tbuckley/cabot-search huggingface dataset:
Performance of whole genome sequencing for respiratory syncytial virus: insights from the first external quality assessment, France, 2024
Authors: Alice Moisan, Hadrien Regue, Yannis Rahou, Alexandre Gaymard, Antoine Oblette, Léa Avon, Nathalie Bergaud, Richard Chalvignac, Quentin Le Hingrat, Sonia Burrel, Aude Jary, Philippe Colson, Pierre Cappy, Luc Deroche, Véronique Brodard, Charlotte Pronier, Elodie Alessandri-Gradt, Maud Salmona, Lionel Chollet, Pauline Trémeaux, Lynda Handala, Slim Fourati, Bruno Lina, Jean-Sébastien Casalegno, Marie-Anne Rameix-Welti, Laurence Josset, Antonin Bal, Naël Zemali, Pantxika Bellecave, Lucie Mazarguil, Valentine Lesourd-Aubert, Stéphane Marot, Valentin Leducq, Théophile Cocherie, Antoine Fauchois, Vincent Calvez, Anne-Geneviève Marcelin, Nadhira Houhou, Romane Guilbaud, Thibault Saint-Joannis, Bernard La Scola, Céline Boschi, Sarah Seng, Arnaud Ly, Hélène Moret, Mme Magda Curci, Mme Marion Couteau, Claire Grolhier, Vincent Thibault, Mohamed Sassi, Chloé Dubus, Marie Leoz, Fanny Lermechain, Jean-Christophe Plantier, Fabienne Tombette, Nere Marie-Laure, Audrey Gabassi, Abdeljalil Senhaji Rachik, Sarah Mafi, Jérôme Le Goff, Thibault Guinoiseau, Yoan Laforgue, Sophie Trouillet Assant, Quentin Semanas, Gregory Destras, Jerome Bourret, Samar Berreira Ibraim, Emilie Yab, Emma Bezot, Florian Prejean, Cécile Poggi, Anne Lise Toyer, Marie Domine, Vincent Gardan, Romain Carcenac, Sofia Demmou, Justine Latour, Camille Vellas
Journal: Clinical Microbiology and Infection (2024)
Hippocampal avoidance prophylactic cranial irradiation (HA-PCI) for small cell lung cancer better preserves white matter networks compared to conventional PCI
Authors: R Colaes, J Blommaert, M Lambrecht, M B de Ruiter, P Pullens, D de Ruysscher, J Belderbos, S Sunaert, S B Schagen, S Deprez
Journal: Neuro-Oncology (2024)

Hippocampal avoidance during prophylactic cranial irradiation (HA-PCI) is proposed to reduce neurocognitive decline, while preserving the benefits of PCI. We evaluated whether (HA-)PCI induces changes in white matter (WM) microstructure and whether sparing the hippocampus has an impact on preserving brain network topology. Additionally, we evaluated associations between topological metrics with hippocampal volume and neuropsychological outcomes.
Hybrid Membrane Based Biomimetic Nanodrug with High-Efficient Melanoma-Homing and NIR-II Laser-Amplified Peroxynitrite Boost Properties for Enhancing Antitumor Therapy via Effective Immunoactivation
Authors: Qi Lin, Yu Zhang, Yina Zeng, Yongchao Zha, Wei Xue, Siming Yu
Journal: Biomaterials (2024)
Characterization of the first unambiguous HIV-1 CRF07_BC/CRF08_BC circulating recombinant form (CRF160_0708) in Yunnan, China
Authors: Min Chen, Yanling Ma, Huichao Chen, Jie Dai, Lijuan Dong, Manhong Jia, Wenfei Ding
Journal: Journal of Infection (2024)
Characterization of a new HIV-1 second-generation circulating recombinant form (CRF135_0107) and its next-generation recombinant in Heilongjiang, China
Authors: Qing-Hai Li, Yun-Qi Zhang, En-Long Li, Ran-Ran Lu, Xiao-Hong Chen, Fu-Xiang Wang, Jia-Ye Wang
Journal: Journal of Infection (2024)
Mutations in tumor suppressor genes Vhl and Rassf1a cause DNA damage, chromosomal instability and induce gene expression changes characteristic of clear cell renal cell carcinoma.
Authors: Antonella Catalano, Laura S Haas, Kyra Zodel, Mojca Adlesic, Francesca Cuomo, Asin Peighambari, Patrick Metzger, Hsin Huang, Stefan Haug, Anna Köttgen, Natalie Köhler, Melanie Boerries, Ian J Frew
Journal: Kidney International (2024)

