Researchers at Science Tokyo have identified two separate stem cell lineages responsible for forming tooth roots and the alveolar bone that anchors teeth in the jaw.
By using genetically modified mice and lineage-tracing methods, the team uncovered how specific signaling pathways direct stem cells to specialize during tooth development. Their findings provide valuable insight that could help advance the field of regenerative dentistry in the future.
Our skin protects us from everyday mechanical stresses, like friction, cuts, and impacts. A key part of this function—standing as a bulwark against the outside world—is the skin’s amazing ability to regenerate and heal. But where does this healing ability begin?
In a new study published in Nature Communications, an interdisciplinary team led by the laboratories of Kaelyn Sumigray, Ph.D., and Stefania Nicoli, Ph.D., discovered that, during the earliest stages of embryonic development, skin stem cells contribute to forming a protective skin layer that accelerates healing as the embryo grows.
Their findings reveal one of the earliest steps in how skin stem cells learn to repair tissue—knowledge that could help engineer improved skin grafts for transplantation.
Researchers at McMaster University and the Massachusetts Institute of Technology (MIT) have made two scientific breakthroughs at once: they not only discovered a brand-new antibiotic that targets inflammatory bowel diseases (IBD), but also successfully used a new type of AI to predict exactly how the drug works. To their knowledge, this is a global first for the AI.
Detailed in the journal Nature Microbiology, the discovery unveils a promising new treatment option for millions of people affected by Crohn’s disease and other related conditions, while also showcasing important new applications for AI in drug discovery research.
“This work shows that we’re still just scratching the surface as far as AI-guided drug discovery goes,” says Jon Stokes, an assistant professor in McMaster’s Department of Biochemistry and Biomedical Sciences and principal investigator on the new study.
Cancer is a challenging enough diagnosis, but many patients are dealt a second blow, even as they heal: “chemo brain.”
Also called “brain fog,” this mix of cognitive issues— memory problems, struggling to find words, an inability to concentrate—affects up to three-in-four cancer patients, according to multiple studies. For many, the effects last years beyond cancer treatment.
A new study offers new models for studying causes of chemo brain and points to the effects of chemotherapy drugs on the brain’s lymphatic system, which is a network of tiny vessels in the brain’s protective membranes that help remove waste and transport immune cells. The study was published Oct. 13 in Communications Biology.
Cutaneous squamous cell carcinoma (CSCC) is a prevalent skin cancer with aggressive progression that poses significant challenges, especially in metastatic cases. Single-cell DNA sequencing (scDNA-seq) has become an advanced technology for elucidating tumor heterogeneity and clonal evolution. However, comprehensive scDNA-seq studies and tailored mutation panels for CSCC are lacking.
We analyzed the genomic landscape of Chinese CSCC patients via a Multi-Patient-Targeted (MPT) scDNA-seq approach. This method combined bulk exome sequencing with Tapestri scDNA-seq. Mutations identified through bulk sequencing were used to design a targeted panel for scDNA-seq. Comparative analysis was conducted to explore the associations between specific gene mutations and clinical characteristics such as tumor stage and patient sex. Clonal evolution analysis was performed to understand the evolutionary trajectories of the tumors.
Bulk sequencing revealed a diverse spectrum of somatic mutations in CSCC tumors, with missense mutations being predominant. The top tumor mutations, such as those in NOTCH1, TP53, NOTCH2, TTN, MUC16, RYR2, PRUNE2, DMD, HRAS, and CDKN2A, presented similar frequencies to those reported in studies in Korean and Caucasian populations. However, the mutation frequencies of HRAS, TTN, MUC16 and MUC4 were significantly different from the Korean and Caucasian populations. Comparative analysis revealed associations between specific gene mutations and clinical characteristics such as tumor stage and patient sex. Clonal evolution analysis via scDNA-seq revealed distinct evolutionary trajectories and their potential correlation with tumor development and patient prognosis. Furthermore, scDNA-seq identified two low-frequency mutation clones, NLRP5 and HMMR, which play important roles in the clonal evolution of CSCC.
