October 30, 2024

Genetic Landscape of Cancer Drug

Base editing screens define the genetic landscape of cancer drug resistance mechanisms


Drug resistance is a principal limitation to the long-term efficacy of cancer therapies. Cancer genome sequencing can retrospectively delineate the genetic basis of drug resistance, but this requires large numbers of post-treatment samples to nominate causal variants. Here we prospectively identify genetic mechanisms of resistance to ten oncology drugs from CRISPR base editing mutagenesis screens in four cancer cell lines using a guide RNA library predicted to install 32,476 variants in 11 cancer genes. We identify four functional classes of protein variants modulating drug sensitivity and use single-cell transcriptomics to reveal how these variants operate through distinct mechanisms, including eliciting a drug-addicted cell state. We identify variants that can be targeted with alternative inhibitors to overcome resistance and functionally validate an epidermal growth factor receptor (EGFR) variant that sensitizes lung cancer cells to EGFR inhibitors. Our variant-to-function map has implications for patient stratification, therapy combinations and drug scheduling in cancer treatment.

Main

Resistance to molecularly targeted anti-cancer treatments remains a major clinical challenge1. Drug resistance is frequently caused by DNA single nucleotide variants (SNVs) in the cancer genome2, leading to point mutations in the drug target or proteins within the same signaling pathway3. The study of drug resistance can inform drug mechanism of action, the design of second-generation inhibitors targeting drug-resistant proteins, the development of combination therapies and patient stratification for second-line therapies. Current approaches often depend on sequencing tumor biopsies from patients that relapse on treatment. These are challenging samples to acquire, meaning it can take years to accrue enough to infer variant function. These analyses are generally restricted to frequently observed variants and must be individually experimentally validated to establish a causal link to drug resistance. This is a slow process that does not allow for the direct comparison of different variant effects. These challenges limit the interpretation of cancer biopsy and circulating tumor DNA sequencing data. Rapid, prospective and systematic functional annotation of variants would accelerate the discovery of drug resistance mechanisms.

CRISPR-based gene editing approaches such as base editing can be used to directly interpret the function of variants of unknown significance (VUS)4,5,6,7,8,9,10,11,12 and study genetic mechanisms of resistance to cytokines and inhibitors8,13,14. Cytidine and adenine base editors use a Cas9 nickase fused to a deaminase, facilitating the programmed installation of C>T and A>G SNVs in the genome at high efficiency in physiologically relevant cell types9,10,11,12,15,16,17,18. Here we use base editing at scale to investigate genetic mechanisms of acquired resistance to molecularly targeted cancer therapies, identifying VUS conferring drug resistance and drug sensitization in cancer cells. We classify cancer variants modulating drug sensitivity into four functional classes, thus providing a systematic framework for interpreting drug resistance mechanisms.

Results

Base editing screens map functional domains in cancer genes


We investigated drug resistance to ten molecularly targeted cancer drugs that are currently approved by the United States Food and Drug Administration (FDA) or are under clinical investigation (Fig. 1a). We selected four cancer cell lines that are sensitive to these agents19 and harbor diverse oncogenic drivers20: H23 (lung; KRAS-G12C), PC9 (lung; EGFR amplification and exon19 deletion), HT-29 (colon; BRAF V600E) and MHH-ES-1 (Ewing sarcoma; EWS-FLI1 fusion). We mutagenized 11 cancer genes that encode common drug targets or genes within the same signaling pathway for interrogation with a guide RNA (gRNA) library (n = 22,816), tiling these genes and their 5′ and 3′ untranslated regions (UTRs). As controls, we included nontargeting gRNAs (NT gRNAs) (n = 57), intergenic-targeting gRNAs (n = 168) and gRNAs predicted to introduce splice variants21 in nonessential (n = 87) and essential (n = 316) genes22,23 (Supplementary Table 1). To maximize the saturation of targeted mutagenesis, the gRNA library was introduced into cancer cell lines expressing doxycycline-inducible cytidine base editor (CBE) or adenine base editor (ABE)8 with relaxed PAM requirements (Cas9–NGN)24. We analyzed the potential functional effects of thousands of gene variants on drug resistance in parallel by performing base editing screens with a proliferation read-out in the presence of targeted anti-cancer drugs from 46 independent pooled genetic screens (Fig. 1a and Supplementary Table 2). Base editing screen replicates were highly correlated (Extended Data Fig. 1), and control gRNAs targeting essential genes were depleted, indicating efficient base editing (Fig. 1b and Extended Data Fig. 2a).
genetic landscape, cancer, drug response, genetic mutations, drug resistance, cancer therapies, tumor growth, personalized treatment, drug metabolism, next-generation sequencing, molecular profiling, actionable mutations, precision oncology, treatment efficacy, adverse effects, genetic variations, targeted therapies, therapeutic resistance, cancer genomics, molecular oncology,

#CancerGenetics, #DrugResponse, #GeneticMutations, #CancerTherapy, #DrugResistance, #TumorGrowth, #PersonalizedTreatment, #DrugMetabolism, #NextGenSequencing, #MolecularProfiling, #ActionableMutations, #PrecisionOncology, #TreatmentEfficacy, #GeneticVariations, #TargetedTherapies, #TherapeuticResistance, #CancerGenomics, #MolecularOncology, #CancerResearch, #OncologyBreakthroughs

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    Scientists Identify Six Novel Genes

    Scientists identify six novel genes linked to cancer risk


    Scientists at deCODE genetics/Amgen, and their collaborators have discovered six novel genes with rare germline variants that associate with cancer risk. The findings are published today in Nature Genetics under the title "Gene-based burden tests of rare germline variants identify six cancer susceptibility genes."

    A subset of cancers arises in individuals who are born with rare sequence variants that significantly alter their cancer risk. The discovery of such variants, like those in the BRCA1- and BRCA2 genes, has led to improved early cancer detection and the development of targeted therapies, ultimately reducing the cancer burden and improving prognosis of those carrying these mutations.

    In this study, the scientists analyzed three large genetic datasets from individuals of European descent, including 130,991 cancer patients and 733,486 controls.