RASSF1A is frequently biallelically inactivated in clear cell renal cell carcinoma (ccRCC) due to loss of chromosome 3p and promoter hypermethylation. Here we investigated the cellular and molecular consequences of single and combined deletion of the Rassf1a and Vhl tumor suppressor genes to model the common ccRCC genotype of combined loss of function of RASSF1A and VHL. In mouse embryonic fibroblasts and in primary kidney epithelial cells, double deletion of Rassf1a and Vhl caused chromosomal segregation defects and increased formation of micronuclei, demonstrating that pVHL and RASSF1A function to maintain genomic integrity. Combined Rassf1a and Vhl deletion in kidney epithelial cells in vivo increased proliferation and caused mild tubular disorganization, but did not lead to the development of kidney tumors. Single cell RNA-sequencing unexpectedly revealed that Rassf1a or Vhl deletion both induce the expression of an overlapping set of genes in a sub-population of proximal tubule cells. Many of these genes are also upregulated in the Vhl/Trp53/Rb1 deficient mouse model of ccRCC. In other subsets of proximal tubule cells, combined Vhl/Rassf1a deletion induced the expression of additional genes that were not upregulated in each of the single knockouts. The expression of the human homologues of Rassf1a-regulated genes correlate negatively with RASSF1 expression levels in human ccRCC. Our results suggest that the loss of RASSF1A function establishes a ccRCC-characteristic gene expression pattern.
Response to Kang et al.’s “Efficacy of low-dose oral minoxidil in the management of anticancer therapy-induced alopecia in patients with breast cancer: A retrospective cohort study”
Authors: Caitlin A Kearney, Anna L Brinks, Carli D Needle, Jerry Shapiro, Mario E Lacouture, Kristen I Lo Sicco
Journal: Journal of the American Academy of Dermatology (2024)
Non-V600E BRAF mutations and treatment for Hairy Cell Leukemia
Authors: Evgeny Arons, Chin-Hsien Tai, Joshi Suraj, Yuelin Liu, Chi-Ping Day, Mark Raffeld, Liqiang Xi, Mory Gould, Isaac David Shpilman, Christopher C. Oakes, Seema Ali Bhat, Michael Rhodes Grever, Daniel Jones, Kerry A Rogers, Hao-Wei Wang, Constance M Yuan, S. Cenk Sahinalp, Robert J. Kreitman
Journal: Blood (2024)

We found 18 patients with immunophenotype consistent with classic hairy cell leukemia (HCL) and BRAF mutations other than just V600E. Twelve had 1 non-V600E BRAF mutation and 6 had V600E with 1 (n=5) or 2 (n=1) non-V600E BRAF co-mutations.
Injection of ROS-Responsive Hydrogel Loaded with IL-1β-targeted nanobody for ameliorating myocardial infarction
Authors: Lu Wang, Changjiang Yu, Ting You, Xinkui Zhang, Haotao Su, Bihui Cao, Sainiwaer Anwaier, Hongmo Xiang, Chengming Dai, Xiang Long, Linjiang Han, Dengfeng Zhang, Junwei Wang, Peng Zhu, Xinjian Yan, Jialiang Liang, Zerui Chen, Huanlei Huang, Shuoji Zhu, Tucheng Sun, Jimei Chen, Ping Zhu
Journal: Bioactive Materials (2024)
A de novo gene promotes seed germination under drought stress in Arabidopsis
Authors: Guang-Teng Jin, Yong-Chao Xu, Xing-Hui Hou, Juan Jiang, Xin-Xin Li, Jia-Hui Xiao, Yu-Tao Bian, Yan-Bo Gong, Ming-Yu Wang, Zhi-Qin Zhang, Yong E Zhang, Wang-Sheng Zhu, Yong-Xiu Liu, Ya-Long Guo
Journal: Molecular Biology and Evolution (2024)

