A Mayo Clinic study demonstrated how the deficiency of the enzyme CDK12 or its regulation by cyclin K causes the expression of mutations related to resistance to endocrine therapy in prostate cancer. Prostate tumors with CDK12 deficiency are more aggressive, recurrent, produce metastases and are associated with castration-resistant prostate cancer (CRPC). CDK12 deficiency impairs DNA repair and increases genomic instability, causing an effect known as homologous recombination deficiency or BRCAness.
The coagulation factor XI (FXI) from the liver acts as an endocrine molecule in the heart, protecting it from heart failure. Scientists at the University of California, Los Angeles (UCLA) found that this communication between the two organs is mediated by the interaction between FXI and a heart protein. This interaction activated genes in cardiomyocytes that reduced inflammation, fibrosis and diastolic dysfunction, protecting the heart from a heart attack. That FXI participates in preventing heart failure suggests the possibility of using it as a therapeutic target.
A simple injection of muscle tissue could control glucose in patients with type 2 diabetes (T2D). Genetic modification of skeletal muscle and subsequent intramuscular implantation could increase blood sugar absorption and become an effective and long-lasting treatment for this pathology. “We took mice satellite cells and we genetically altered to overexpress GLUT4,” Hagit Shoyhet, researcher at the Levenberg lab of stem-cell and tissue engineering, Technion (Israel), said at the European Association for the study of Diabetes (EASD) 58th Annual Meeting.
Synthetic cells (SCs) armed with recombinant growth factors could contribute to tissue regeneration and healing by promoting angiogenesis. This technology opens the door to its application in other therapies such as transplants that require the remodeling or formation of new blood vessels. In addition, they mark the way to produce intracorporeal biological drugs or the inhibition of the angiogenesis process itself when it comes to blocking the irrigation of a tumor.
Scientists from the University of Lisbon have described how telomeres can establish the maximum damage that a cancer cell can suffer. Above this threshold, the cell would stop dividing and die. The damage comes from the transcription of the telomeres themselves of an RNA molecule called TERRA. When TERRA’s levels increase, the cell can no longer multiply. This mechanism occurs in ALT (alternative lengthening of telomeres) cells, which do not elongate their telomeres through telomerase.
Sex differences at the cellular level could explain why men respond less well to glioblastoma (GBM) treatments, according to a study led by the Washington University School of Medicine in St. Louis (WUSTL). The researchers found that male and female GBM tumor cells had different metabolic needs. GBM cells from male surgical samples absorbed more glutamine and had different nutritional preferences for amino acids.
A new study has unveiled the signaling cascade involved in the progression of brain metastasis from breast cancer. A family of connexins participates in the process that regulate the expression of laminins that favor metastatic cells to colonize the brain.
The design of genetically modified exosomes that combine multiple targets killed cancer cells and conferred immunity against them. Scientists at the University of Southern California (USC) applied bioengineering techniques to introduce up to four antitumor functions in the same type of extracellular vesicles and destroy EGFR-positive triple-negative breast cancer (TNBC) tumor cells.
A new vaccine that uses the native-like HIV-1 envelope (Env) trimer CH505 and a Toll-like receptor (TLR) 7/8 agonist adjuvant, successfully evaluated in macaques, generated potent polyclonal neutralizing antibodies (nAbs) and a high protection against the infection of the homologous simian-human immunodeficiency virus (SHIV).
Surviving apoptosis after administration of a drug triggered a previously unknown evolutionary process that gave tumor cells greater resistance to subsequent therapies. A cancer cell that does not die gets stronger. Cancer reappears with those cells that escape death thanks to a mechanism that, at the same time, offers a potential therapeutic target. According to a study led by St. Jude Children's Research Hospital in collaboration with the University of Glasgow and University of Oxford, the alternative to the cell death program is a stress response pathway that generates a persister cell phenotype not described before.