    Through a gene-based burden association analysis across 22 different cancer types, they found four novel genes associated with a risk of developing cancer; the pro-apoptotic BIK for prostate cancer, the autophagy involved ATG12 for colorectal cancer, TG for thyroid cancer, and CMTR2 for both lung cancer and cutaneous melanoma.

    The relative increase in cancer risk conferred by these variants was substantial (90%–295%), but it should be noted that the design of the study does not allow accurate assessment of absolute lifetime cancer risk.

    Additionally, the researchers found the first genes with rare variants that are associated with a decreased risk of cancer. Specifically, loss of AURKB was found to protect against any cancer type, and loss of PPP1R15A was associated with a 53% lower risk of breast cancer. This suggests that inhibition of PPP1R15A may be a therapeutic option for breast cancer.

    The study revealed new insight into the biological mechanisms involved in cancer predisposition that will hopefully lead to better screening and treatment strategies.

    cancer genetics, gene discovery, cancer risk, novel genes, cancer susceptibility, molecular mechanisms, genetic mutations, early detection, personalized treatment, cancer research, risk assessment, precision medicine, targeted therapy, cancer prevention, oncogenes, tumor suppressor genes, genomic sequencing, cancer biomarkers, genetic screening, healthcare innovation,

    #CancerGenetics, #GeneDiscovery, #CancerRisk, #NovelGenes, #GeneticResearch, #CancerSusceptibility, #MolecularMechanisms, #GeneticMutations, #EarlyDetection, #PersonalizedMedicine, #CancerResearch, #RiskAssessment, #PrecisionMedicine, #TargetedTherapy, #CancerPrevention, #Oncogenes, #TumorSuppressor, #GenomicSequencing, #CancerBiomarkers, #GeneticScreening

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    October 28, 2024

    Anti-Tumor Effects

    A PD-L1 tropism-expanded oncolytic adenovirus enhanced gene delivery efficiency and anti-tumor effects

    Recombinant adenovirus serotype 5 (Ad5)-mediated virotherapy is a maturing technique in cancer treatment. However, the utility of adenovirus (Ad) has been limited by low expression of coxsackievirus and adenovirus receptor (CAR) in cancer cells resulting in poor infectivity of Ads. To overcome the problem, we aimed to develop a novel tropism-modified oncolytic adenovirus, ZD55-F-HI-sPD-1-EGFP, which contains the epitope of PD-1 (70-77aa) at the HI-loop of Ad fiber. Trimerization of Fiber-sPD-1 was confirmed by immunoblot analysis. ZD55-F-HI-sPD-1-EGFP shows a remarkable improvement in viral infection rate and gene transduction efficiency in the PD-L1-positive cancer cells. Competition assays with a PD-L1 protein reveals that cell internalization of ZD55-F-HI-sPD-1-EGFP is mediated by both CAR and PD-L1 at a high dose. The progeny virus production capacity showed that sPD-1 incorporated fiber-modified oncolytic Ad replication was not affected. Furthermore, treating with ZD55-F-HI-sPD-1-EGFP significantly increased viral infection rate and enhanced anti-tumor effect in vivo. This study demonstrates that the strategy to expand tropism of oncolytic Ad may significantly improve therapeutic profile for cancer treatment.

    Oncolytic virotherapy is considered as one of the most promising cancer therapies, because of their ability to selectively replicate and lyse tumor cells, induce inflammatory response, release tumor-associated antigens to activate host’s adaptive anti-tumor immunity, and promote lymphocyte infiltration in tumors [1], [2], [3], [4], [5]. Adenovirus serotype 5 (Ad5) based oncolytic adenovirus are widely applied to pre-clinical and clinical trials [6], [7]. Ad5 infection of cells is initiated by the formation of a complex between the fiber protein knob domain of the virus and the host cell surface coxsackievirus and adenovirus receptor (CAR) [8], [9]. However, CAR is expressed at low levels in many types of cancer cells [10], [11], [12], [13], which limits the infectivity and oncolytic efficiency of Ad5-mediated oncolytic adenovirus [14], [15]. Therefore, the methods to increase infectivity of Ad5 are required to maximize the therapeutic efficacy of oncolytic Ad in cancers with CAR-deficient.
    To broaden the native tropism of oncolytic Ad, several genetic modifications of Ads have been studied, which are mainly focused on fiber proteins. Considering that the tropism of infection often differed between adenovirus subgroups [16], fiber knob serotype switching is one of the main approaches to broaden the tropism of Ad5-based vectors. Numerous Ad5-based oncolytic vectors with chimeric fibers have been developed, such as replacement of Ad5 knob to Ad37 enhanced viral infectivity against glioma cell [17], and replacement of Ad5 knob to Ad35 knob enhanced CD46-dependent Ad gene transfer efficiency [18]. Chimeric fibers of Ad5/3 [19], [20] and Ad5/35 [21], [22] also have been developed as cancer therapies. In addition, insertion of a peptide to the C-terminus or HI-loop of the fiber protein is another main approach to expand the tropism of Ad5-based vectors. Incorporating the vesicular stomatitis virus glycoprotein (VSV-G) epitope onto the C terminus of the fiber knob facilitated the specificity binding of the virus to phosphatidylserine (PS) moieties on the cellular plasma membrane [23]. Addition a cationic polylysine sequence (pK7) to the fiber knob facilitated viral binding to negatively charged cell surface molecules, such as heparin sulfates and increased Ad infection to endothelial cells and fibroblasts [24]. Similarly, insertion a peptide of arginine-glycineaspartate (RGD) integrin recognition site to the C-terminus or HI-loop of the fiber protein signally increased Ad infection in wide range of cells such as fibroblasts, endothelial cells, and smooth muscle cells [25]. However, the current fiber protein modification aimed at increasing the Ad infectivity cannot satisfy all tumor cell types due to the diversity of tumors. Therefore, more fiber protein modification studies are needed to expand the tropism of adenovirus to invade different tumor cells. Structure of the complex of human PD-1 and its ligand PD-L1 showed that the 70–77 amino acid peptide (70 to 77, MSPSNQTD) of PD-1 plays a role in interacting with PD-L1 [26]. Therefore, we hypothesized that insertion short PD-1 (sPD-1, 70-77aa) to HI-loop of the fiber knob can expand the tropism of Ad to PD-L1 positive tumor cells.