Abstract The origin of genes from non-coding sequences is a long-term and fundamental biological question. However, how de novo genes originate and integrate into the existing pathways to regulate phenotypic variations is largely unknown. Here, we selected seven genes from 782 de novo genes for functional exploration based on transcriptional and translational evidence. Subsequently, we revealed that SWK, a de novo gene that originated from a non-coding sequence in Arabidopsis thaliana, plays a role in seed germination under osmotic stress. SWK is primarily expressed in dry seed, imbibing seed and silique. SWK can be fully translated into an 8 kDa protein, which is mainly located in the nucleus. Intriguingly, SWK was integrated into an extant pathway of hydrogen peroxide content (folate synthesis pathway) via the upstream gene cytHPPK/DHPS, an Arabidopsis-specific gene that originated from the duplication of mitHPPK/DHPS, and downstream gene GSTF9, to improve seed germination in osmotic stress. In addition, we demonstrated that the presence of SWK may be associated with drought tolerance in natural populations of Arabidopsis. Overall, our study highlights how a de novo gene originated and integrated into the existing pathways to regulate stress adaptation.
Re: Michael Baboudjian, Hashim Hashim, Nikita Bhatt, et al. Summary Paper on Underactive Bladder from the European Association of Urology Guidelines on Non-neurogenic Male Lower Urinary Tract Symptoms. Eur Urol 2024;86:213–20
Authors: Aravindh Rathinam, Jonathan Katz, Robert Marcovich, Hemendra N Shah
Journal: European Urology (2024)
Corrigendum to “EGFR-targeted stearoyl gemcitabine nanoparticles show enhanced anti-tumor activity” [Journal of Controlled Release, 157 (2012), 287–296]
Authors: Michael A. Sandoval, Brian R. Sloat, Dharmika S.P. Lansakara-P, Amit Kumar, B. Leticia Rodriguez, Kaoru Kiguchi, John DiGiovanni, Zhengrong Cui
Journal: Journal of Controlled Release (2024)
ACK1/TNK2 kinase: molecular mechanisms and emerging cancer therapeutics
Authors: Dhivya Sridaran, Nupam P Mahajan
Journal: Trends in Pharmacological Sciences (2024)

Activated CDC42-associated kinase 1 (ACK1), encoded by the TNK2 gene, is a cytoplasmic non-receptor tyrosine kinase whose aberrant activation correlates positively with cancer severity. Recent research has revealed the functional relevance of this oncokinase - it is an epigenetic regulator that drives cancer progression in multiple malignancies. Although ACK1 is an attractive target for therapeutic intervention, incomplete knowledge of its diverse signaling mechanisms and the lack of specific inhibitors have challenged its clinical success. We summarize recent breakthroughs in understanding ACK1 regulation and cellular signaling, and shed light on its immunomodulatory role in balancing T cell activation. We provide a comprehensive overview of preclinical, proof-of-concept studies of potent ACK1-targeting small-molecule inhibitors that are expected to enter clinical trials for cancer patients.
Ru‐Ph Nanozyme‐Based Hydrogels for Tumor Chemodynamic Therapy by Enhancing Enzyme Catalytic Efficiency Through Multiple Pathways
Authors: Min Xiao, Yiqun Zhang, Jianghao Xing, Kun Qiao, Yuling Ba, Xianwen Wang, Song Gao, Zhennan Yuan
Journal: Advanced Healthcare Materials (2024)

Abstract The discovery of nanozymes has opened new possibilities for tumor therapy. However, their reliance on the tumor microenvironment and limited catalytic efficiency hinder broader applications. In this study, ruthenium‐phenanthroline nanoparticles (Ru‐Phs) are synthesized by combining ruthenium with phenanthroline and subsequently coloaded with the proton pump inhibitor (PPI) pantoprazole into sodium alginate (ALG) to form a Ru‐Phs‐PPI‐ALG hydrogel for in situ tumor therapy. This hydrogel demonstrates excellent chemodynamic properties, forming a gel within tumor tissues and gradually releasing Ru‐Phs, which generates highly toxic reactive oxygen species (ROS) via peroxidase‐like (POD‐like) activity. The inclusion of PPI reduced the intracellular pH of tumor cells, accelerating the Fenton reaction and ROS accumulation. Additionally, the high photothermal conversion efficiency of Ru‐Phs‐PPI‐ALG enables heat generation under near‐infrared (NIR) irradiation, which not only disrupts tumor cell structures but also further enhances the POD‐like catalytic activity of Ru‐Phs. The hydrogel effectively killed 4T1 cells in vitro, and transcriptomic analysis confirms its potent chemodynamic efficacy. In vivo experiments demonstrate significant tumor ablation and excellent biocompatibility. This multipathway strategy to increase enzyme activity and improve chemodynamic effects provides a promising approach for advancing nanozyme applications in tumor therapy.
Optimizing dosing in atopic dermatitis therapy: Looking for the cream of the crop
Authors: Jose Manuel Carrascosa
Journal: British Journal of Dermatology (2024)

