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Cooper, C.

Publications and source records attributed to Cooper, C..

34 records · Page 2Linked to original sources

Therapeutic targeting of SETD2-deficient cancer cells with the small-molecule compound RITA

The histone methyltransferase SETD2 and its associated histone mark H3 lysine 36 trimethylation (H3K36me3) are frequently lost in certain cancer types, identifying SETD2 as an important therapeutic target. Here we show that SETD2-deficient cancer cells are profoundly sensitive to the compound RITA, resulting in significant p53 induction and apoptosis. This is further associated with defects in DNA replication, leading to delays in S-phase progression, increased recruitment of replication stress markers, and reduced replication fork progression. RITA sensitivity is linked to the phenol sulphotransferase SULT1A1, which we find to be highly upregulated in cells that lack SETD2. Depletion of SULT1A1 or addition of the phenol sulphotransferase inhibitor DCNP abolishes these phenotypes and suppresses the sensitivity of SETD2-deficient cancer cells, identifying SULT1A1 activity to be critical in mediating the potent cytotoxicity of RITA against SETD2-deficient cells. These findings define a novel therapeutic strategy for targeting the loss of SETD2 in cancer. Significance StatementThe histone-modifying enzyme SETD2 has emerged as an important tumour suppressor in a number of different cancer types, identifying it as a promising therapeutic target. The concept of synthetic lethality, a genetic interaction in which the simultaneous loss of two genes or pathways that regulate a common essential process renders the cell nonviable, is a valuable tool for killing cancer cells that have known mutations. In this study, we conducted a synthetic lethality screen for compounds that specifically target SETD2-deficient cancer cells. The top hit, a compound called RITA, reduces cell viability and induces cell death only in the context of SETD2 loss, thereby highlighting a potential novel therapeutic strategy for treating SETD2-deficient cancers.

cell biology↗

Placental uptake and metabolism as determinants of pregnancy vitamin D status

Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes. Using physiological human placental perfusion and villous explants, we investigate the role of the placenta in regulating the relationships between maternal 25(OH)D and fetal physiology. We demonstrate active placental uptake of 25(OH)D3 by endocytosis, placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the maternal and fetal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than simply the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta, with widespread effects on the placenta itself. These data demonstrate a complex interplay between vitamin D and the placenta and will inform future interventions using vitamin D to support fetal development and maternal adaptations to pregnancy.

physiology↗

Single-cell analysis reveals diverse stromal subsets associated with immune evasion in triple-negative breast cancer

The tumour stroma regulates nearly all stages of carcinogenesis. Stromal heterogeneity in human triple-negative breast cancers (TNBCs) remains poorly understood, limiting the development of stromal-targeted therapies. Single cell RNA-sequencing of five TNBCs revealed two cancer-associated fibroblast (CAF) and two perivascular-like (PVL) subpopulations. CAFs clustered into two states, the first with features of myofibroblasts and the second characterised by high expression of growth factors and immunomodulatory molecules. PVL cells clustered into two states consistent with a differentiated and immature phenotype. We showed that these stromal states have distinct morphologies, spatial relationships and functional properties in regulating the extracellular matrix. Using cell-signalling predictions, we provide evidence that stromal-immune crosstalk acts via a diverse array of immunoregulatory molecules. Importantly, the investigation of gene signatures from inflammatory-CAFs and differentiated-PVL cells in independent TNBC patient cohorts revealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively. Such insights present promising candidates to further investigate for new therapeutic strategies in the treatment of TNBCs.

cancer biology↗

Serotonin suppresses slow oscillations by activating somatostatin interneurons via the 5-HT2A receptor