    Here, we constructed a tropism expanded oncolytic adenovirus (ZD55-F-HI-sPD-1-EGFP), which incorporated a short peptide of PD-1 (sPD-1, 70-77aa) in HI-loop of fiber knob and contained an exogenous reporter gene, EGFP. We verified that fiber trimer formation and viral replication ability of ZD55-F-HI-sPD-1-EGFP were not affected compared to the control virus ZD55-EGFP with wild-type fiber. ZD55-F-HI-sPD-1-EGFP increased viral infectivity, gene transduction efficiency and antitumoral efficacy, in comparison to control oncolytic adenovirus, ZD55-EGFP, in PD-L1-positive cancer cells. This is the first report to demonstrate sPD-1 epitope incorporated oncolytic Ad has expanded tropism that can improve viral infection and gene transduction efficiency in PD-L1-positive cancer cells and strengthened its therapeutic applications.

    #PDL1, #OncolyticAdenovirus, #GeneDelivery, #AntiTumor, #CancerImmunotherapy, #PrecisionOncology, #ImmuneResponse, #AdenovirusEngineering, #TumorTargeting, #GeneTherapy, #CancerTreatment, #ViralTropism, #OncolyticVirus, #ImmuneCheckpoint, #PDL1Expression, #TumorLysis, #TargetedTherapy, #AdenoviralVectors, #TherapeuticGenes, #Oncology

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    October 26, 2024

    Idiopathic Osteoporosis

    Genetic variants in melatonin receptor linked to idiopathic osteoporosis


    Osteoporosis is a common bone disorder characterized by low bone mass and increased fracture risk, usually affecting postmenopausal women and men over the age of 60.

    Idiopathic osteoporosis (IOP) is a rare form of early-onset osteoporosis that is seen in individuals under 50 years of age without any known metabolic or hormonal causes. Family histories of osteoporosis and childhood fractures suggest a genetic basis for IOP, though many cases remain unexplained despite previous genetic studies.

    In the study, "Melatonin receptor 1A variants as genetic cause of idiopathic osteoporosis," published in Science Translational Medicine, researchers examined melatonin receptor variants as a potential genetic cause of IOP. They focused on the variant rs374152717, found in an Ashkenazi family with IOP, and rs28383653, identified in unrelated IOP patients.

    Whole-exome sequencing was conducted on an Ashkenazi family affected by IOP, as well as a cohort of 75 unrelated women with IOP. The rs374152717 variant was present in individuals with IOP in the Ashkenazi family but absent in unaffected relatives.

    This mutation was more frequent in the Ashkenazi population (0.9%) than in the general population (0.0004%). In the unrelated cohort, the rs28383653 variant was found in 4% of IOP patients.

    A mouse model was used to investigate the functional consequences of the rs374152717 mutation. Mice carrying the human mutation exhibited low bone mass, a hallmark of osteoporosis, which the scientists traced to defects in osteoblast function.

    Osteoblasts are the cells responsible for bone formation. These cells were found to experience senescence, an accelerated aging or premature shutting down of cellular activity due to the mutation. This senescent state impaired their ability to differentiate and build bone properly.

    Further analysis in human cells confirmed that the rs374152717 mutation disrupted melatonin signaling, leading to the production of a dysfunctional MTNR1A protein and subsequent bone degeneration.

    Melatonin signaling normally promotes bone formation and inhibits bone resorption, but the mutations caused abnormal regulation of cyclic AMP, calcium signaling, and mitogen-activated protein kinase pathways, which triggered osteoblast senescence and bone loss.

    The findings point to a possible source for the mysterious idiopathic osteoporosis condition and suggest that genetic screening for MTNR1A variants could be a primary investigation for individuals with unexplained bone loss.



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    October 24, 2024

    Stressed Bees Experience Human-like Emotions

    Stressed bees may experience human-like emotions



    Researchers from Newcastle University in Newcastle upon Tyne, England, have discovered that bumblebees’ responses to adverse events resemble human emotions. Findings of the study show that bees lower their expectations of rewards when they become agitated or stressed, which scientists say could impact their approach to pollination. The study offers significant evidence for judgement biases in bees.1,2

    “Our study shows that bees are more pessimistic after stress as their behavior suggests that they do not expect to get rewards,” Vivek Nityananda, PhD, a Biotechnology and Biological Sciences Research Council (BBSRC) David Phillips research fellow who worked on the study, said in a university release.1 “Emotions are complex states and, in humans, involve a subjective understanding of what you are feeling. We might never know if bees feel something similar, however, what this research can say is that bees have similar responses when they are stressed and make pessimistic choices. The best explanation for their behavior is that they expect high rewards to be less likely and exhibit traits of pessimistic people.”

    In the study, published in the journal Proceedings of the Royal Society B, bumblebees were required to make an active choice as part of a novel judgement bias test.2 The bees were trained to associate high-tier and low-tier rewards, in 2 separate reward chambers, with distinct colors. One of the colors was associated with a sweet reward location, and the other with a much lower-tier reward. Bees learned the difference and visited the favorable location when shown both colors.1,2

    After learning these associations, 2 groups of bees were subjected to a simulated predatory attack—they were shaken and trapped by a robotic arm wielding a sponge—while a third group was left alone, not experiencing any added stress.1,2 When presented ambiguous colors that fell somewhere between the 2 familiar colors, bees in the 2 groups that had experienced the attacks, and were under more stress, were less likely to interpret the ambiguous colors as indicators of high-tier rewards. Therefore, they visited low-tier reward locations more frequently than bees in the control group.

    “Our research suggests that, like other animals, including humans, bees may experience emotion-like states when stressed, as demonstrated by a clear shift towards pessimism,” Olga Procenko, PhD, a researcher at the University of Birmingham who led the study, said in a university release.1 “When faced with ambiguity, stressed bees, much like someone seeing the glass as ‘half empty,’ are more likely to expect negative outcomes. Besides suggesting that states akin to emotion may be evolutionarily conserved, our study opens up new possibilities for understanding how stress affects insect cognition and behavior, which could provide insights into their responses to environmental challenges and inform conservation efforts.”

