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Category: biotech/medical – Page 2

Researchers at the University of Oklahoma have made a discovery that could potentially revolutionize treatments for antibiotic-resistant infections, cancer and other challenging gram-negative pathogens without relying on precious metals.

Currently, precious metals like platinum and rhodium are used to create synthetic carbohydrates, which are vital components of many approved antibiotics used to combat , including Pseudomonas aeruginosa, a notorious hospital-acquired infection responsible for the deaths of immunocompromised patients. However, these elements require harsh reaction conditions, are expensive to use and are harmful to the environment when mined.

In an innovative study published in the journal Nature Communications, an OU team led by Professor Indrajeet Sharma has replaced these with either blue light or iron, achieving similar results with significantly lower toxicity, reduced costs, and greater appeal for researchers and .

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During viral infection, the innate immune system utilizes a variety of specific intracellular sensors to detect virus-derived nucleic acids and activate a series of cellular signaling cascades that produce type I IFNs and proinflammatory cytokines and chemokines. Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus that has been associated with a variety of human malignancies, including Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman disease. Infection with KSHV activates various DNA sensors, including cGAS, STING, IFI16, and DExD/H-box helicases. Activation of these DNA sensors induces the innate immune response to antagonize the virus. To counteract this, KSHV has developed countless strategies to evade or inhibit DNA sensing and facilitate its own infection. This review summarizes the major DNA-triggered sensing signaling pathways and details the current knowledge of DNA-sensing mechanisms involved in KSHV infection, as well as how KSHV evades antiviral signaling pathways to successfully establish latent infection and undergo lytic reactivation.

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A research team has unveiled a crucial mechanism that helps regulate DNA damage repair, with important implications for improving cancer treatment outcomes.

The result was published in Cell Death & Differentiation. The team was led by Professor Zhao Guoping at the Hefei Institutes of Physical Science of the Chinese Academy of Sciences.

The efficacy of radiotherapy is largely limited by the DNA damage repair capacity of tumor cells. When ionizing radiation induces DNA double-strand breaks—the primary lethal damage—tumor cells often exhibit abnormal overexpression of DNA repair proteins, establishing a robust damage response system that drives clinical radioresistance. To address this challenge, the team deciphered the regulatory network of epigenetic modifications in DNA damage repair.

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But classic risk factors do not seem to fully explain the recent rise in early-onset cancers, says Dr. Cathy Eng, director of the Young Adult Cancers Program at Vanderbilt University’s Ingram Cancer Center in Tennessee. Some of the trends are baffling; young, nonsmoking women, for example, are being diagnosed with lung cancer in strangely high numbers. Many times, Eng’s patients were extremely healthy: vegetarians, marathon runners, avid swimmers. “That’s why I really believe there’s other risk factors to account for this,” she says.

There’s no shortage of theories about what those may be. Many scientists point to modern diets, which tend to be heavy on potentially carcinogenic products—including ultra-processed foods, red meat, and alcohol—and may also contribute to weight gain, another cancer risk factor. The foods we eat can also affect the gut microbiome, the colony of microbes that lives in the digestive system and appears linked to overall health. Alterations to the gut microbiome via diet, or perhaps exposure to drugs like antibiotics, have also been implicated.

Other researchers blame the microplastics littering our environment and leaching into our food and water supplies, some of which, according to a 2024 study, have even shown up in cancer patients’ tumors. Other environmental factors could also be to blame, given that everything from cosmetics to food packaging contains substances that many researchers aren’t convinced are safe. Even our near constant exposure to artificial light could be messing with normal biological rhythms in ways that have profound health consequences, some research suggests.

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One of the challenges of fighting pancreatic cancer is finding ways to penetrate the organ’s dense tissue to define the margins between malignant and normal tissue. A new study uses DNA origami structures to selectively deliver fluorescent imaging agents to pancreatic cancer cells without affecting normal cells.

