Glioblastoma is one of the most common and lethal brain cancers. Using a glioblastoma model, the scientists at the University of Texas MD Anderson Cancer Center have discovered the path by which cancer cells grow and spread in the brain. According to Baoli Hu, Ph.D., senior research scientist, the study might open new possibilities for cancer treatment.
Baoli Hu, Y. Alan Wang, Ronald A. DePinho and Qianghu Wang made a glioblastoma model that located glioma stem cells that have the ability to develop into other cell types. The scientists further discovered that when a gene known as WNT5A is activated, it allowed glioma cells to change, leading to aggressive tumor growth.
According to the researchers, they have uncovered a process through which glioma stem cells turn into endothelial-like cells. The new cells referred to as GdECs, the researchers said, recruit endothelial cells, forming a niche that support the growth of glioma cells away from the main tumor, and lead to disease recurrence and satellite “lesions”.
Clinical data shows higher GdECs and WNT5A expression in the recurrent tumors and satellite than was seen in the main tumors, confirming the link between glioma cell spread in the brain and WNT5A-mediated stem cell variation. The study revealed that WNT5A is the main factor in glioma stem cells changing to GdECs. The scientists believe this will lead to a new therapeutic strategy for people suffering from glioblastoma.
A team of scientists have made a comprehensive computational model of congestive heart failure, a primary cause of death. According to a study that was published in PLOS Computational Biology, this ‘virtual heart’ might help scientists study new drugs therapies.
Scientists from the University of California made a model that simulates changes from the heart, down to the tissue and cellular levels of the heart, then show the associated electrocardiogram (ECG) results, helping doctors to diagnose heart abnormalities.
At the tissue and cellular levels, the model shows what occurs in the heart when the flow and levels of calcium, sodium, and potassium ions are changed. At the level of an organ, the scientists made an anatomically comprehensive model of the heart, which allows researchers to see the big picture of what occurs when critical electrophysiologic components of a well working heart are tweaked.
In addition, during the study, the researchers discovered that ventricular fibrillation, when excitation waves pump blood of the heart are dis-coordinated and fragmented, results from heart failure-associated slowdown in processes of the cell at the top part of heart. The scientists also used their model to design a new drug strategy to control this heart failure.
Researchers have identified DNA genomic mutations likely caused by smoking of tobacco in seventeen types of cancerous tumours. A detailed study of tobacco-linked mutations by researchers at the Wellcome Trust Sanger Institute and the Los Alamos National Laboratory was published in science. The study helped in understanding how tobacco smoke causes mutations that lead to cancer in tissues that are exposed to it.
The researchers used genome sequences of 610 tumours and the exomes of 4,633 tumours, adding up to 17 smoking-linked forms of cancer. The scientist examined tumours as a mixture of many genomic mutations signatures observed in a previous study. Of the 5,243 growths, the scientists examined, 1,063 were derived from non-smokers and 2,490 from tobacco smokers.
The hypothesis of the study is that tobacco smoke directly destroys DNA tissues that are directly exposed to it. However, the study did not reveal how chemicals in tobacco increase the risk of cancer in tissues that are not directly exposed to tobacco smoke like kidneys, and bladder.
The tumour forms with the highest probability of causing cancer in people who smoke over 30 cigarettes per day are those occurring in tissues directly in contact with tobacco smoke, the scientists showed. Counting the number of mutations seen in lung tissues samples, the study estimated that about 150 mutations collect in a particular lung cell in an individual who smoke a pack of cigarettes per day.
Cells are adept at detecting and responding to their neighbors. Cells must be tuned to their environment, using indications from outside themselves to drive essential cellular milestones such as whether or when to divide, where and whether to migrate and even when to die.
Even single-celled organism— algae, yeast, bacteria—need to sense and respond to outside signals to survive. To perceive and respond to any signals, cells must interpret external signals into a molecular language inside their borders. The internal signals are then transmitted from the cell’s’ surface to its nucleus, the decision-making center.
A new study which was led by computational biologist Dr. Steven Andrews and molecular biologist Dr. Roger Brent, addresses the events that follow when a cell receive external information. Using computational modeling, the biologists discovered the mechanism cells use to transmit some type of signals from their surface to their nucleus, where genetic information of a cell is stored.
To their surprise, they discovered that the mechanism that the cells use is not the obvious and simple way scientists would engineer such a system. They found that the mechanism, known as push-pull control, transmits accurate signals via bags of goo, instead of a wire or something that biologist would use.
Although the mechanism may appear illogical, the push-pull type of signaling could explain why some cancer drugs work as they do, the biologists said.