Genomic Screening Research Articles

Advances in CRISPR-enabled genome-wide screens in yeast.

CRISPR-Cas genome-wide screens are powerful tools for unraveling genotype-phenotype relationships, enabling precise manipulation of genes to study and engineer industrially-useful traits. Traditional genetic methods, such as random mutagenesis or RNA interference, often lack the specificity and scalability required for large-scale functional genomic screens. CRISPR systems overcome these limitations by offering precision gene targeting and manipulation, allowing for high-throughput investigations into gene function and interactions. Recent work has shown that CRISPR genome editing is widely adaptable to several yeast species, many of which have natural traits suited for industrial biotechnology. In this review, we discuss recent advances in yeast functional genomics, emphasizing advancements made with CRISPR tools. We discuss how the development and optimization of CRISPR genome-wide screens have enabled a host-first approach to metabolic engineering, which takes advantage of the natural traits of non-conventional yeast - fast growth rates, high stress tolerance, and novel metabolism - to create new production hosts. Lastly, we discuss future directions, including automation and biosensor-driven screens, to enhance high-throughput CRISPR-enabled yeast engineering.

Genomic Screening at a Single Health System

Completion of the Human Genome Project prompted predictions that genomics would transform medicine, including through genomic screening that identifies potentially medically actionable findings that could prevent disease, detect it earlier, or treat it better. However, genomic screening remains anchored in research and largely unavailable as part of routine care. To summarize 11 years of experience with genomic screening and explore the landscape of genomic screening efforts. This cohort study was based in Geisinger's MyCode Community Health Initiative, a genomic screening program in a rural Pennsylvania health care system in which patient-participants exomes are analyzed. Genomic screen-positive rates were evaluated and stratified by condition type (cancer, cardiovascular, other) and US Centers for Disease Control and Prevention (CDC) Tier 1 designation. The proportion of participants previously unaware of their genomic result was assessed. Other large-scale population-based genomic screening efforts with genomic results disclosure were compiled from public resources. A total of 354 957 patients participated in Geisinger's genomic screening program (median [IQR] age, 54 [36-69] years; 194 037 [59.7%] assigned female sex at birth). As of June 2024, 175 500 participants had exome sequencing available for analysis, and 5934 participants (3.4%) had a pathogenic variant in 81 genes known to increase risk for disease. Between 2013 and July 2024, 5119 results were disclosed to 5052 eligible participants, with 2267 (44.2%) associated with risk for cardiovascular disease, 2031 (39.7%) with risk for cancer, and 821 (16.0%) with risk for other conditions. Most results (3040 [59.4%]) were in genes outside of those with a CDC Tier 1 designation. Nearly 90% of participants (4425 [87.6%]) were unaware of their genomic risk prior to disclosure. In a survey of large-scale biobanks with genomic and electronic health record (EHR) data, only 25.0% (6 of 24) disclosed potentially actionable genomic results. In this large, genomics-informed cohort study from a single health system, 1 in 30 participants had a potentially actionable genomic finding. However, nearly 90% were unaware of their risk prior to screening, demonstrating the utility of genomic screening in identifying at-risk individuals. Most large-scale biobanks with genomic and EHR data did not return genomic results with potential medical relevance, missing opportunities to significantly improve genomic risk ascertainment for these individuals and to perform longitudinal studies of clinical and implementation outcomes in diverse settings.

Nanopore sequencing technology in clinical diagnostics and genomic research: Opportunities and challenges

Nanopore sequencing technology, an advanced third-generation sequencing technology, is a revolutionary sequencing method widely used in clinical diagnosis and genomic research because of its features such as real-time sequencing, direct sequencing, long read length and portability. This paper outlines the basic principles and advantages of the technology, and briefly introduces its applications in clinical medicine such as diagnosis of diseases rare and genetic diseases, detection of infectious disease pathogens, public health emergency response, and cancer genomics screening. In genomics, nanopore sequencing is instrumental in genome assembly, structural variation detection, recovery of DNA from ancient organisms, and microbiological research. It enables direct sequencing and analysis of molecules, allowing for the identification of complex structural variations within the genome. This study finds that the technology also suffers from low accuracy, high cost associated with large data volumes, and significant requirements for data processing capabilities. These limitations can potentially be addressed through innovations such as improved nanopore materials and design, and integration with artificial intelligence. Finally, the latest innovations of the technology are analyzed, and the development trend and application prospects are outlooked.

