Lifeboat Foundation

OneSkin, founded by Brazilian PhD scientists in 2016, reports that it has now closed a Series A funding round led by Selva Ventures, together with contributions from PLUS Capital, Unilever Ventures, Able Partners, SOSV, and Meta Planet. This brings the accumulated capital of the firm to 20 million US dollars.

The goal of the OneSkin team is the research and development of topical treatments that promote skin longevity. The brand’s efforts have led to the development of the peptide OS-01, which is claimed to reverse the aging of the skin by preventing the accumulation of “old”, non-dividing senescent cells, as well as shield skin cells from DNA damage. OS-01 is already available on the market in several different products offered by the company.

Senescent cells have been the focus of a significant amount of biogerontological research in recent years. Scientists claim that every cell in the human body has a limited capacity for division, governed by genetic factors. When the cells reach the point in their lifecycle where their ability to divide is permanently halted, they remain in a minimally-functional state in the tissue types they inhabit.

Skull bone marrow expands during adult life, exhibits lifelong vascular growth and increases its haematopoietic potential during ageing.

A new drug strategy that regulates the tumor immune microenvironment may transform a tumor that resists immunotherapy into a susceptible one, according to a study by researchers from the Johns Hopkins Kimmel Cancer Center and Oregon Health & Science University.

The immune microenvironment around a pancreatic tumor has suppressed immune activity, allowing the tumor to evade attacks by the immune system. The cancer evades the immune system by attracting suppressive cells into the tumor, which limits access of tumor-killing T cells. Because of that so-called immune desert environment, pancreatic ductal adenocarcinoma (PDA), the most common type of pancreatic cancer, has been resistant to immune-based therapies that have successfully treated a variety of other cancers, including melanoma and lung cancer.

In a phase 2 clinical trial, a research team led by Nilofer Azad, M.D., professor of oncology and co-leader of the Kimmel Cancer Center’s Cancer Genetics and Epigenetics Program, and Marina Baretti, M.D., the Jiasheng Chair in Hepato-Biliary Cancer at the Kimmel Cancer Center, tested the safety and efficacy of the combination of two drugs: an immunotherapy, nivolumab, and an epigenetic drug, entinostat — a histone deacetylase inhibitor (HDACi). The combination was studied in a group of 27 patients with advanced PDA who had previously been treated with chemotherapy.

As people who research aging like to quip, the best thing you can do to increase how long you live is to pick good parents. After all, it has long been recognized that longer-lived people tend to have longer-lived parents and grandparents, suggesting that genetics influence longevity.

Complicating the picture, however, is that we know that the sum of your lifestyle, specifically diet and exercise, also significantly influences your health into older age and how long you live. What contribution lifestyle versus genetics makes is an open question that a recent study in Nature has shed new light on.

Scientists have long known that reducing calorie intake can make animals live longer. In the 1930s, it was noted that rats fed reduced calories lived longer than rats who could eat as much as they wanted. Similarly, people who are more physically active tend to live longer. But specifically linking single genes to longevity was until recently a controversial one.

Microbial systems have been synthetically engineered to deploy therapeutic payloads in vivo.

To enable effective cancer vaccination, we developed an engineered bacterial system in probiotic Escherichia coli Nissle 1917 (EcN) to enhance expression, delivery and immune-targeting of arrays of tumour exonic mutation-derived epitopes highly expressed by tumour cells and predicted to bind major histocompatibility complex (MHC) class I and II (Fig. 1a). This system incorporates several key design elements that enhance therapeutic use: optimization of synthetic neoantigen construct form with removal of cryptic plasmids and deletion of Lon and OmpT proteases to increase neoantigen accumulation, increased susceptibility to phagocytosis for enhanced uptake by antigen-presenting cells (APCs) and presentation of MHC class II-restricted antigens, expression of listeriolysin O (LLO) to induce cytosolic entry for presentation of recombinant encoded neoantigens by MHC class I molecules and T helper 1 cell (T_H1)-type immunity and improved safety for systemic administration due to reduced survival in the blood and biofilm formation.

To assemble a repertoire of neoantigens, we conducted exome and transcriptome sequencing of subcutaneous CT26 tumours. Neoantigens were predicted from highly expressed tumour-specific mutations using established methods^14,15, with selection criteria inclusive of putative neoantigens across a spectrum of MHC affinity^16,17. Given the importance of both MHC class I and MHC class II binding epitopes in antitumour immunity^15,18,19, we integrated a measure of wild-type-to-mutant MHC affinity ratio—termed agretopicity^17,20—for both epitope types derived from a given mutation, to help estimate the ability of adaptive immunity to recognize a neoantigen. Predicted neoantigens were selected from the set of tumour-specific mutations satisfying all criteria, notably encompassing numerous recovered, previously validated CT26 neoantigens¹⁵ (Extended Data Fig. 1a).

Continue reading “Probiotic neoantigen delivery vectors for precision cancer immunotherapy” »

Google DeepMind has unexpectedly released the source code and model weights of AlphaFold 3 for academic use, marking a significant advance that could accelerate scientific discovery and drug development. The surprise announcement comes just weeks after the system’s creators, Demis Hassabis and John Jumper, were awarded the 2024 Nobel Prize in Chemistry for their work on protein structure prediction.

AlphaFold 3 represents a quantum leap beyond its predecessors. While AlphaFold 2 could predict protein structures, version 3 can model the complex interactions between proteins, DNA, RNA, and small molecules — the fundamental processes of life. This matters because understanding these molecular interactions drives modern drug discovery and disease treatment. Traditional methods of studying these interactions often require months of laboratory work and millions in research funding — with no guarantee of success.

Continue reading “Google DeepMind open-sources AlphaFold 3, ushering in a new era for drug discovery and molecular biology” »

How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.

The authors have declared no competing interest.

Surprising findings on bacterial aging have emerged from a study carried out by a team of researchers led by the biologist Dr. Ulrich Steiner at Freie Universität Berlin. In a new paper published in Science Advances, the team demonstrated that even genetically identical bacterial cells living in the same environment react differently to the aging process and that changes occur at different rates within different regions of the cell.

Scientists from Vilnius University’s (VU) Life Sciences Center (LSC) have discovered a unique way for cells to silence specific genes without cutting DNA. This research, led by Prof. Patrick Pausch and published in the journal Nature Communications, reveals a new way to silence genes that is akin to pressing a “pause” button on certain genetic instructions within cells.