The study, led by University of Illinois Urbana-Champaign mechanical science and engineering professor Bumsoo Han and professor Jong Hyun Choi at Purdue University, found that specially engineered DNA origami structures carrying imaging dye packets can specifically target human KRAS mutant cancer cells, which are present in 95% of pancreatic cancer cases.

“This research highlights not only the potential for more accurate cancer imaging, but also selective chemotherapy delivery, a significant advancement over current pancreatic ductal adenocarcinoma treatments,” said Han, who is also affiliated with the Cancer Center at Illinois. “The current process of cancerous tissue removal through can be improved greatly by more accurate imaging of tumor margins.”

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Somewhere in the body of a patient, a small clump of cells, growing undetected, has begun to form a tumor. It has yet to cause pain or visible symptoms of illness. Several months from now, or perhaps years, those first signs will prompt a doctor’s inquiry, a referral to a specialist, and an eventual diagnosis. Treatment will depend on how long the cancer has gone unnoticed and how far it has spread.

There were early signs, though not ones the patient or doctor could have noticed. Small fragments of RNA, cast off from dying cells or spit out of the tumor’s twisted transcriptions, floating about in the bloodstream—early signals of a tissue in distress.

A new method developed by Stanford researchers aims to bring the moment of detection much closer to the beginning. They have developed a blood-based method called RARE-seq that detects tumor-derived cell-free RNA with around 50 times the sensitivity of standard sequencing techniques.

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Breast cancer is becoming increasingly treatable, but in some cases the disease can resurface even decades after a patient has been declared cancer free. This is because of cells that detach from the original tumor and hide in a dormant state in the breast or other organs.

Little is known about the mechanisms responsible for dormancy in , and even less is known about what causes these cells to suddenly wake up. A new study from the laboratory of Israel Prize laureate Prof. Yosef Yarden at the Weizmann Institute of Science, published in Science Signaling, reveals the mechanism that puts to sleep, as well as the reason that they emerge from dormancy more aggressive than they were before they became dormant.

From the earliest stage of embryonic development, through sexual maturation to the production of breast milk during pregnancy and after childbirth, breast tissue changes throughout a woman’s life. These changes are made possible by the metamorphosis that breast tissue cells undergo, from the early developmental stage, known as mesenchymal, when the cells are round, highly mobile and dividing rapidly, to the more mature, epithelial stage, when they are somewhat cubical, less active and dividing slowly.

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The pair decided to conduct a clinical trial that could be more compelling. In 12 people with early Alzheimer’s who took 3TC for 6 months, the drug didn’t boost cognitive abilities. But other indicators suggested some benefits, as Frost, Sullivan, and their colleagues revealed last month in npj Dementia. For instance, levels of one key neurodegeneration indicator dipped, suggesting 3TC protects patients’ brain cells. “That was the change I was most excited to see,” Frost says.

Their recent study was the first clinical test of an antitransposon strategy for Alzheimer’s to reach the finish line. But it’s just one of a growing number of trials launched by academic researchers and biotechs to gauge the effects of throttling transposons—so-called jumping genes. These vagrant sequences, some of which are relics of viruses that invaded cells long ago or may even be derived from symbiotic bacteria, make up more than 40% of the human genome but were once seen as largely harmless. However, a variety of evidence from human cell lines, lab animals, and epidemiological studies has implicated their antics in illnesses such as lupus, amyotrophic lateral sclerosis (ALS), Parkinson’s disease, and cancer, as well as in aging.

Encouraging results are trickling in. In 2022, a phase 2 trial determined that 3TC halted tumor growth in some patients with colorectal cancer. Last year, Transposon Therapeutics revealed that a different drug that stymies replication of these sequences slowed one sign of physical decline in people with ALS or another neurodegenerative disease, frontotemporal dementia. “It’s really amazing how quickly the story has developed,” says John Sedivy, a molecular biologist at Brown and the company’s co-founder.

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