Lytic coelomocyte death is tuned by cleavage but not phosphorylation of MLKL in echinoderms.

Lytic cell death including necroptosis and pyroptosis is induced by mixed lineage kinase domain-like protein (MLKL) phosphorylation and inflammatory caspase specific cleavage Gasdermins in higher mammals, respectively. In this study, we identified a novel MLKL homolog containing a tetrapeptide recognition motif (14-LVAD-17) of inflammatory caspase from Apostichopus japonicus,which was absent of Gasdermins member by genome screening. Functional analysis revealed that AjMLKL was involved in the regulation of Vibrio splendidus AJ01 infection induced lytic coelomocyte death in a cleavage-dependent manner, but not through RIPK3-dependent phosphorylation as mammals. Mechanistically, the activated form of cysteine-aspartic specific proteases-1 (AjCASP-1) bound to the tetrapeptide site of AjMLKL and cleaved it at Asp17. Cleaved AjMLKL18-491 displayed higher binding affinities towards phosphatidylinositol phosphate and cardiolipin compared to those of un-cleaved form. In addition, cleaved AjMLKL18-491 exerted stronger ability in disrupting the membrane integrity of liposome. More importantly, AjMLKL18-491 caused a large non-selective ionic coelomocyte pore and could directly kill the invasive AJ01. Moreover, activation of inflammatory AjCASP-1 was further found to be dependent on forming an inflammasome-like complex via CASc domain of AjCASP-1 and the N-terminal Ig domains of internalized AjNLRC4. All our results proved first evidence that lytic cell death was activated through MLKL cleavage, not MLKL phosphorylation in echinoderm, which offered insights into the functional, evolutionary mechanisms of lytic cell death in invertebrates.

Comprehensive genomic dependency landscape of a human colon cancer organoid

Identifying genetic dependencies in human colon cancer could help identify effective treatment strategies. Genome-wide CRISPR-Cas9 dropout screens have the potential to reveal genetic dependencies, some of which could be exploited as therapeutic targets using existing drugs. In this study, we comprehensively characterized genetic dependencies present in a colon cancer organoid avatar, and validated tumor-specific selectivity of select pharmacologic agents. We conducted a genome-wide CRISPR dropout screen to elucidate the genetic dependencies that interacted with select driver somatic mutations. We found distinct genetic dependencies that interacted with WNT, MAPK, PI3K, TP53, and mismatch repair pathways and validated targets that could be exploited as treatments for this specific subtype of colon cancer. These findings demonstrate the utility of functional genomic screening in the context of personalized medicine.

The acceptability of blood spot screening and genome sequencing in newborn screening: a systematic review examining evidence and frameworks.

Population-wide newborn blood spot screening programmes are a successful public health intervention used to detect whether the baby is at risk of certain rare conditions, with the aim of earlier diagnosis and provision of optimal care and treatment. Evaluating candidate conditions to include in newborn blood spot and genetic sequencing raises questions regarding acceptability to parents/carers. In the context of the possible expansion of the newborn blood spot screening programme in the United Kingdom, this review aimed to systematically review research on the acceptability to parents of newborn blood spot screening and genetic sequencing. A protocol was developed prior to commencing the review and was registered on the PROSPERO database. A team of researchers carried out the review, with checking at all stages carried out by at least two individuals. We included research published after 2013 with participants who were pregnant or a recent parent of a newborn and were resident in a high-income country. We included quantitative and qualitative studies that investigated the acceptability to parents/carers of newborn blood spot screening or genetic sequencing. Quantitative studies were narratively synthesised, and theories/frameworks identified and evaluated. Qualitative studies were analysed for recurring themes, and a meta-synthesis was carried out to compare and contrast these two types of data. We quality appraised included articles using tools appropriate for their study design. Searches were carried out in September to November 2023 and screening identified 25 relevant research articles. Just over half were from North America, with four existing reviews and nine qualitative studies. Domains of acceptability described in the literature were: support for screening; level of anxiety, information and knowledge; consent; views of the procedure; and support after screening. The research indicated consensus support for blood spot screening, and for expanding to some other conditions, although some parental anxiety was reported. Parents/carers mostly perceived that they had received sufficient information, but the timing of this could be improved. While parents indicated interest in genomic screening, studies highlighted the need for clearer consent procedures and greater support for parents following genomic screening than for blood spot screening. Only three included studies reported using any kind of theoretical framework. Most parents/carers found newborn blood spot screening programmes to be acceptable and favoured their large-scale implementation. A minority of parents/carers expressed concerns regarding the acceptability of processes underpinning newborn blood spot screening, such as consent, the timing of receiving information and support available after testing. More research is needed regarding the acceptability of newborn genomic sequencing screening programmes, which are less established compared with newborn blood spot screening programmes. The over-representation of studies conducted in the United States has implications for the applicability of findings to other countries where testing is not typically mandatory and health systems differ considerably. Most studies were of cross-sectional design and there was limited representation of people from lower incomes and non-white ethnicity. While the inclusion of studies only in populations of future or very recent parents provided coherence to the findings, unclear reporting of participants may have resulted in under- or overinclusion of some studies. This article presents independent research funded by the National Institute for Health and Care Research (NIHR) Health Technology Assessment programme as award number NIHR159927.

