The first comprehensive study comparing the outcomes of robotic surgery to those of traditional open surgery in any organ has found that the surgeries are equally effective in treating bladder cancer.
The work has important implications for understanding how human cancer cells develop resistance to natural product-based chemotherapies.
An analysis co-led led by a UNC Lineberger Comprehensive Cancer Center researcher linked higher body mass index, or BMI, to lower breast cancer risk for younger women, even for women within a normal weight range.
A new synthetic enzyme, crafted from DNA rather than protein, flips lipid molecules within the cell membrane, triggering a signal pathway that could be harnessed to induce cell death in cancer cells. This is the first such synthetic enzyme to outperform its natural counterpart -- and it does so by three orders of magnitude.
How can elimination of therapeutics from the bloodstream or their early enzymatic degradation be avoided in systemic delivery? Chinese scientists have new developed a method to bind an established cancer therapeutic, floxuridine, with natural serum albumin for its transport and delivery to target cancer cells. In the journal Angewandte Chemie, the authors demonstrate the automated synthesis of a conjugated floxuridine polymer, its successful transport and delivery, and its efficiency in stopping tumor growth.
The bottleneck of cationic antimicrobial peptides as anticancer therapeutics is their limited ability to penetrate cell membranes. Tokyo Medical and Dental University (TMDU) researchers discovered a cyclic decapeptide (termed peptide 1) that serves as a promising lead compound as a new intracellular delivery vehicle for therapeutically effective peptides. When conjugated with another membrane impermeable proapoptotic domain (PAD) peptide, the compound was found to have significantly inhibitory activity in cancer cell lines.
A discovery about how human cells are 'triggered' to undergo an inflammatory type of cell death could have implications for treating cancer, stroke and tissue injury, and immune disorders. A research team from the Walter and Eliza Hall Institute in Melbourne identified the molecular trigger in human cells that drives necroptosis, and implicated defects in this molecular trigger as potentially playing a role in cancer development.
When cells grow and divide to ensure a biological function, DNA must be unwound from its typical tightly packed form and copied into RNA to create proteins. When this process goes awry, the result could be diseases such as cancers. University of North Carolina School of Medicine researchers have discovered that a protein called Spt6 facilitates RNA degradation so that cells have just the right amount of RNA for the creation of proteins.
A surprising form of cell-to-cell communication in glioblastoma promotes global changes in recipient cells, including aggressiveness, motility, and resistance to radiation or chemotherapy. Paradoxically, the sending cells in this signaling are glioblastoma cells undergoing programmed cell death. The apoptotic cancer cells release extracellular vesicles. These vesicle, or exosomes, carry components that alter RNA splicing in the recipient glioblastoma cells, and this altered splicing promotes therapy resistance and aggressive migration.
Oxidative stress can help tumors thrive, but one way novel cancer treatments work is by pushing levels to the point where it instead helps them die, scientists report.