Journal Article Accepted manuscript Optimizing dosing in atopic dermatitis therapy: Looking for the cream of the crop Get access Jose Manuel Carrascosa Jose Manuel Carrascosa Dermatology Department, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain Email:[email protected] https://orcid.org/0000-0003-4266-0771 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, ljae514, https://doi.org/10.1093/bjd/ljae514 Published: 25 December 2024 Article history Received: 20 December 2024 Accepted: 23 December 2024 Published: 25 December 2024
Early-life microRNA signatures in cord blood associated with allergic rhinitis and asthma development
Authors: Hooman Mirzakhani, Alberta L Wang, Rinku Sharma, Maoyun Sun, Ronald Panganiban, Quan Lu, Michael McGeachie, Zheng Lu, Augusto A Litonjua, Kelan G Tantisira, Scott T Weiss
Journal: Journal of Allergy and Clinical Immunology (2024)
The Hippo pathway: organ size control and beyond
Authors: Pengfei Guo, Sicheng Wan, Kun-Liang Guan
Journal: Pharmacological Reviews (2024)

The Hippo signaling pathway is a highly conserved signaling network for controlling organ size, tissue homeostasis, and regeneration. It integrates a wide range of intracellular and extracellular signals, such as cellular energy status, cell density, hormonal signals, and mechanical cues, to modulate the activity of YAP/TAZ transcriptional coactivators. A key aspect of Hippo pathway regulation involves its spatial organization at the plasma membrane, where upstream regulators localize to specific membrane subdomains to regulate the assembly and activation of the pathway components. This spatial organization is critical for the precise control of Hippo signaling, as it dictates the dynamic interactions between pathway components and their regulators. Recent studies have also uncovered the role of biomolecular condensation in regulating Hippo signaling, adding complexity to its control mechanisms. Dysregulation of the Hippo pathway is implicated in various pathological conditions, particularly cancer, where alterations in YAP/TAZ activity contribute to tumorigenesis and drug resistance. Therapeutic strategies targeting the Hippo pathway have shown promise in both cancer treatment, by inhibiting YAP/TAZ signaling, and regenerative medicine, by enhancing YAP/TAZ activity to promote tissue repair. The development of small molecule inhibitors targeting the YAP-TEAD interaction and other upstream regulators offers new avenues for therapeutic intervention. SIGNIFICANCE STATEMENT: The Hippo signaling pathway is a key regulator of organ size, tissue homeostasis, and regeneration, with its dysregulation linked to diseases such as cancer. Understanding this pathway opens new possibilities for therapeutic approaches in regenerative medicine and oncology, with the potential to translate basic research into improved clinical outcomes.
<i>Clostridioides difficile</i> binary toxin CDT induces biofilm-like persisting microcolonies
Authors: Jazmin Meza-Torres, Jean-Yves Tinevez, Aline Crouzols, Héloïse Mary, Minhee Kim, Lise Hunault, Susan Chamorro-Rodriguez, Emilie Lejal, Pamela Altamirano-Silva, Déborah Groussard, Samy Gobaa, Johann Peltier, Benoit Chassaing, Bruno Dupuy
Journal: Gut Microbes (2024)