    The study emphasized the need for further research to fully understand the implications for the pollination of flowers and plants. It’s critical to understand if the pessimistic judgements made by the bees could be adaptive, potentially to avoid dangerous or unpredictable environments.2 Further research should prioritize an understanding of how emotion-like states in bees are generated and sustained. With a deeper understanding of these mechanisms and their origin, researchers will be able to determine whether there is a common ancestry and similar states in other vertebrates, or whether they are distinct and the result of convergent evolution.2

    “We need to figure out how bees evaluate rewards when stressed and whether these states in bees show other properties we see in emotions,” Nityananda said.1 “We also need to investigate the neural mechanisms involved and see if bees in the wild show similar responses.”

    #StressedBees, #BeeBehavior, #HumanLikeEmotions, #CognitiveAbilities, #EmotionalResponses, #BeeResearch, #StressInBees, #InsectBehavior, #PessimismInBees, #CognitiveComplexity, #EnvironmentalStress, #PredatorThreat, #InsectCognition, #AnimalEmotions, #StressResponse, #EmotionalExperience, #BeeCognition, #SurvivalSkills, #InsectResearch, #BeeConservation

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    October 23, 2024

    Evolution of Vertebrates

    Turtle genome provides new clues on the evolution of vertebrates


    Scientists from the UAB and Iowa State University have generated the genome assemblies of two hidden-neck turtles, unpublished until now. The results, which revealed a new three-dimensional structure of the genome within the phylogenetic group of reptiles, birds and mammals, will contribute to the development of more effective turtle conservation strategies, and to the study of the evolution of the genome and chromosomal organisation of vertebrates.

    The study was led by researchers Aurora Ruiz-Herrera (UAB) and Nicole Valenzuela (Iowa State University), with the participation of researchers from the Institute of Evolutionary Biology (CSIC-UPF) and Earlham College. Published in Genome Research, it highlights the important role of chromatin, a three-dimensional structure into which genetic material folds and is packaged within the cell nucleus, in the regulation of gene function and its impact on evolution and speciation.

    The researchers generated de novo assemblies (with no previous reference model) of the complete genome of two cryptodiran turtle species, commonly named short-necked turtles, by combining gene sequencing and expression techniques. The two turtles represent two lineages in which the sex chromosomes have evolved independently: one with XX/XY chromosomes, the type humans and other mammals have, and another with ZZ/ZW, present in birds and butterflies. In addition, researchers identified a new three-dimensional chromatin conformation in both lineages: beyond the fusion/fission events in linear genomes, they detected a chromosomal folding pattern that allows for centromere-telomere interactions. These discoveries provide new clues on the 3D chromatin structure in amniotes, a phylogenetic group to which reptiles, birds and mammals belong.

    “We suggest that the divergent pattern found in the turtles originated from an existing amniote ancestral state defined by a nuclear configuration with extensive associations between its chromosomes that were preserved during linear genome reshuffling in turtles and other vertebrates”, states Nicole Valenzuela, researcher in the Department of Ecology, Evolution and Organismal Biology at Iowa State University.

    “These findings broaden our knowledge about the evolution of sex chromosomes and provide a solid foundation for future research on genome evolution and chromosome organisation in vertebrates”, highlights Aurora-Ruiz Herrera, researcher in the Department of Cell Biology, Physiology and Immunology and the Institute of Biotechnology and Biomedicine (IBB) of the UAB.

    Key model for scientific research

    The researchers note in the article that the study of turtle genomes provides crucial information that could transform our understanding of biology and evolution. With their longevity and resistance to disease, they offer a unique model for scientific studies ranging from biomedicine to species conservation. Deciphering their genome is key to identifying the genes responsible for these traits, and could advance human medicine, especially in areas such as ageing and disease resistance.

    In addition, the turtle genome offers a unique window into evolution: these reptile species have existed for more than 250 million years, surviving mass extinction events and adapting to diverse environments. Studying their DNA helps better to understand the mechanisms of adaptation and survival, which are key to the conservation of both, the turtles themselves and other species.

    The first turtle genome assemblies were published more than a decade ago. Since then, twelve Chelonian genome assemblies have been reported, nine of them with their gene sequence identified. “The newly generated assemblies are now added to this list and reflect the importance of high-quality genomic resources for the advancement of evolutionary and developmental biology,” concludes Aurora Ruiz-Herrera.

    #SexDifferences, #ParasiticDiseases, #ImmuneResponse, #Estrogen, #Testosterone, #ImmuneModulation, #ChronicInfections, #ParasiteClearance, #AutoimmuneReactions, #GeneticFactors, #ImmuneGenes, #Microbiome, #InnateImmunity, #AdaptiveImmunity, #Cytokines, #SexHormones, #PathogenSusceptibility, #Immunology, #DiseaseOutcomes, #HormonalInfluence

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    October 22, 2024

    Genetic Databases

    ‘Anonymous’ genetic databases vulnerable to privacy leaks


    A study has raised concerns that a type of genetic database that is increasingly popular with researchers could be exploited to reveal the identities of its participants, or link private health information to their public genetic profiles.

    Single-cell data sets can contain information on gene expression in millions of cells collected from thousands of people. They are often freely accessible, providing a valuable resource for researchers who study the effects of diseases at a cellular level. The data are supposed to be anonymized, but a study published on 2 October in Cell shows how genetic data from one study “can be exploited to uncover private information about individuals in another study”, the authors write.

    The findings highlight the difficulty of balancing the interests of researchers with the privacy of donors. “Our genomes are very identifying. They can tell a lot about us, our traits, our predisposition to diseases,” says study co-author Gamze Gürsoy, a bioinformatics researcher at Columbia University in New York City. “You can change your credit-card number if it leaks, but you cannot change your genome.”
    Sensitive data

    Concerns around privacy in genetic data sets have been raised before, but they mainly focused on ‘bulk’ genetic data sets. These contain information on gene activity averaged across a large population of cells rather than data of an individual cell.

    It was previously thought that single-cell data sets wouldn’t be as vulnerable to privacy leaks, owing to the level of ‘noise’, or variation in gene expression, between different cells. But Gürsoy and her colleagues demonstrated that was not the case.