Serotonin (5-HT) is one of the major neuromodulators present in the mammalian brain and has been shown to play a role in multiple physiological processes. The mechanisms by which 5-HT modulates cortical network activity, however, are not yet fully understood. We investigated the effects of 5-HT on slow oscillations (SOs), a synchronized cortical network activity universally present across species. SOs are observed during anesthesia and are considered to be the default cortical activity pattern. We discovered that ({+/-})3,4-methylenedioxymethamphetamine (MDMA) and fenfluramine, two potent 5-HT releasers, inhibit SOs within the entorhinal cortex (EC) in anesthetized mice. Combining opto- and pharmacogenetic manipulations with in vitro electrophysiological recordings, we uncovered that somatostatin-expressing (Sst) interneurons activated by the 5-HT2A receptor (5-HT2AR) play an important role in the suppression of SOs. Since 5-HT2AR signaling is involved in the etiology of different psychiatric disorders and mediates the psychological effects of many psychoactive serotonergic drugs, we propose that the newly discovered link between Sst interneurons and 5-HT will contribute to our understanding of these complex topics.

neuroscience↗

Distinct Predictive Patterns of Antidepressant Response to Sertraline, Placebo and Bupropion using Pre-Treatment Reward Processing as examined through Functional MRI and Deep Learning: Key Results from the EMBARC Study

ImportanceThe lack of antidepressant-specific biomarkers to inform treatment selection is a key obstacle in the treatment of Major Depressive Disorder. Quantitative measurements of reward processing neural activity with task-based functional magnetic resonance imaging (fMRI) may allow prediction of individual outcomes for specific antidepressants. ObjectiveTo build and validate predictors of individual outcomes for sertraline, bupropion, and placebo using reward processing task-based fMRI, clinical assessments, and deep learning. DesignThis is a secondary analysis of data from the Establishing Moderators and Biosignatures of Antidepressant Response in Clinical Care (EMBARC) study, a placebo-controlled, double-blind randomized clinical trial. The study ran from July 2011 to December 2015 and this analysis was performed between December 2018 and July 2019. SettingThe EMBARC study was conducted at 4 academic medical centers. ParticipantsA random sample of 296 un-medicated participants meeting DSIM-IV criteria for depression was enrolled. InterventionSubjects were randomized to sertraline or placebo during phase 1. In phase 2, non-responders to placebo were treated with sertraline and non-responders to sertraline were treated with bupropion. Each phase lasted for 8 weeks. Main outcomes and measuresThe primary outcome was the change in the 17-item Hamilton Rating Scale for Depression ({Delta}HAMD) after 8 weeks of treatment. Task-related brain activation measures, computed from pre-treatment reward processing task fMRI, and clinical measurements were used to train deep learning predictive models for each treatment group. ResultsThe current analysis includes 222 participants with complete imaging, clinical, and treatment outcome data (146 female, mean age 16.4 {+/-} 13.4 years). The predictive model for sertraline, trained on 106 participants, achieved an R2 of 35% (95% CI 20-50%, p < 10-3) in predicting {Delta}HAMD and a number-needed-to-treat (NNT) of 4.31 in predicting remission. The placebo model, trained on 116 participants, achieved an R2 of 23% (95% confidence interval of 11-37%, p < 10-3) and an NNT of 2.78. The bupropion model achieved an R2 of 37% (95% CI 12-61%, p < 10-3) and an NNT of 2.35. Reward processing activity in regions such as the medial frontal cortex, insula, and thalamus were important predictors of sertraline outcome, while the anterior cingulate cortex, striatum, insula, and thalamus were important regions for predicting bupropion outcome. These are consistent with previously reported findings, while regions not previously implicated such as the temporal pole and paracentral lobule were also found to be predictive. Conclusions and relevanceThese findings demonstrate the utility of reward processing measurements and deep learning in predicting individual antidepressant outcomes with high accuracy. They also present potential composite biomarkers for these treatments based on neuroimaging and clinical features. Trial registrationClinicalTrials.gov identifier: NCT01407094 KEY POINTSO_ST_ABSQuestionC_ST_ABSCan pre-treatment fMRI measurements of reward processing, in combination with multi-dimensional clinical assessments, be used to form personalized predictions of antidepressant outcomes? FindingsDeep learning predictive models trained on pre-treatment reward processing task-based neuroimaging and clinical data from a randomized clinical trial were able to explain up to 37% of the variance in individual treatment outcomes and predict remission with NNT of 2-4. Specific clinical variables and brain regions with reward processing activity important for the model predictions were identified, which may form composite biomarkers of antidepressant response. MeaningQuantitative measures of reward processing, as identified through deep learning, may move us closer to a precision medicine approach that enables clinicians to select the appropriate antidepressant for each patient with greater certainty.

