

Previous studies have found taking aspirin can cut the risk of developing colon or bowel cancer and suggested it does so by blocking the enzyme cyclooxygenase2 which promotes inflammation and cell division and is found in high levels in tumors.

Other scientists have previously found it can reduce the risk of developing colon cancer and suggested it does so by blocking the enzyme cyclooxygenase2, or COX - 2, which promotes inflammation and cell division and is found in high levels in tumors.