Clinical symptoms of Clostridioides difficile infection (CDI) range from diarrhea to pseudomembranous colitis. A major challenge in managing CDI is the high rate of relapse. Several studies correlate the production of CDT binary toxin by clinical strains of C. difficile with higher relapse rates. Although the mechanism of action of CDT on host cells is known, its exact contribution to CDI is still unclear. To understand the physiological role of CDT during CDI, we established two hypoxic relevant intestinal models, Transwell and Microfluidic Intestine-on-Chip systems. Both were challenged with the epidemic strain UK1 CDT+ and its isogenic CDT- mutant. We report that CDT induces mucin-associated microcolonies that increase C. difficile colonization and display biofilm-like properties by enhancing C. difficile resistance to vancomycin. Importantly, biofilm-like microcolonies were also observed in the cecum and colon of infected mice. Hence, our study shows that CDT induces biofilm-like microcolonies, increasing C. difficile persistence and risk of relapse.
Silent circulation of plasmid-borne tet(X6) and blaOXA-58 genes in a community-acquired Acinetobacter baumannii strain
Authors: Huiqiong Jia, Qingchao Tong, Le Wang, Yuye Wu, Xinyang Li, Shuangshuang Li, Yingying Kong, Yingying Zhang, João Pedro Rueda Furlan, Nwai Oo Khine, Patrick Butaye, Jun Zhang, Qing Yang, Zhi Ruan
Journal: Drug Resistance Updates (2024)
AYVM to AYMM transition on HER2 exon 20 insertion induces TKI resistance in NSCLC
Authors: Shiqi Mao, Xinyu Liu, Lin Wang, Yan Wang, Shuo Yang, Tao Jiang, Xingya Li, Qiming Wang, Xuefei Li, Fengying Wu, Guanghui Gao, Xiaoxia Chen, Chunyan Wu, Wei Zhang, Jiao Zhang, Xiang Lin, Xiaoyu Zhu, Baobin Li, Fei Li, Caicun Zhou, Shengxiang Ren
Journal: Journal of Thoracic Oncology (2024)
Wip1 phosphatase activator QGC-8-52 specifically sensitizes p53-negative cancer cells to chemotherapy while protecting normal cells
Authors: Ke Wu, Xiao-Xiao Ge, Xiao-Fan Duan, Jie-Qing Li, Kun Wang, Qiao-Hong Chen, Zhi-Min Huang, Wei-Yan Zhang, Yong Wu, Qun Li
Journal: Drug Resistance Updates (2024)
Menin inhibitors in the treatment of acute myeloid leukemia
Authors: Gerwin A Huls, Carolien M Woolthuis, Jan Jacob Schuringa
Journal: Blood (2024)

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by the (oligo)clonal expansion of myeloid progenitor cells. Despite advances in treatment, AML remains challenging to cure, particularly in patients with specific genetic abnormalities. Menin inhibitors have emerged as a promising therapeutic approach, targeting key genetic drivers of AML such as KMT2A rearrangements and NPM1 mutations. Here, we review the clinical value of menin inhibitors, highlighting their mechanism of action, efficacy, safety, and potential to transform AML treatment.
Multiplex sample-sparing assay for detecting type-specific antibodies to Zika and dengue viruses: an assay development and validation study
Authors: Lindsay Dahora Hein, Izabella N Castillo, Freddy A Medina, Frances Vila, Bruno Segovia-Chumbez, Jorge L Muñoz-Jordán, Stephen S Whitehead, Laura E Adams, Gabriela Paz-Bailey, Aravinda M de Silva, Lakshmanane Premkumar
Journal: The Lancet Microbe (2024)
The Monogenic Landscape of Human Infectious Diseases
Authors: Stéphanie Boisson-Dupuis, Paul Bastard, Vivien Béziat, Jacinta Bustamante, Aurélie Cobat, Emmanuelle Jouanguy, Anne Puel, Jérémie Rosain, Qian Zhang, Shen-Ying Zhang, Bertrand Boisson
Journal: Journal of Allergy and Clinical Immunology (2024)
Esophageal epithelial Ikkβ deletion promotes eosinophilic esophagitis in experimental allergy mouse model
Authors: Margarette H Clevenger, Cenfu Wei, Adam L Karami, Lia E Tsikretsis, Dustin A Carlson, John E Pandolfino, Nirmala Gonsalves, Deborah R Winter, Kelly A Whelan, Marie-Pier Tétreault
Journal: Journal of Allergy and Clinical Immunology (2024)
CELL CYCLE DYSREGULATION IN CANCER
Authors: Antonino Glaviano, Samarendra K Singh, E Hui Clarissa Lee, Elena Okina, Hiu Yan Lam, Daniela Carbone, E Premkumar Reddy, Mark J O'Connor, Andrew Koff, Garima Singh, Justin Stebbing, Gautam Sethi, Karen Carmelina Crasta, Patrizia Diana, Khandan Keyomarsi, Michael B Yaffe, Seth A Wander, Aditya Bardia, Alan Prem Kumar
Journal: Pharmacological Reviews (2024)