Abstract B019: Cyclin E1 amplification promotes chromosomal instability and distinct vulnerabilities in gastroesophageal adenocarcinoma

Abstract Background: Gastroesophageal adenocarcinomas (GEA) are characterized by chromosomal instability (CIN) predominantly consisting of high amplitude focal amplifications of oncogenes, including Cyclin E1. An initial pan-cancer analysis revealed that CCNE1 is one of the top genes whose expression correlates with focal CIN. Objective: We proposed a causal role for excess CCNE1 as a driver of CIN and gastroesophageal tumorigenesis, and investigated the therapeutic vulnerabilities of CCNE1 amplification/overexpression. Design: We engineered a novel CCNE1-overexpressing mouse gastric organoid model with Trp53 deletion and studied the functional effects on tumor initiation and progression. Whole genome sequencing of tumors was performed to characterize the effects of CCNE1 overexpression on genomic instability. To identify dependencies of CCNE1-amplified GEA, we executed a CRISPRi functional genomic screen. Top genetic dependencies were translated into potential pharmacologic vulnerabilities and tested in monotherapy and combination. Results: CCNE1 overexpression accelerated tumor initiation and progression of mouse gastric organoids with Trp53 deletion. These tumors demonstrated increased chromosomal complexity, mainly focal amplifications. Our functional genomic screen identified specific genetic dependencies of CCNE1-amplified GEA, including CCNE1/CDK2 as the strongest hits, and SKP2 as a novel dependency likely through its function as a p27 degrader. Pharmacologic inhibition of CDK2 was insufficient and antagonistic with concurrent inhibition of the DNA damage response via targeting the ATR/CHEK1 axis. However, staggered inhibition of these distinct vulnerabilities demonstrated efficacy. Conclusions: Our study identifies CCNE1 as a driver of CIN in GEA and builds a foundation for further exploration of therapies for CCNE1-amplified GEA characterized by genomic instability. Citation Format: ZHONG WU, Ankur Nagaraja, Chunyang Bao, Jin Zhou, Adam Bass. Cyclin E1 amplification promotes chromosomal instability and distinct vulnerabilities in gastroesophageal adenocarcinoma [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Functional and Genomic Precision Medicine in Cancer: Different Perspectives, Common Goals; 2025 Mar 11-13; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2025;85(5 Suppl):Abstract nr B019.

The Intersection Between Genetic Reproductive Carrier Screening and Genomic Newborn Screening: Implications for Clinical Practice.

The Intersection Between Genetic Reproductive Carrier Screening and Genomic Newborn Screening: Implications for Clinical Practice.