    The team reviewed three publicly available single-cell data sets, which included blood cells from people with lupus, a chronic autoimmune disease. The researchers found that they could use data on gene expression to predict the structure of a person’s genome, by combining these values with information on expression quantitative trait loci (eQTLs). The details of eQTLs — variations on the chromosome that correlate with gene expression — are also publicly available on single-cell data sets.

    To test the reliability of their work, the researchers checked their genome predictions against a genome database corresponding with the cells they used. They were able to link most of the data sets to their corresponding genome, with an accuracy rate of more than 80%.

    Unlike the data on gene expression and eQTLs, full-genome databases can usually be accessed only by scientists, to protect donor’s identifying information. But the researchers point out that a participant’s genome data can be publicly available elsewhere. For example, they might have uploaded it to a genealogy website in which users send DNA samples to learn more about their ancestry. In this case, an attacker could identify an individual whose cells are in a single-cell data set using their genome. This could reveal personal data related to a sensitive trait such as a psychiatric disorder, given that research participants are often selected to study the biology of these complex conditions.

    Privacy breaches such as these could have real-world implications, including causing employment discrimination, says Gürsoy. She adds that any leaks could even have repercussions for future generations, given that genetic traits can be passed to offspring. “Anything that leaks about us will perpetuate through generations,” she says.

    Bradley Malin, who researches large-scale genomic data sharing at Vanderbilt University in Nashville, Tennessee, says that the study is a “novel extension and contribution to the literature”. He adds that future research could explore whether genomic data could still be linked in larger data sets that include samples from thousands or millions of people.

    Competing interests

    Scientists are unsure about how best to tackle these privacy concerns. “There’s the desire to protect individual privacy, but also the desire to collectively advance medical research, and those are, unfortunately, at odds with each other,” says Mark Gerstein, who researches medical data science at Yale University in New Haven, Connecticut. The simplest solution would be to stop making genetic data so easily accessible, but this would negatively affect research, he says. “We need to share and aggregate large amounts of information.” he says. “Locking it down and making it more private, really, just gums that whole process up.”

    In their study, Gürsoy and her colleagues say that there should be greater transparency about the risks for participants who share their genomic data, and suggest that researchers should ensure that donors give consent for their data being shared. Another way forward could be encrypting personal data when it is part of a public database. The authors acknowledge that doing this would complicate the process of building and maintaining data sets, but say that it could help to protect participants’ privacy.

    #GeneticPrivacy, #DataLeaks, #AnonymousDatabases, #PrivacyConcerns, #GeneticInformation, #ReIdentification, #GenomicStudies, #DataSecurity, #PrivacyLeaks, #DataVulnerability, #SecurityRisks, #GeneticResearch, #ConsentMatters, #IdentityTracing, #GenomicPrivacy, #GeneticData, #PublicDataRisks, #DataProtection, #GeneticSecurity, #HealthData

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    October 21, 2024

    Scientists discover unexpected link between genes

    Scientists discover unexpected link between genes involved in human brain evolution and developmental disorders


    The human brain stands out among mammals for its remarkably prolonged development. Synapses – critical connections between neurons of the cerebral cortex, the brain’s main hub for cognition – take years to mature in humans, compared to just months in species like macaques or mice. This extended development, also known as neoteny, is thought to be central to humans' advanced cognitive and learning abilities. On the other hand, it has been hypothesized that disruptions of brain neoteny could be linked to neurodevelopmental disorders such as intellectual disability and autism spectrum disorder.

    The lab of Pierre Vanderhaeghen at the VIB-KU Leuven Center for Brain & Disease Research previously discovered that the prolonged development of the human cerebral cortex is mainly due to human-specific molecular mechanisms in neurons. Now, they are investigating these molecular timers in human neurons.

    Unlocking the secrets to slow synapse development

    In their latest study, the team tested the involvement of two genes, SRGAP2B and SRGAP2C, which are unique to humans. First identified by Cécile Charrier in the laboratory of Professor Franck Polleux (Columbia University, USA), these genes have been found to slow down synapse development when artificially introduced into mouse neurons of the cerebral cortex. The question if these genes function the same way in human neurons has remained unanswered.

    To address this, Dr. Baptiste Libé-Philippot, a Postdoctoral Fellow in the Vanderhaeghen lab, switched off SRGA2B and SRGAP2C in human neurons, transplanted them into mouse brains, and carefully monitored synapse development over an 18-month period.

    'We discovered that when you turn off these genes in human neurons, synaptic development speeds up at remarkable levels', says Dr. Libé-Philippot. 'By 18 months, the synapses are comparable to what we would expect to see in children between five and ten years old! This mirrors the accelerated synapse development observed in certain forms of autism spectrum disorder'.

    Clues to human-specific brain disorder susceptibility

    The team then investigated the underlying genetic mechanisms behind the pronounced effects of SRGAP2B and SRGAP2C on human neuron neoteny. They focused on the SYNGAP1 gene, an important disease gene known to be involved in intellectual disability and autism spectrum disorder.

    Remarkably, they discovered that the SRGAP2 and SYNGAP1 genes act together to control the speed of human synapse development. Most strikingly, they found that SRGAP2B and SRGAP2C increase the levels of the SYNGAP1 gene and can even reverse some defects in neurons lacking SYNGAP1. This finding increases our understanding of how human-specific molecules influence neurodevelopmental disease pathways, shedding light on why such disorders are more prevalent in our species.

    Professor Pierre Vanderhaeghen is looking forward to the future: 'This work gives us a clearer picture of the molecular mechanisms that shape the slow development of human synapses. It is amazing to find out that the same genes that are involved in the evolution of the human brain also have the potential to modify the expression of specific brain diseases. This could have important clinical relevance: more research is needed to understand how human-specific mechanisms of brain development affect learning and other behaviors and how their dysregulation can lead to brain disorders. It becomes conceivable that some human-specific gene products could become innovative drug targets'.

    brain evolution, human evolution, developmental disorders, autism spectrum disorder, intellectual disability, epilepsy, genetic pathways, cognitive abilities, neurodevelopmental conditions, genetic research, evolutionary biology, human cognition, brain development, gene discovery, neurogenetics, brain complexity, risk factors, neurological disorders, mutation, gene expression,

    #BrainEvolution, #HumanEvolution, #DevelopmentalDisorders, #Autism, #IntellectualDisability, #Epilepsy, #GeneticPathways, #CognitiveAbilities, #Neurodevelopment, #GeneticResearch, #EvolutionaryBiology, #HumanCognition, #BrainDevelopment, #GeneDiscovery, #Neurogenetics, #BrainComplexity, #RiskFactors, #NeurologicalDisorders, #GeneExpression, #BrainGenes

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    October 19, 2024

    Genomic Prediction screened for IQ

    What is genomic prediction and can embryos really be ‘screened for IQ’?