Cancer is a systemic manifestation of aberrant cell cycle activity and dysregulated cell growth. Genetic mutations can determine tumor onset by either augmenting cell division rates or restraining normal controls such as cell cycle arrest or apoptosis. As a result, tumor cells not only undergo uncontrolled cell division but also become compromised in their ability to exit the cell cycle accurately. Regulation of cell cycle progression is enabled by specific surveillance mechanisms known as cell cycle checkpoints, and aberrations in these signaling pathways often culminate in cancer. For instance, DNA damage checkpoints, which preclude the generation and augmentation of DNA damage in the G1, S, and G2 cell cycle phases, are often defective in cancer cells, allowing cell division in spite of the accumulation of genetic errors. Notably, tumors have evolved to become dependent on checkpoints for their survival. For example, checkpoint pathways such as the DNA replication stress checkpoint and the mitotic checkpoint rarely undergo mutations and remain intact because any aberrant activity could result in irreparable damage or catastrophic chromosomal missegregation leading to cell death. In this review, we initially focus on cell cycle control pathways and specific functions of checkpoint signaling involved in normal and cancer cells and then proceed to examine how cell cycle control and checkpoint mechanisms can provide new therapeutic windows that can be exploited for cancer therapy. SIGNIFICANCE STATEMENT: DNA damage checkpoints are often defective in cancer cells, allowing cell division in spite of the accumulation of genetic errors. Conversely, DNA replication stress and mitotic checkpoints rarely undergo mutations because any aberrant activity could result in irreparable damage or catastrophic chromosomal missegregation, leading to cancer cell death. This review focuses on the checkpoint signaling mechanisms involved in cancer cells and how an emerging understanding of these pathways can provide new therapeutic opportunities for cancer therapy.
Shared molecular, cellular, and environmental hallmarks in cardiovascular disease and cancer: any place for drug repurposing?
Authors: Elisa Avolio, Barbara Bassani, Marzia Campanile, Khaled Ak Mohammed, Paola Muti, Antonino Bruno, Gaia Spinetti, Paolo Madeddu
Journal: Pharmacological Reviews (2024)

Cancer and cardiovascular disease (CVD) are the 2 biggest killers worldwide. Specific treatments have been developed for the 2 diseases. However, mutual therapeutic targets should be considered because of the overlap of cellular and molecular mechanisms. Cancer research has grown at a fast pace, leading to an increasing number of new mechanistic treatments. Some of these drugs could prove useful for treating CVD, which realizes the concept of cancer drug repurposing. This review provides a comprehensive outline of the shared hallmarks of cancer and CVD, primarily ischemic heart disease and heart failure. We focus on chronic inflammation, altered immune response, stromal and vascular cell activation, and underlying signaling pathways causing pathological tissue remodeling. There is an obvious scope for targeting those shared mechanisms, thereby achieving reciprocal preventive and therapeutic benefits. Major attention is devoted to illustrating the logic, advantages, challenges, and viable examples of drug repurposing and discussing the potential influence of sex, gender, age, and ethnicity in realizing this approach. Artificial intelligence will help to refine the personalized application of drug repurposing for patients with CVD. SIGNIFICANCE STATEMENT: Cancer and cardiovascular disease (CVD), the 2 biggest killers worldwide, share several underlying cellular and molecular mechanisms. So far, specific therapies have been developed to tackle the 2 diseases. However, the development of new cardiovascular drugs has been slow compared with cancer drugs. Understanding the intersection between pathological mechanisms of the 2 diseases provides the basis for repurposing cancer therapeutics for CVD treatment. This approach could allow the rapid development of new drugs for patients with CVDs.