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Category: biotech/medical – Page 48

MIT chemists synthesize a fungal compound that holds promise for treating brain cancer

“We have a much better appreciation for how those subtle structural changes can significantly increase the synthetic challenge,” says Mohammad Movassaghi, an MIT professor of chemistry. “Now we have the technology where we can not only access them for the first time, more than 50 years after they were isolated, but also we can make many designed variants, which can enable further detailed studies.”

In tests in human cancer cells, a derivative of verticillin A showed particular promise against a type of pediatric brain cancer called diffuse midline glioma. More tests will be needed to evaluate its potential for clinical use, the researchers say.

Genetic testing trifecta predicts risk of sudden cardiac death and arrhythmia

The study involving 1,119 participants will be published in Cell Reports Medicine.

Currently, genetic testing is divided into three distinct approaches:

In a new study, scientists have developed a more precise genetic risk score to determine whether a person is likely to develop arrhythmia, an irregular heartbeat that can lead to serious conditions such as atrial fibrillation (AFib) or sudden cardiac death.

Their approach not only improves the accuracy of heart disease risk prediction but also offers a comprehensive framework for genetic testing that, according to the scientists, could be applied to anything, including other complex, genetically influenced diseases like cancer, Parkinson’s Disease and autism.

“It’s a very cool approach in which we are combining rare gene variants with common gene variants and then adding in non-coding genome information. To our knowledge, no one has used this comprehensive approach before, so it’s really a roadmap of how to do that,” said co-corresponding author.

The Role of αvβ3 Integrin in Cancer Therapy Resistance

A relevant challenge for the treatment of patients with neoplasia is the development of resistance to chemo-, immune-, and radiotherapies. Although the causes of therapy resistance are poorly understood, evidence suggests it relies on compensatory mechanisms that cells develop to replace specific intracellular signaling that should be inactive after pharmacological inhibition. One such mechanism involves integrins, membrane receptors that connect cells to the extracellular matrix and have a crucial role in cell migration. The blockage of one specific type of integrin is frequently compensated by the overexpression of another integrin dimer, generally supporting cell adhesion and migration.

Mitochondrial Respiratory Supercomplex Assembly Factor COX7RP Contributes to Lifespan Extension in Mice

COX7RP is a critical factor that assembles mitochondrial respiratory chain complexes into supercomplexes, which is considered to modulate energy production efficiency. Whether COX7RP contributes to metabolic homeostasis and lifespan remains elusive. We here observed that COX7RP-transgenic (COX7RP-Tg) mice exhibit a phenotype characterized by a significant extension of lifespan. In addition, metabolic alterations were observed in COX7RP-Tg mice, including lower blood glucose levels at 120 min during the glucose tolerance test (GTT) without a significant difference in the area under the curve (AUC), as well as reduced serum triglyceride (TG) and total cholesterol (TC) levels. Moreover, COX7RP-Tg mice exhibited elevated ATP and nicotinamide adenine dinucleotide levels, reduced ROS production, and decreased senescence-associated β-galactosidase levels. Single-nucleus RNA-sequencing (snRNA-seq) revealed that senescence-associated secretory phenotype genes were downregulated in old COX7RP-Tg white adipose tissue (WAT) compared with old WT WAT, particularly in adipocytes. This study provides a clue to the role of mitochondrial respiratory supercomplex assembly factor COX7RP in resistance to aging and longevity extension.

Cancer-promoting DNA circles hitchhike on chromosomes to spread to daughter cells

Small, cancer-associated DNA circles “hitchhike” on chromosomes during cell division to spread efficiently to daughter cells by co-opting a process used to maintain cellular identity through generations, Stanford Medicine-led research has found.

These circles, known as extrachromosomal or ecDNA, are major drivers in human cancers. Blocking their ability to associate with chromosomes causes the loss of the circles during cell division and the death of lab-grown cancer cells. Targeting this weak link in the circles’ proliferation could lead to new classes of cancer therapies, the researchers predict.

“Unfortunately, ecDNAs have developed a crafty mechanism that allows them to wreak havoc on human health,” said professor of pathology Paul Mischel, MD. “They are using nature’s own method of gene expression and cell fate to ensure they are safely distributed into the next generation of cells and not lost into the cytoplasm or extracellular space when a cell divides.”

A BCL-xL/BCL-2 PROTAC effectively clears senescent cells in the liver and reduces MASH-driven hepatocellular carcinoma in mice

Yang, Jn-Simon, He et al. report that the dual BCL-xL/BCL-2 PROTAC 753b is a potent and liver-tropic senolytic, which (unlike other inhibitors of BCL-xL) does not cause severe thrombocytopenia. They evaluate its efficacy in natural aging and in reducing progression from steatotic liver disease to hepatocellular carcinoma, using mouse models.

Researchers confirm new Rickettsia species found in dogs

Researchers from North Carolina State University have confirmed that a species of Rickettsia first seen in dogs in 2018 is a new species of bacteria. The new species, dubbed Rickettsia finnyi, is associated with symptoms similar to those of Rocky Mountain spotted fever (RMSF) in dogs, but has not yet been found in humans.

The work appears in Emerging Infectious Diseases.

Rickettsia pathogens are categorized into four groups; of those, the spotted-fever group Rickettsia (which is transmitted by ticks) is the most commonly known and contains the most identified species. There are more than 25 species of tick-borne, spotted-fever group Rickettsia species worldwide, with R. rickettsii—which causes RMSF—being one of the most virulent and dangerous.

Cell nucleus shape may influence cancer treatment success

Cancer cells with a cell nucleus that is easily deformed are more sensitive to drugs that damage DNA. These are the findings of a new study by researchers at Linköping University in Sweden. The results may also explain why combining certain cancer drugs can produce the opposite of the intended effect. The study has been published in the journal Nature Communications.

A few years ago, a new type of drug was introduced that exploits deficiencies in cancer cells’ ability to repair damage to their DNA. These drugs, called PARP1 inhibitors, are used against cancers that have mutations in genes involved in DNA repair, such as the breast cancer gene 1 (BRCA1).

This gene has such a central role in the cell’s ability to repair serious DNA damage that mutations in it greatly increase the risk of developing cancer, often at a young age. The risk is so high that some women with a mutated BRCA1 gene choose to have their breasts and ovaries surgically removed to prevent cancer.

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