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Antisense oligonucleotides (ASOs) are a new generation of drugs that can treat human diseases by blocking the transmission of harmful information from the body's genes. In cancer patients, ASOs have the potential to block messages that drive tumors to grow and spread. However, ASOs have not yet been used to treat human cancer. First, they must be transported into cancer cells, but the cancer cells will not let them in.
Recently, a research team at the Massachusetts Institute of Technology (MIT) developed a new method that uses light signals instead of electrical signals to stimulate muscles. Compared to electrical stimulation, this optogenetic technology provides more precise muscle control while significantly reducing muscle fatigue. Relevant research was recently published in the journal Science Robotics, titled "Closed-loop optogenetic neuromodulation enables high-fidelity fatigue-resistant muscle control."
In a new study, researchers from the Johns Hopkins University School of Medicine used human breast and lung cells to map a molecular pathway that tricks the cells into taking a dangerous path. That is, making too many copies of their genome, which is a characteristic of cancer cells. The discovery sheds light on what can go wrong when a group of molecules and enzymes trigger and regulate what's called the cell cycle. They believe their findings could be used to develop therapies that interrupt cell cycle disorders and potentially halt cancer growth. Relevant research results were recently published in the journal Science. The paper is titled "CDK4/6 activity is required during G2 arrest to prevent stress-induced endoreplication".
As understanding of immune activity at the tumor site increases, immunotherapy has received widespread attention as an effective cancer treatment strategy, leading to a major shift in cancer research and clinical trials. The main purpose of tumor immunotherapy is to stimulate host anti-tumor immunity, establish an immune-sensitive microenvironment, and ultimately achieve tumor shrinkage while improving the overall survival rate of patients.
Cancer has a profound impact on human life, and immune checkpoint therapy (ICT) has made significant progress in cancer therapy. However, ICT will face various consequences, such as lower overall response rate and immune-related adverse events. To overcome these obstacles, researchers have been exploring novel immune checkpoints. CD300A is a type I transmembrane protein that carries an immunoreceptor tyrosine-based inhibitory motif. It can serve as a potential immune checkpoint and negatively regulate the function of NK cells through its interaction with phosphatidylserine.
A specific genetic change called an ALK fusion causes non-small cell lung cancer (NSCLC) in some patients. This abnormality causes the ALK protein to be overactive. These tumors can be treated with ALK inhibitors, but the cancer cells quickly develop resistance. Now, in a new study, researchers from the German Cancer Research Center have demonstrated in mouse and human tumor cells that simultaneous treatment with ALK and SRC inhibitors can improve the therapeutic response of lung cancer cells and delay the development of drug resistance. This combination therapy, which strongly interferes with the protein composition of cancer cells, could improve clinical outcomes in some forms of non-small cell lung cancer. Relevant research results were recently published in Drug Resistance Updates. The paper is titled "Concurrent inhibition of ALK and SRC kinases disrupts the ALK lung tumor cell proteome."
CDK4/6 inhibitors (CDK4/6i, CDK4/6 inhibitors) can improve the survival rate of patients with estrogen receptor-positive (ER+) breast cancer. However, patients treated with CDK4/6i eventually develop drug tolerance and disease progression. Loss-of-function alterations in RB1 confer resistance to CDK4/6i, but optimal therapies for these patients have yet to be developed.
Nuclear factor κB (NF-κB) plays an important role in the occurrence of various human diseases. Various inflammatory signals, including circulating lipopolysaccharides (LPSs), can activate the expression of NF-κB through special receptors. Recently, in a research report titled "Positive selection CRISPR screens reveal a druggable pocket in an oligosaccharyltransferase required for inflammatory signaling to NF-κB" published in the international journal Cell, scientists from Dana-Farber Cancer Institute and other institutions are expected to help develop new targeted therapies to inhibit the activation of NF-κB.
Researchers from Shanghai Jiao Tong University in China recently published a research paper titled "Dendritic-cell-targeting virus-like particles as potent mRNA vaccine carriers" online in Nature Biomedical Engineering. This study reports the design and performance of a virus-like particle targeting dendritic cells (DCs). The particles feature the Sindbis viral glycoprotein engineered to recognize surface proteins on DCs and package mRNA encoding the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein or herpes simplex virus 1 glycoproteins B and D.
Bejamine Deverman's team at the Broad Institute recently published a research paper titled "An AAV capsid reprogrammed to bind human transferrin receptor mediates brain-wide gene delivery" online in Science. The study designed an AAV capsid, BI-hTFR1, that binds to the human transferrin receptor (TfR1), a protein expressed on the blood-brain barrier (BBB). Compared with AAV9, BI-hTFR1 has a higher active transport capacity across the human brain endothelial cell layer and provides a 40-50-fold enhancement of reporter gene expression in the CNS of mice carrying a human TFRC knock-in. This enhanced tropism is CNS specific and is not present in wild-type mice.
