Apoptosis is programmed cell death, the body's normal method of disposing of damaged, unwanted, or unneeded cells.
One way to tackle cancer, the second-leading cause of death in the United States, is to target oncogenes -- genes that have the potential to cause cancer.
The Jan. 17 issue of the Journal of the American Medical Association features an important study about sepsis with an accompanying editorial by a University of Nebraska Medical Center expert.
The white blood cells are potent fighters that protect the body against foreign invaders, including pathogens and cancer cells. Scientists have found that the presence of B cells, which are powerhouses, in tumor cells, combat the disease from within.
University of California San Diego School of Medicine researchers have identified the molecular mechanism activated by the presence of tetrahydrocannabinol (THC) - the ingredient that causes people to feel the euphoria or "high" associated with cannabis - in the bloodstream that accelerates cancer growth in patients with human papillomavirus (HPV)-positive head and neck squamous cell carcinoma.
Dying cells in the body can keep the immune system in check, thus preventing unwanted immune responses against the body's own tissues.
A new study has shown that regular use of aspirin may protect against heart disease, reduce colorectal tumor growth and prevent relapse.
The protein, called syndecan-4, combines with fellow cell membrane proteins, called integrins, to form protruding 'hands' that sense the environment outside the cell.
The benefits of a daily aspirin may extend beyond heart health to colorectal cancer treatment, say City of Hope researchers who have found aspirin appears to reduce tumor growth and inhibit recurrence of the disease.
Certain bacteria can override a defense mechanism of the immune system, so called programmed cell death, through inhibition of death effector molecules by their outer membranes components.
Scientists at St. Jude Children's Research Hospital have discovered a new way that the molecule RIPK1 leads to cell death in infected, damaged or unwanted cells showing that more than one mechanism can trigger the process.
The p53 gene, which researchers had thought was less relevant in kidney cancer, may play an important role after all – a discovery that could lead to new treatments.
In laboratory experiments, a metabolic inhibitor was able to kill a variety of human cancer cells of the skin, breast, lung, cervix and soft tissues through a non-apoptotic route -- catastrophic macropinocytosis.
Investigators at Rutgers Cancer Institute of New Jersey have found that a treatment based on a novel cellular product programmed to deliver an overabundance of chimeric antigen receptor causes cell death in non-Hodgkin lymphoma models that are sensitive or resistant to standard therapies.
Every cell contains a vast number of proteins, each of which has a specific function, for example as a receptor for another molecule or an enzyme that catalyzes chemical reactions.
Colon cancer cells deficient in p53, one of the most important control proteins in cell growth, activate a particular metabolic pathway to adapt to the lack of oxygen and nutrients inside the tumor. Statins, which are often prescribed to lower cholesterol, block this metabolic pathway and cause the cancer cells to die, as scientists from the German Cancer Research Center have now discovered.
The cover for issue 63 of Oncotarget features Figure 6, "Inverse relationship between ETV7 and SERPINE1 in OSCC," by Salameti, et al.
Apoptosis is a form of “cell suicide”, where a cell self-terminates, ideally as planned or programmed, enabling multi-cellular organisms to continue to live, develop and thrive.
All neurodegenerative diseases have a common thread: the appearance of protein clumps in the brain such as amyloid-beta plaques in Alzheimer's disease and alpha synuclein aggregates in Parkinson's.
The growing trend of implementing immunotherapy into oncology has resulted in various new therapeutic cancer treatments utilizing antibodies.
Abnormal scarring is a serious threat resulting in non-healing chronic wounds or fibrosis. Scars form when fibroblasts, a type of cell of connective tissue, reach wounded skin and deposit plugs of extracellular matrix.