Conservation Genomics of West Virginia Walleye (Sander vitreus): Impact of Minor Allele Frequency Thresholds on Population Structure and Potential Adaptive Divergence Inferences

Background: Walleye (Sander vitreus), a valuable sportfish and an important ecological apex predator, exhibits genetic structuring across their range and localized structuring as a result of stocking. Methods: Walleye from 17 sampling locations across West Virginia were sequenced using a ddRAD protocol, generating various SNP datasets to assess population structuring and genomic diversity, with specific emphasis on the native Eastern Highlands strain. Different minor allele frequency filter thresholds were tested to assess impacts on genetic diversity and differentiation metrics. Results: High genetic differentiation was observed between the Eastern Highlands and Great Lakes strains, with further sub-structuring within the Eastern Highlands strain between the Ohio River populations and the other populations. Increasing MAF thresholds generally reduced the distinctiveness of clusters, but the overall inference of the number of clusters was minimally impacted. Genetic diversity metrics indicated some variability among Eastern Highlands walleye populations, with isolated populations, including the New River and Summersville Lake, showing higher inbreeding coefficients. MAF filters generally increased diversity metrics, but the trend of diversity metrics among populations remained relatively consistent. Several SNPs were found to be potentially undergoing selection, with the minor allele frequencies of these SNPs being found to be highest in Summersville Lake, highlighting potential adaptive divergence between the riverine populations and a large lentic system. Conclusions: The use of any MAF filter generated the same trends of population structuring and genomic diversity inferences regardless of the MAF threshold used. Further management of Eastern Highlands walleye in West Virginia needs to emphasize protecting the genetic integrity of the Kanawha River population and ongoing genomic screening of broodstock to conserve native genetic diversity.

Efficacy of EGFR tyrosine kinase inhibitors in patients with non-small cell lung cancer with EGFR exon 19 insertions: clinical-genomic, preclinical analysis through LC-SCRUM-Asia (multi-institutional genomic screening registry).

Efficacy of EGFR tyrosine kinase inhibitors in patients with non-small cell lung cancer with EGFR exon 19 insertions: clinical-genomic, preclinical analysis through LC-SCRUM-Asia (multi-institutional genomic screening registry).

(Limited) Predictability of thermal adaptation in invertebrates.

Evolutionary genomic approaches provide powerful tools to understand variation in and evolution of physiological processes. Untargeted genomic or transcriptomic screens can identify functionally annotated candidate genes linked to specific physiological processes, in turn suggesting evolutionary roles for these processes. Such studies often aim to inform modeling of the potential of natural populations to adapt to climate change, but these models are most accurate when evolutionary responses are repeatable, and thus predictable. Here, we synthesize the evolutionary genetic and comparative transcriptomic literature on terrestrial and marine invertebrates to assess whether evolutionary responses to temperature are repeatable within populations, across populations and across species. There is compelling evidence for repeatability, sometimes even across species. However, responses to laboratory selection and geographic variation across thermal gradients appear to be highly idiosyncratic. We also survey whether genetic/transcriptomic studies repeatedly identify candidate genes in three functional groups previously associated with the response to thermal stress: heat shock protein (Hsp) genes, proteolysis genes and immunity genes. Multiple studies across terrestrial and marine species identify candidates included in these gene sets. Yet, each of the gene sets are identified in only a minority of studies. Together, these patterns suggest that there is limited predictability of evolutionary responses to natural selection, including across studies within species. We discuss specific patterns for the candidate gene sets, implications for predictive modeling, and other potential applications of evolutionary genetics in elucidating physiology and gene function. Finally, we discuss limitations of inferences from available evolutionary genetic studies and directions for future research.

Current situation and new steps in newborn screening in Spain.

Current situation and new steps in newborn screening in Spain.

Predicted Risk of Ventricular Arrhythmias in a Genome-First Population With Genetic Risk for Arrhythmogenic Right Ventricular Cardiomyopathy.

Population genomic screening for desmosome variants associated with arrhythmogenic right ventricular cardiomyopathy (ARVC) may facilitate early disease detection and protective intervention. The validated ARVC risk calculator offers a novel means to risk stratify individuals with diagnosed ARVC, but predicted risk in the context of genomic screening identification has not been explored. Individuals harboring a pathogenic/likely pathogenic variant in a desmosome gene (PKP2, DSP, DSG2, or DSC2) were identified through the Geisinger MyCode Genomic Screening and Counseling program. The ARVC risk calculator was applied to patients with a subsequent evaluation of right ventricular function. This predicted risk was compared with outcomes in the first 5 years (range, 0.3-5.0 years) after genetic result return. Of 254 individuals with a clinically confirmed pathogenic/likely pathogenic desmosome variant, 113 (median age, 56 [interquartile range, 42-66]; 71% female) had cardiac imaging in follow-up and no prior sustained ventricular arrhythmia (VA). Eighty-two (73%) had no ARVC task force criteria (TFC) besides the variant (possible diagnosis), 22 (19%) had a single additional minor criterion (borderline diagnosis), and 9 (8%) met criteria for definite diagnosis. The median 5-year predicted VA risk was 3.9% (2.3%-6.6%), notably lower than that of the calculator derivation cohort (20.6%). The risk of fast VA was 1.6% (1.0%-2.9%). The predicted VA risk was higher in individuals with any nongenetic ARVC task force criteria (6.3% [2.5-13.2%]) versus those without (3.7% [2.2-5.6%]; P=0.01), and in individuals with DSP variants (6.1% [3.9-7.8%] versus PKP2 3.4% [2.2-5.3%]; P=0.01). Over a median 3.0 years of follow-up (≤5 years only), no sustained VA events were observed in this cohort. The predicted 5-year risk of VA in individuals ascertained via population genomic screening for desmosome variants is low (3.9%; 1.6% for fast VA) but may vary by affected gene and ARVC task force criteria burden.