bioinformatics↗

The Genomic Loci of Specific Human tRNA Genes Exhibit Ageing-Related DNA Hypermethylation

The epigenome deteriorates with age, potentially impacting on ageing-related disease. Here, we interrogate the DNA methylation state of the genomic loci of human tRNA. Whilst arising from only ~46kb (<0.002% genome), this information transfer machinery is the second most abundant cellular transcript. tRNAs also control metabolic processes known to affect ageing, through core translational and additional regulatory roles. We identified a genomic enrichment for age-related DNA hypermethylation at tRNA loci. Analysis in 4,350 MeDIP-seq peripheral-blood DNA methylomes (16-82 years), classified 44 and 21 hypermethylating specific tRNAs at study- and genome-wide significance, respectively, contrasting with 0 hypomethylating. Validation and replication (450k array & independent targeted Bisuphite-sequencing) supported thehypermethylation of this functional unit. The strongest consistent signals, also independent of major cell-type change, occur in tRNA-iMet-CAT-1-4 and tRNA-Ser-AGA-2-6. This study is this first comprehensive evaluation of the genomic DNA methylation state of human tRNA genes and reveals a discreet hypermethylation with advancing age.

genomics↗

Generation of transgenic quails by in vivo transfection of primordial germ cells

During development, dynamic changes in tissue shapes known as morphogenesis result from the exquisite orchestration of signalling pathways, cell-cell interactions, cell divisions, and coordinated movements. How cells within embryos adopt a vast array of cell fates and tissue shapes in such an ever-changing environment has fascinated scientists for generations, yet the ability to observe and characterize those rapid changes has proven technically challenging in higher vertebrates. The japanese quail (Coturnix coturnix japonica) is an attractive model where basic rules driving morphogenesis in amniotes can be deciphered using genetic approaches. Similar to the more popular chicken model, the quail embryo is easily accessible to a wide range of manipulations and live imaging. A decisive asset of quail over chicken is a much shorter life cycle, which makes its use as genetic model for basic research extremely appealing. To date, all existing transgenic quail lines were generated using replication-deficient lentiviruses, but diverse limitations of this approach have hindered the widespread expansion of such technology. Here, we successfully used a plasmid-based in vivo transfection of quail primordial germ cells (PGCs) to generate a number of transgenic quail lines over a short period of time. The plasmid-based approach is simple, efficient and it allows using the infinite variety of genome engineering approaches developed in other models, such as strategies to facilitate transgenic bird selection, shown here. This major technological development completes the vast panel of techniques applicable to the avian model, making it one of the most versatile experimental systems available.

developmental biology↗

Semi-quantitative characterisation of mixed pollen samples using MinION sequencing and Reverse Metagenomics (RevMet)

1. The ability to identify and quantify the constituent plant species that make up a mixed-species sample of pollen has important applications in ecology, conservation, and agriculture. Recently, metabarcoding protocols have been developed for pollen that can identify constituent plant species, but there are strong reasons to doubt that metabarcoding can accurately quantify their relative abundances. A PCR-free, shotgun metagenomics approach has greater potential for accurately quantifying species relative abundances, but applying metagenomics to eukaryotes is challenging due to low numbers of reference genomes. 2. We have developed a pipeline, RevMet (Reverse Metagenomics), that allows reliable and semi-quantitative characterization of the species composition of mixed-species eukaryote samples, such as bee-collected pollen, without requiring reference genomes. Instead, reference species are represented only by genome skims: low-cost, low-coverage, short-read sequence datasets. The skims are mapped to individual long reads sequenced from mixed-species samples using the MinION, a portable nanopore sequencing device, and each long read is uniquely assigned to a plant species. 3. We genome-skimmed 49 wild UK plant species, validated our pipeline with mock DNA mixtures of known composition, and then applied RevMet to pollen loads collected from wild bees. We demonstrate that RevMet can identify plant species present in mixed-species samples at proportions of DNA [&ge;]1%, with few false positives and false negatives, and reliably differentiate species represented by high versus low amounts of DNA in a sample. 4. The RevMet pipeline could readily be adapted to generate semi-quantitative datasets for a wide range of mixed eukaryote samples, which could include characterising diets, quantifying allergenic pollen from air samples, quantifying soil fauna, and identifying the compositions of algal and diatom communities. Our per-sample costs were {pound}90 per genome skim and {pound}60 per pollen sample, and new versions of sequencers available now will further reduce these costs.

