Tag Archives: cell

One protein, two personalities: Team identifies new mechanism of cancer spread

A new finding by University of Pennsylvania scientists has identified key steps that trigger this disintegration of cellular regulation. Their discovery — that a protein called Exo70 has a split personality, with one form keeping cells under tight control and another contributing to the ability of tumors to invade distant parts of the body — points to new possibilities for diagnosing cancer metastasis. The research, published in the journal Developmental Cell, was conducted by a team of researchers from the School of Arts and Sciences’ Department of Biology; the Perelman School of Medicine’s pathobiology and laboratory medicine, medicine and genetics departments, and China’s Hangzhou Normal University School of Medicine. …

First step of metastasis halted in mice with breast cancer

"Metastasis is what most threatens breast cancer patients, and we have found a way to stop the first part of the process in mice," says Andrew Ewald, Ph.D., assistant professor of cell biology at the Johns Hopkins School of Medicine. Before metastasis occurs, single cells on the edge of a tumor, termed leader cells, form protrusions into the surrounding tissue, like someone dipping a toe in to test the water before deciding to venture farther, Ewald says. If the conditions are right, the leader cells act as guides, with many tumor cells following behind, as they escape the confines of the tumor into the healthy tissue beyond. Full metastasis occurs when the cells succeed in migrating to a new location — the lungs, for example — and set up shop, creating a new tumor…

Cancer ‘avalanche effect’ refuted

Cancer is due to changes in the DNA of cells, which causes them to divide in an uncontrolled manner. It is also true that the cancer cells in certain common tumours, such as in colon cancer, can have over 100 chromosomes instead of the 46 chromosomes normally present in a human cell. But does a single, initial change in the number of chromosomes set off a sequence of unstoppable changes that lead to cancer? The answer to this question is important; in order to ensure that cancer research is on the right track…

Drug-antibody pair has promising activity in non-Hodgkin lymphoma

The ongoing open-label phase 2 study presented at the American Society of Hematology (ASH) meeting was designed to test the activity of brentuximab vedotin (Adcetris) in relapsed or refractory non-Hodgkin lymphoma (NHL) including B-cell cancers such as diffuse large B cell lymphoma (DLBCL). The antibody-toxin compound has been approved for treatment of relapsed or refractory Hodgkin lymphoma and anaplastic T cell lymphoma, and its success prompted the trial in NHL, said Eric Jacobsen, MD, of Dana-Farber, senior author of the study. First author is Nancy Bartlett, MD, of Washington University School of Medicine. …

Researchers uncover why combination drug treatment ineffective in cancer clinical trials

Faculty of Medicine & Dentistry researcher Michael Sawyer and his colleagues, including first author Vijaya Damaraju, recently published their findings in the peer-reviewed journal, Clinical Cancer Research. In the ’80s and ’90s, cancer research focused on finding out which proteins "drove" cancers. New drugs targeting these proteins worked well by themselves, and some in the field believed combining the new drugs with the older chemotherapy drugs would work better than either drug by itself. …

Detailed image shows how genomes are copied

Genomes are built from pairs of long strands of DNA. In previous collaborations with American researchers, Umeå University scientists have shown that DNA polymerase epsilon is one of the three enzymes that build DNA strands in all higher-level organisms from yeast to humans. When the DNA of an organism’s genome is copied, DNA polymerase epsilon is responsible for building about half of the DNA. This process occurs quickly and with very high accuracy to avoid producing mutations that can be detrimental to the cell and to the organism as a whole. …

Dysfunctional mitochondria may underlie resistance to radiation therapy

Maxim Frolov, associate professor of biochemistry and molecular genetics at the University of Illinois at Chicago, and colleagues investigated the effects of a mutation in a gene called E2F, which controls other genes responsible for initiating programmed cell death, a normal function in most cells. Cells undergo programmed cell death — or apoptosis — when they are no longer needed, as a normal part of aging, or in response to environmental factors like radiation that damage cellular DNA. …

Low-fat fish oil changes cancer tissue in prostate cancer, study shows

The findings are important because lowering the cell cycle progression (CCP) score may help prevent prostate cancers from becoming more aggressive, said study lead author William Aronson, a clinical professor of urology at UCLA and chief of urologic oncology at the West Los Angeles Veterans Affairs Medical Center. "We found that CCP scores were significantly lower in the prostate cancer in men who consumed the low-fat fish oil diet as compare to men who followed a higher fat Western diet," Aronson said…

Biologists ID new cancer weakness

A new study from MIT biologists has found that tumor cells with mutated p53 can be made much more vulnerable to chemotherapy by blocking another gene called MK2. In a study of mice, tumors lacking both p53 and MK2 shrank dramatically when treated with the drug cisplatin, while tumors with functional MK2 kept growing after treatment. The findings suggest that giving cancer patients a combination of a DNA-damaging drug and an MK2 inhibitor could be very effective, says Michael Yaffe, the David H. Koch Professor in Science and senior author of a paper describing the research in the Nov…