A research team at CiQUS (University of Santiago de Compostela, Spain) has unveiled an innovative molecular approach that enables anticancer drugs to reach the nucleus of tumor cells, where they can exert their therapeutic effect. The study focused on doxorubicin, a widely used chemotherapy agent. Prolonged exposure to this drug often leads to the emergence of resistant cells, a major clinical challenge that this strategy successfully overcomes while preserving the drug’s antitumor activity.
The approach builds on a simple but powerful concept: the ability of cyclic peptides —small amino acid rings— to stack and self-assemble into hollow cylindrical structures (nanotubes) on the surface of cancer cell membranes. The system, developed by the team led by Juan R. Granja, couples doxorubicin to these peptides and directs it to the cell nucleus through a delivery pathway that differs from the drug’s usual mechanism. This allows the drug to bypass the cellular resistance mechanisms that would normally deactivate it.
Compared with healthy cells, cancer cell membranes contain higher levels of negatively charged lipids. The cyclic peptides used in this study display a strong affinity for these anionic surfaces, facilitating their interaction with tumor cells. As a result, the peptide–drug conjugates enter resistant cells and travel towards the nucleus, where doxorubicin intercalates with DNA to trigger its cytotoxic effect.
Cellular senescence occurs in response to endogenous or exogenous stresses and is characterized by stable cell cycle arrest, alterations in nuclear morphology and secretion of proinflammatory factors, referred to as the senescence-associated secretory phenotype (SASP). An increase of senescent cells is associated with the development of several types of cancer and aging-related diseases. Therefore, senolytic agents that selectively remove senescent cells may offer opportunities for developing new therapeutic strategies against such cancers and aging-related diseases. This review outlines senescence inducers and the general characteristics of senescent cells. We also discuss the involvement of senescent cells in certain cancers and diseases. Finally, we describe a series of senolytic agents and their utilization in therapeutic strategies.
Predicting future tumor growth from initial imaging of incidentally discovered meningioma (IDM) could inform treatment decisions. However, most factors identified in prior studies on meningioma growth are qualitative. The aim of this study is to identify factors associated with tumor growth using quantitative radiomics features from MRI data.
MRI T2 features from initial imaging of 24 tumor growth cases were compared with those of 25 cases without growth. An in-house program was developed to reduce the time required for data analysis. This program is based on the open-source software 3D Slicer 5.6.2 and PyRadiomics 3.1.0. It enables semi-automatic batch t-test analyses for each feature to compare tumor growth and non-growth groups. Regions of interest (ROIs) were placed in the tumor, outer tumor edge, whole brain, and white matter contralateral to the tumor. A total of 107 features were analyzed across seven classifications: First Order, Shape, Gray Level Co-occurrence Matrix, Gray Level Run Length Matrix, Gray Level Size Zone Matrix, Gray Level Dependence Matrix, and Neighboring Gray Tone Difference Matrix. A t-test was used to identify significant predictors.
Ten features across five classifications showed significant differences (p 0.05): 2 First Order statistics, 2 Shape features, 4 Gy Level Co-occurrence Matrices, 1 Gy Level Size Zone Matrix, and 1 Neighboring Gray Tone Difference Matrix.
The cells in the human body are continuously challenged by a variety of genotoxic attacks. Erroneous repair of the DNA can lead to mutations and chromosomal aberrations that can alter the functions of tumor suppressor genes or oncogenes, thus causing cancer development. As a central tumor suppressor, p53 guards the genome by orchestrating a variety of DNA-damage-response (DDR) mechanisms. Already early in metazoan evolution, p53 started controlling the apoptotic demise of genomically compromised cells. p53 plays a prominent role as a facilitator of DNA repair by halting the cell cycle to allow time for the repair machineries to restore genome stability. In addition, p53 took on diverse roles to also directly impact the activity of various DNA-repair systems. It thus appears as if p53 is multitasking in providing protection from cancer development by maintaining genome stability.