    A startup in the US, Heliospect, appears to be preparing to launch a service to enable parents to select ‘desirable’ traits


    There is broad scientific consensus that intelligence is partly inherited and that genes play a significant role. But pinning this incredibly complex trait down to precise contributions from specific genes is a far more thorny scientific challenge – and claims of being able to produce meaningful IQ “gains” in the context of embryo screening are widely viewed as contentious.

    Despite the science being unsettled, it has emerged that at least one company, the US startup Heliospect, appears to be preparing to publicly launch a service that allows parents who have conceived several embryos through IVF to select those most likely to have “desirable” traits, such as height and IQ.

    Complex traits, such as IQ, are not determined by a single mutation, but are influenced by the tiny contributions of thousands of genes that have only become detectable with the advent of vast genetic databases, such as UK Biobank.

    The testing is done by taking samples of DNA and looking for patterns. In the case of an embryo, a few cells are extracted to provide DNA results, which a company like Heliospect would run through its prediction algorithm.

    Scientists can use the data to seek out statistical correlations between genes and a person’s educational attainment (sometimes used as an IQ proxy), risk of psychiatric disorders and a whole host of other traits.

    The genetic contributions can be summed up to give a so-called polygenic score. But these scores are based on probability, rather than being a guarantee. Environmental and random biological variation also play a role. An embryo with a mediocre score could turn out to be a genius, and vice versa.

    And, in the wider context of society, access to healthcare, education, and a supportive family environment can have as large an impact as inherited traits.

    The company appears to have suggested that couples who use their service might expect to have a child who is, on average, six IQ points smarter than the child they would have had through natural conception. This is significantly higher than the 2.5 IQ point expected gain estimated in a 2019 study, that considered this hypothetical scenario. The validity of Heliospect’s claim is impossible to establish, although independent experts have expressed scepticism.

    One issue is that genes linked to good parenting – genes that are also passed on to children – also contribute to academic outcomes. But these genes benefit a child by helping provide a kind, nurturing home environment rather than by directly making them smarter.

    Prof Hank Greely, of Stanford University in California, said he didn’t believe that studies to date demonstrate an ability to make genetic predictions of the future intelligence of embryos precisely enough to produce anything other than “trivial” gains. “My first reaction is that it’s not real,” he said.

    Even accepting the claimed six IQ point gain, this assumes that 10 embryos would translate into 10 viable pregnancies, which is not the reality for most couples. For women, aged 18-34, the average live birth rate per embryo transferred is 33%, according to Human Fertilisation & Embryology Authority figures, and this falls to less than 10% for women over 40. There is also attrition between eggs retrieved and embryos created. Many couples do not have 10 viable embryos to chose between and, for others, this would require an unusually intensive series of IVF cycles, which is not risk free.

    Beyond possible medical risks, IQ screening of embryos poses a host of broader ethical questions. Some fear the technology could lead to a Gattaca-style stratified society. The 1997 science fiction film presented a world with a genetically enhanced upper class and a naturally conceived lower class.

    Supporters of polygenic screening of embryos often cite the success of animal breeding schemes as evidence for the potentially considerable benefits of trait selection. But others note that pedigree programmes can produce unexpected “ride-along” effects. In one case, in the 2010s, scientists bred so-called “superchickens”, after selecting successive generations of prolific egg layers in an effort to boost livestock productivity. But the superchickens also turned out to be incredibly aggressive. When introduced into a farmyard environment the flock descended into disarray, with some of the hens pecking each other to death. There is no guarantee that selecting for high IQ in humans would not also produce unanticipated outcomes.

    interprofessional education, genetics, nursing curriculum, genetic counseling, personalized medicine, genomics, ethical considerations, genetic testing, patient care, healthcare collaboration, team-based learning, undergraduate nursing, clinical practice, healthcare education, curriculum design, critical thinking, communication skills, holistic care, nursing education, disease prevention,

    #InterprofessionalEducation, #GeneticsInNursing, #NursingCurriculum, #GeneticCounseling, #PersonalizedMedicine, #Genomics, #GeneticTesting, #PatientCare, #HealthcareCollaboration, #TeamBasedLearning, #NursingEducation, #EthicalGenetics, #ClinicalPractice, #HealthcareEducation, #CriticalThinking, #CommunicationSkills, #HolisticCare, #GeneticsAndNursing, #DiseasePrevention, #UndergraduateNursing

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    October 18, 2024

    Bacterial cells transmit

    Bacterial cells transmit memories to offspring


    Bacterial cells can “remember” brief, temporary changes to their bodies and immediate surroundings, a new Northwestern University and University of Texas-Southwestern study has found.

    And, although these changes are not encoded in the cell’s genetics, the cell still passes memories of them to its offspring — for multiple generations.

    Not only does this discovery challenge long-held assumptions of how the simplest organisms transmit and inherit physical traits, it also could be leveraged for new medical applications. For example, researchers could circumvent antibiotic resistance by subtly tweaking a pathogenic bacterium to render its offspring more sensitive to treatment for generations.

    “A central assumption in bacterial biology is that heritable physical characteristics are determined primarily by DNA,” said Northwestern’s Adilson Motter, the study’s senior author. “But, from the perspective of complex systems, we know that information also can be stored at the level of the network of regulatory relationships among genes. We wanted to explore whether there are characteristics transmitted from parents to offspring that are not encoded in DNA, but rather in the regulatory network itself. We found that temporary changes to gene regulation imprint lasting changes within the network that are passed on to the offspring. In other words, the echoes of changes affecting their parents persist in the regulatory network while the DNA remains unchanged.”