Abstract B078: APMAP functions as a tumor-intrinsic target sensitizing cancer cells to macrophage-mediated phagocytosis

Abstract Macrophage-mediated phagocytosis plays a critical role in cancer cell elimination. Here, we developed an in vitro tumor-macrophage co-culture platform for unbiased identification of factors that impede macrophage phagocytosis using genome-wide CRISPR knockout. From the functional genomics screen, we identified APMAP as a tumor-intrinsic phagocytosis sensitizer. In vitro experiments validated that APMAP depletion in tumor cells enhances direct engulfment and selective killing of tumor cells by macrophages. In vivo experiments showed that APMAP depletion attenuates tumor growth and displays combinational effects with cetuximab in an MDA-MB-468 orthotopic model. To dissect the mechanism of action, we conducted a whole genome anchor screen using an APMAP-WT/KO isogenic pair and identified fatty acid biosynthesis pathway genes (including FASN, ACLY and ACC) that are required for APMAP deficiency-induced phenotypes; the metabolomics analysis suggests that sphingolipids are potential APMAP substrates. To inform drug discovery, we demonstrated that enzymatic activity is required for APMAP-enhanced phagocytosis. We further demonstrated that as a transmembrane protein, intracellularly localized APMAP was functional as a phagocytosis sensitizer, thereby suggesting that a small molecule inhibitor is preferred over a blocking antibody as a therapeutic strategy for disrupting APMAP activity. Citation Format: Rachel Davidson, Ye Wang, Lei Ji, Grace Trombley, Wenrong Zhou, Binzhang Shen, Ashley Choi, Hannah Stowe, Shangtao Liu, Samuel R. Meier, Brian Doyon, Douglas A. Whittington, Yi Yu, Teng Teng, Jannik N. Andersen, Alan Huang, Chengyin Min, Salam Shaaban, Serge Gueroussov. APMAP functions as a tumor-intrinsic target sensitizing cancer cells to macrophage-mediated phagocytosis [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B078.

CellFIE: Integrating Pathway Discovery With Pooled Profiling of Perturbations Uncovers Pathways of Huntington's Disease, Including Genetic Modifiers of Neuronal Development and Morphology.

Genomic screens and GWAS are powerful tools for identifying disease-modifying genes, but it is often challenging to understand the pathways by which these genes function. Here, we take an integrated approach that combines network analysis and an imaging-based pooled genetic perturbation study to examine modifiers of Huntington's disease (HD). The computational analysis highlighted several genes in a subnetwork enriched for modifiers of neuronal development and morphology. To test the functional roles of these genes, we developed an experimental pipeline that allows pooled CRISPRi KD of 21 genes in human iPSC-derived neurons followed by optical analysis of genotypes, neuronal arborization, multiplexed pathway activity and morphological fingerprint readout. This approach recovered known genes involved in morphology and confirmed unexpected links from the network between several genetic modifiers of HD and morphology. Our approach overcomes challenges in pooled measurement of neuronal function and health and could be adapted for other phenotypes in HD and other neurological diseases.

Optical Pooled Screening for the Discovery of Regulators of the Alternative Lengthening of Telomeres Pathway.

