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Scientists develop off-the-shelf immunotherapy for ovarian cancer

Ovarian cancer is the leading cause of death among women with gynecological cancers. The current medical playbook—surgery followed by chemotherapy—initially shows promise. Tumors shrink, sometimes disappearing entirely. But in more than 80% of patients, the cancer not only comes back, but returns more aggressive and increasingly resistant to the very treatments that once seemed effective.

But now, there could be new hope. In a study published in the journal Med, UCLA researchers have detailed their development of a new type of immune cell , called CAR-NKT cell therapy, that could transform care by delivering superior cancer-fighting power.

“This is the culmination of over a decade of work in my lab and represents over six years of collaboration with gynecologic oncologist Dr. Sanaz Memarzadeh,” said co-senior author Lili Yang, a professor of microbiology, immunology and and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

New Study Suggests Cancer Drug Could Be Used to Target Protein Connection That Spurs Parkinson’s Disease

In studies with genetically engineered mice, Johns Hopkins Medicine researchers say they have identified a potentially new biological target involving Aplp1, a cell surface protein that drives the spread of Parkinson’s disease-causing alpha-synuclein.

The findings, published May 31 2024 in Nature Communications, reveal how Aplp1 connects with Lag3, another cell surface receptor, in a key part of a process that helps spread harmful alpha-synuclein proteins to brain cells. Those protein buildups are hallmarks of Parkinson’s disease.

Notably, the researchers say, Lag3 is already the target of a combination cancer drug approved by the U.S. Food and Drug Administration (FDA) that uses antibodies to “teach” the human immune system what to seek and destroy.

Adult Neurogenesis: Beyond Rats and Mice

Basically I believe that the flatworm could give the genetic code for essentially brain immortality other just nad plus. But it would have to be made in the brain and controlled possibly with nanotransfection which would scan the body and modify the human brain cells to have its characteristics that may already exist in the human brain also.


Powerful genetic tools in classical laboratory models have been fundamental to our understanding of how stem cells give rise to complex neural tissues during embryonic development. In contrast, adult neurogenesis in our model systems, if present, is typically constrained to one or a few zones of the adult brain to produce a limited subset of neurons leading to the dogma that the brain is primarily fixed post-development. The freshwater planarian (flatworm) is an invertebrate model system that challenges this dogma. The planarian possesses a brain containing several thousand neurons with very high rates of cell turnover (homeostasis), which can also be fully regenerated de novo from injury in just 7 days. Both homeostasis and regeneration depend on the activity of a large population of adult stem cells, called neoblasts, throughout the planarian body. Thus, much effort has been put forth to understand how the flatworm can continually give rise to the diversity of cell types found in the adult brain. Here we focus on work using single-cell genomics and functional analyses to unravel the cellular hierarchies from stem cell to neuron. In addition, we will review what is known about how planarians utilize developmental signaling to maintain proper tissue patterning, homeostasis, and cell-type diversity in their brains. Together, planarians are a powerful emerging model system to study the dynamics of adult neurogenesis and regeneration.

The adult brain has long been thought to be a fixed structure due to its immense complexity as is illustrated succinctly in the following quote from prominent nineteenth century neuroscientist and Nobel laureate Santiago Ramón y Cajal:

“Once the development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably. In the adult centers, the nerve paths are something fixed, ended, and immutable. Everything may die, nothing may be regenerated. It is for the science of the future to change, if possible, this harsh decree.”

Without Gene Therapies it Will Not be Possible to Extend Life | 071 Liz Parrish, Mba

Dr. Esra Çavuşoğlu, PhD’s 71st Ayık Kafa podcast guest is Liz Parrish explores the transformative potential of gene therapy in extending human longevity and enhancing healthspan.

Liz Parrish MBA, is the Founder and CEO of BioViva Sciences USA Inc. BioViva is committed to extending healthy lifespans using gene therapy and works on combinatorial gene therapies with its proprietary CMV gene therapy delivery platform.

Liz is a humanitarian, entrepreneur, author, and innovator. In addition, she is a proponent of the Best Choice Medicine plan (BCM), a more efficient and streamlined regulatory model around the use of genetic therapies.

She shares her personal journey, the scientific basis for gene therapy, and the economic implications of aging-related diseases. The podcast also takes a closer look at the four different gene therapies that Liz Parrish administered to herself: Klotho, Follistatin, PGC-1α, and Telomerase Reverse Transcriptase. The discussion covers the various gene therapies being developed, their safety, ethical considerations, and the importance of early intervention. Liz emphasizes the need for public awareness and investment in longevity research to make these therapies accessible to all.

#EsraÇavuşoğlu #AyıkKafa #ElevatingLifeEvolvingHealth #Longevilab #LizParrish #Longevity #genetherapy.

Liz Parrish:

EnsembleAge: enhancing epigenetic age assessment with a multi-clock framework

Several widely used epigenetic clocks have been developed for mice and other species, but a persistent challenge remains: different mouse clocks often yield inconsistent results. To address this limitation in robustness, we present EnsembleAge, a suite of ensemble-based epigenetic clocks. Leveraging data from over 200 perturbation experiments across multiple tissues, EnsembleAge integrates predictions from multiple penalized models. Empirical evaluations demonstrate that EnsembleAge outperforms existing clocks in detecting both pro-aging and rejuvenating interventions. Furthermore, we introduce EnsembleAge HumanMouse, an extension that enables cross-species analyses, facilitating translational research between mouse models and human studies. Together, these advances underscore the potential of EnsembleAge as a robust tool for identifying and validating interventions that modulate biological aging.

A Boost for the Precision of Genome Editing

The FDA’s recent approval of the first CRISPR-Cas9–based gene therapy has marked a major milestone in biomedicine, validating genome editing as a promising treatment strategy for disorders like sickle cell disease, muscular dystrophy, and certain cancers.

CRISPR-Cas9, often likened to “molecular scissors,” allows scientists to cut DNA at targeted sites to snip, repair, or replace genes. But despite its power, Cas9 poses a critical safety risk: the active enzyme can linger in cells and cause unintended DNA breaks—so-called off-target effects—which may trigger harmful mutations in healthy genes.

Now, researchers in the labs of Professor Ronald T. Raines (MIT Department of Chemistry) and Professor Amit Choudhary (Harvard Medical School) have engineered a precise way to turn Cas9 off after its job is done—significantly reducing off-target effects and improving the clinical safety of gene editing. Their findings are detailed in a new paper published this week in the Proceedings of the National Academy of Sciences (PNAS).


Researchers used cells that glow green due to a green fluorescent protein (GFP) gene. If Cas9 is working, it disrupts the GFP gene and the cells stop glowing. If LFN-Acr blocks Cas9, the cells keep glowing. These images depict cells in different conditions: some with active Cas9 (which stopped the green glow), some with Cas9 and LFN-Acr (glow stayed on).

Image courtesy of the researchers.

Lifestyle and environmental factors affect health and ageing more

A new study led by researchers from Oxford Population Health has shown that a range of environmental factors, including lifestyle (smoking and physical activity) and living conditions, have a greater impact on health and premature death than our genes.

The researchers used data from nearly half a million UK Biobank participants to assess the influence of 164 environmental factors and genetic risk scores for 22 major diseases on ageing, age-related diseases, and premature death. The study is published in Nature Medicine.

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