    Motter is the Charles E. and Emma H. Morrison Professor of Physics at Northwestern’s Weinberg College of Arts and Sciences and director of the Center for Network Dynamics. The study’s co-first authors are postdoctoral fellow Thomas Wytock and graduate student Yi Zhao, who are both members of Motter’s laboratory. The study also involves a collaboration with Kimberly Reynolds, a systems biologist at the University of Texas Southwestern Medical Center.

    Learning from a model organism

    Since researchers first identified the molecular underpinnings of genetic code in the 1950s, they have assumed traits are primarily — if not exclusively — transmitted through DNA. However, after the completion of the Human Genome Project in 2001, researchers have revisited this assumption.

    Wytock cites the World War II Dutch famine as a famous example pointing to the possibility of heritable, non-genetic traits in humans. A recent study showed that the children of men, who were exposed to the famine in utero, exhibited an increased tendency to become overweight as adults. But isolating the ultimate causes for this type of non-genetic inheritance in humans has proved challenging.

    “In the case of complex organisms, the challenge lies in disentangling confounding factors such as survivor bias,” Motter said. “But perhaps we can isolate the causes for the simplest single-cell organisms, since we can control their environment and interrogate their genetics. If we observe something in this case, we can attribute the origin of non-genetic inheritance to a limited number of possibilities — in particular, changes in gene regulation.”

    The regulatory network is analogous to a communication network that genes use to influence each other. The research team hypothesized that this network alone could hold the key to transmitting traits to offspring. To explore this hypothesis, Motter and his team turned to Escherichia coli (E. coli), a common bacterium and well-studied model organism.

    “In the case of E. coli, the entire organism is a single cell,” Wytock said. “It has many fewer genes than a human cell, some 4,000 genes as opposed to 20,000. It also lacks the intracellular structures known to underlie the persistence of DNA organization in yeast and the multiplicity of cell types in higher organisms. Because E. coli is a well-studied model organism, we know the organization of the gene regulatory network in some detail.”

    Reversible stress, irreversible change

    The research team used a mathematical model of the regulatory network to simulate the temporary deactivation (and subsequent reactivation) of individual genes in E. coli. They discovered these transient perturbations can generate lasting changes, which are projected to be inherited for multiple generations. The team currently is working to validate their simulations in laboratory experiments using a variation of CRISPR that deactivates genes temporarily rather than permanently.

    But if the changes are encoded in the regulatory network rather than the DNA, the research team questioned how a cell can transmit them across generations. They propose that the reversible perturbation sparks an irreversible chain reaction within the regulatory network. As one gene deactivates, it affects the gene next to it in the network. By the time the first gene is reactivated, the cascade is already in full swing because the genes can form self-sustaining circuits that become impervious to outside influences once activated.

    “It’s a network phenomenon,” said Motter, who is an expert in the dynamic behaviors of complex systems. “Genes interact with each other. If you perturb one gene, it affects others.”

    Although his team is deactivating genes to test the hypothesis, Motter is clear that different types of perturbations could cause a similar effect. “We also could have changed the cell’s environment,” he said. “It could be the temperature, the availability of nutrients or the pH.”

    The study also suggests that other organisms have the necessary elements to exhibit non-genetic heritability. “In biology, it’s dangerous to assume anything is universal,” Motter contends. “But, intuitively, I do expect the effect to be common because E. coli’s regulatory network is similar or simpler than those found in other organisms.”

    The study, “Irreversibility in bacterial regulatory networks,” was supported by the National Science Foundation (award number MCB-2206974).

    bacterial memory, epigenetic inheritance, horizontal gene transfer, DNA methylation, CRISPR-Cas system, stress response, antibiotic resistance, biofilm formation, quorum sensing, plasmid transfer, microbial evolution, genetic adaptation, bacterial communication, transgenerational inheritance, environmental stress, mutagenesis, molecular mechanisms, cell signaling, host immunity, survival advantage.

    #BacterialMemory #EpigeneticInheritance #HorizontalGeneTransfer #DNAMethylation #CRISPRCas #StressResponse #AntibioticResistance #BiofilmFormation #QuorumSensing #PlasmidTransfer #MicrobialEvolution #GeneticAdaptation #BacterialCommunication #TransgenerationalInheritance #EnvironmentalStress #Mutagenesis #MolecularMechanisms #CellSignaling #HostImmunity #SurvivalAdvantage

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    October 16, 2024

    Genetic insights treatment

    Genetic insights transform treatment for children with developmental disorders


    Thousands of children with severe developmental disorders have benefited from more targeted treatments and support with genetic insights from the large-scale Deciphering Developmental Disorders (DDD) study, finds a new study.

    Researchers from the University of Exeter and the Royal Devon University Healthcare NHS Foundation Trust followed up on the impact of those diagnosed as part of the DDD study, a collaboration between the NHS and the Wellcome Sanger Institute. This large-scale project, which began over a decade ago, has led to life-changing diagnoses for over 5,500 families across the UK and Ireland and the discovery of 60 new genetic conditions.

    The findings, published in Genetics in Medicine Open (14 October), reveal that over a thousand of those diagnosed were able to alter their treatment or undergo further medical testing based on their genetic findings, significantly improving their quality of life.

    The Deciphering Developmental Disorders (DDD) study included 13,500 families, recruited from 24 regional genetics services across the UK and Ireland. All the families had children with a severe developmental disorder, which was undiagnosed despite prior testing and likely to be caused by a single genetic change. The Wellcome Sanger Institute sequenced all the genes in the children's' and parents' genomes to look for answers, a search which is still ongoing.

    In this new study, researchers analysed outcomes for 4,237 of the families who received a genetic diagnosis, finding 76 per cent (3,214 people) were given condition-specific information or support. A further 28 per cent (1,183 people) of people were able to change treatment or get further medical testing because of their diagnosis. Over 20 per cent (880 people) joined patient support groups, such as Unique to connect with others facing similar challenges.

    Additionally, 143 people were able to start, stop or adjust specific therapies, which can have a major impact on quality of life, and even be lifesaving. Researchers expect this number to grow, as new genetic therapies continue to develop.

    Helen Firth, Professor of Clinical Genomics at the University of Cambridge, Honorary Faculty Member at Wellcome Sanger Institute and author of the study, said: "Genomic testing is enabling far more people to receive a molecular genetic diagnosis of their rare disorder. These diagnoses are a launch pad to more tailored management and treatment based on the specific genetic diagnosis. This paper studied the impact of a genetic diagnosis for patients diagnosed by the DDD study. It provides a template for improving care and support following a genetic diagnosis."