Telomere elongation is essential for the proliferation of cancer cells. Telomere length control is achieved by either the activation of the telomerase enzyme or the recombination-based Alternative Lengthening of Telomeres (ALT) pathway. ALT is active in about 10-15% of human cancers, but its molecular underpinnings remain poorly understood, preventing the discovery of potential novel therapeutic targets. Pooled CRISPR-based functional genomic screens enable the unbiased discovery of molecular factors involved in cancer biology. Recently, Optical Pooled Screens (OPS) have significantly extended the capabilities of pooled functional genomics screens to enable sensitive imaging-based readouts at the single cell level and large scale. To gain a better understanding of the ALT pathway, we developed a novel OPS assay that employs telomeric native DNA FISH (nFISH) as an optical quantitative readout to measure ALT activity. The assay uses standard OPS protocols for library preparation and sequencing. As a critical element, an optimized nFISH protocol is performed before in situ sequencing to maximize the assay performance. We show that the modified nFISH protocol faithfully detects changes in ALT activity upon CRISPR knock-out (KO) of the FANCM and BLM genes which were previously implicated in ALT. Overall, the OPS-nFISH assay is a reliable method that can provide deep insights into the ALT pathway in a high-throughput format.

Screening for hearing impairment in newborns using targeted genomic sequencing: a large pilot cohort study.

Current state-run newborn hearing screening (NBHS) programs have limitations in identifying children with mild or late-onset sensorineural hearing impairment (SNHI). As more than 50% of pediatric SNHI cases are attributed to genetic causes, these limitations may be addressed by the increasing accessibility of high-throughput, low-cost genomic sequencing. This study aims to investigate the feasibility of integrating a next-generation sequencing (NGS)-based genomic screening protocol into conventional NBHS and to examine its potential benefits and challenges. A total of 8,261 newborns who underwent simultaneous NBHS and NGSbased genomic screening targeting 46 deafness genes were prospectively enrolled in this study. The genotypes of the subjects were determined, and newborns with conclusive genetic diagnoses were subjected to audiological assessments. A total of 164 subjects were confirmed to have conclusive genetic diagnoses, with 112 subjects carrying variants in GJB2 and MTRNR1, and 52 subjects carrying variants in other deafness genes. Of these, 126 subjects with conclusive genetic diagnoses passed the NBHS, suggesting that an additional 1.5% (126/8,261) of children at risk for SNHI but not detected by conventional physiological NBHS could be identified through targeted genomic screening in the general population. Notably, the father of one subject with the COL4A5 variant and three paternal relatives of another subject with the EDNRB variant, who were unaware of their conditions prior to this study, were diagnosed with Alport and Waardenburg syndromes, respectively, highlighting the benefit to families. Targeted genomic sequencing in newborns may complement the conventional NBHS in identifying children at risk for SNHI and facilitate early diagnosis in families with non-syndromic mimics.

Cranial Neural Crest Cells Three-Dimensional In Vitro Differentiation Protocol for Multiplexed Assay.

With their remarkable capacity to generate both ectodermal and mesenchymal derivatives, cranial neural crest cells (CNCC) have attracted a lot of interest in studying the mechanisms regulating cell fate decisions and plasticity. Originating in the dorsal neuroepithelium, this cell population is transient and relatively rare in the developing embryo - making functional tests, genomic screens, and biochemistry assays challenging to perform in vivo. To overcome these limitations, several methods have been developed to model CNCC development in vitro. Neurosphere (NS) based culturing methods provide a complex microenvironment that recapitulates the developing anterior neuroepithelium in 3D. These systems allow the growth of many NS in the same plate to generate a large amount of CNCC, but the produced NS present a high variability in shape, size, and number of CNCC formed - making quantitative assays difficult to perform. This protocol outlines a reproducible method for generating NS from mouse embryonic stem cells (mESC) in a 96-well format. NS generated in 96-well plates produce cranial neural crest cells (CNCC), which can be further cultured. By controlling the number of starting cells, this approach reduces variability in the size and shape between NS and increases reproducibility across experiments. Finally, this culture system is adaptable to several applications and offers a higher degree of flexibility, making it highly customizable and suitable for multiplexing experimental conditions.

Discovery of novel WRN inhibitors for treating MSI-H colorectal cancers.

Discovery of novel WRN inhibitors for treating MSI-H colorectal cancers.

Families' experiences of receiving adult- and pediatric-onset genetic results.

Families' experiences of receiving adult- and pediatric-onset genetic results.