    Professor Matthew Hurles, Director of the Wellcome Sanger Institute and lead of the DDD study, said: "It is both deeply gratifying and sobering to understand the impact that our research has had on thousands of DDD families. We can feel proud that through the integration of the nationwide scale of the NHS and being on the cutting edge of new genomic technologies, the UK has been pioneering in the application of new genomic technologies to diagnose rare disorders. However, this study also highlights how much more work is needed to find treatments for the majority of rare disorders. Nevertheless, it is clear that even without a disease-specific therapy being available, participating families can benefit substantially from having a definitive molecular diagnosis for their child's condition."

    Sarah Wynn, Chief Executive Officer of Unique, which supports families affected by rare genetic disorders and has been involved in the DDD study from the outset, said: "This study has provided so many families with an explanation for their child's developmental delay, and has also identified numerous genes involved in causing their conditions. Many of these families have waited a long time to get this answer, and they are now able to better understand their child and their needs, enabling access to the appropriate care and support. Families are also understandably desperate for information about how their child may be affected now, and in the future, but for rare conditions such as these, there is often a complete lack of information. A vital output of the DDD project has been the collaboration with Unique to produce much-needed family-friendly patient literature, which benefits not only the project participants, but all those subsequently diagnosed."

    Andrew Gwynne, UK Minister for Public Health and Prevention, said: "Innovative research is vital to increasing our understanding of all illnesses, and saving lives, just like Jaydi's. Helping people get a final diagnosis faster is one of the key priorities in the UK Rare Diseases Framework and we are continuously committed to making improvements to the health and care system for people living with rare conditions."



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    October 15, 2024

    Genetic Insights Into Alopecia Areata

    New Genetic Insights Into Alopecia Areata


    Alopecia areata has a genetic relationship with trace elements, serum metabolites, and inflammatory factors that highlights the potential value of targeted therapeutic strategies and preventive measures, according to a study published in Skin Research and Technology.1

    Genetics, environmental factors, and immune dysregulation influence alopecia areata development. There is an increased risk between alopecia areata and atopy and allergies such as hay fever, eczema, asthma, and allergies to pollen, dust, and cats.2 Hypothyroidism has also been found to contribute to the development of alopecia areata among patients.3 Currently, there is little research that explores the association between developing alopecia areata and the progression of trace elements, serum modalities, and inflammatory cytokines that could be influencing the onset of the disease.1

    Trace elements are essential building blocks for cells that play a crucial role in processes like energy production, tissue repair, and nerve function. They help maintain the balance of immune cells, which is vital for preventing autoimmune diseases. Fluctuations in trace element levels can disrupt these functions and potentially contribute to the development of autoimmune conditions.

    Serum metabolites serve as biomarkers of metabolic activity, reflecting the alterations in metabolic pathways associated with disease states. Monitoring these metabolites in alopecia areata can provide a better understanding of the metabolic underpinnings of the disease and how it will evolve over time.

    Monocytes, a type of immune cell, may play a role in the development of alopecia areata but understanding the connection between these cells could help us better understand the causes of the disease and develop new treatments.

    A Mendelian randomization analysis was conducted to genetically confirm the link between trace elements, metabolites, and inflammatory markers with the risk of alopecia areata. This study aimed to identify novel biological pathways and potential therapeutic targets.

    The study examined 15 common trace elements and a total of 198 single nucleotide polymorphisms were labeled as inverse variance weighted (IVW). The IVW analysis highlights the possible connection between copper levels and the risk of developing alopecia areata (OR, 0.86; 95% CI, 0.75-0.99; P = .041). No heterogeneity was revealed (P = .922) and there was no evidence of horizontal pleiotropy detected (P = .749).

    There was an inverse correlation between alopecia areata development and the levels of Gamma-glutamylglutamine (OR, 0.35; 95% CI, 0.16-0.76; P = .007), X-12707 (OR, 0.55; 95% CI, 0.32-0.93; P = .026), and (N(1) + N (8))-acetylspermidine (OR, 0.61; 95% CI, 0.41-0.91; P = .015). Alopecia areata risk also has possible positive correlations with levels of N-acetylarginine (OR, 1.31; 95% CI, 1.03-1.65; P = .025) and 12 additional serum metabolites.

    Inflammatory factors with an inverse correlation to an increased risk of alopecia areata development included levels of C-C motif chemokine 23 (OR, 0.56; 95% CI, 0.39-0.81; P = .001), monocyte chemoattractant protein-3 (OR, 0.64; 95% CI, 0.42-0.97; P = .035), and Cystatin D (OR, 0.78; 95% CI, 0.61-0.99; P = .042).

    Additional positive correlations with alopecia areata risk were found in transforming growth factor-alpha (OR, 1.72; 95% CI, 1.01-2.94; P = .044), interleukin-2 receptor subunit beta (OR, 1.80; 95% CI, 1.01-3.19; P = .044), and interferon gamma (OR, 2.23; 95% CI, 1.34-3.71; P = .001).

    One of the limitations is the study design because it relies on the effectiveness of genetic tools and may not consider all relevant biological pathways, the authors noted. The largely European population included in the study limits the results to specific ethnicities and geographical locations. Overall data interpretation is limited because the casual mechanism between alopecia areata risk and some biomarkers remains unclear.

    Higher levels of copper were found to be casually associated with a reduced risk of alopecia areata, suggesting its potential protective effect against autoimmune hair loss. Conversely, elevated levels of specific inflammatory markers were linked to a higher risk of hair follicle damage, highlighting the importance of further research to better understand the underlying mechanisms of alopecia areata.

    #Genetics #Neuroanatomy #BrainResearch #GeneExpression #SynapticPlasticity #Neurodevelopment #AutismResearch #Schizophrenia #Neurogenetics #MolecularPathways #Neurodegeneration #Alzheimers #Parkinsons #CRISPR #BrainConnectivity #Neuroplasticity #MentalHealthGenetics #CognitiveNeuroscience #Endophenotypes #GeneEnvironmentInteraction

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