ecology↗

Interaction of HelQ helicase with RPA modulates RPA-DNA binding and stimulates HelQ to unwind DNA through a protein roadblock.

Cells reactivate compromised DNA replication forks using enzymes that include DNA helicases for separating DNA strands and remodelling protein-DNA complexes. HelQ helicase promotes replication-coupled DNA repair in mammals in a network of interactions with other proteins. We report newly identified HelQ helicase activities, when acting alone and when interacting with RPA. HelQ helicase was strongly inhibited by a DNA-protein barrier (BamHIE111A), and by an abasic site in the translocating DNA strand. Interaction of HelQ with RPA activated DNA unwinding through the protein barrier, but not through the abasic site. Activation was lost when RPA was replaced with bacterial SSB or DNA binding-defective RPA, RPAARO1. We observed stable HelQ-RPA-DNA ternary complex formation, and present evidence that an intrinsically disordered N-terminal region of HelQ (N-HelQ) interacts with RPA, destabilising RPA-DNA binding. Additionally, SEC-MALS showed that HelQ multimers are converted into catalytically active dimers when ATP-Mg2+ is bound. HelQ and RPA are proposed to jointly promote replication fork recovery by helicase-catalysed displacement of DNA-bound proteins, after HelQ gains access to ssDNA through its N-terminal domain interaction with RPA.

biochemistry↗

Evaluation of the NCCN guidelines using the RIGHT Statement and AGREE II instrument: a cross-sectional review.

IntroductionRobust, clearly reported clinical practice guidelines (CPGs) are essential for evidence-based clinical practice. The Reporting Items for practice Guidelines in HealThcare (RIGHT) statement and Appraisal of Guidelines for Research and Evaluation (AGREE) II instrument were published to improve the methodological and reporting quality in healthcare CPGs.\n\nMethodsWe applied the RIGHT statement checklist and AGREE II instrument to 48 National Comprehensive Cancer Network (NCCN) guidelines. Our primary objective was to assess the adherence to RIGHT and AGREE II items. Since neither RIGHT nor AGREE-II can judge the clinical usefulness of a guideline, our study is designed to only focus on the methodological and reporting quality of each guideline.\n\nResultsThe NCCN guidelines demonstrated notable strengths and weaknesses. For example, RIGHT statement items 19 (conflicts of interest), 7b (description of subgroups), and 13a (clear, precise recommendations) were fully reported in all guidelines. However, the guidelines inconsistently incorporated patient values and preferences and cost, nor did they consistently describe the method for assessing the quality and certainty of evidence. Regarding the AGREE II instrument, the NCCN guidelines scored highly on the domains 4 (clear, precise recommendations) and 6 (handling of conflicts of interest), but lowest on domain 2 (inclusion of all relevant stakeholders).\n\nConclusionsIn this investigation we found that NCCN CPGs demonstrate key strengths and weaknesses with respect to the reporting of key items essential to CPGs. We recommend the continued use of NCCN guidelines and adherence to the RIGHT and AGREE II items. Doing so serves to improve the evidence delivered to healthcare providers, thus potentially improving patient care.

epidemiology↗

Machine Learning to Predict Osteoporotic Fracture Risk from Genotypes

BackgroundGenomics-based prediction could be useful since genome-wide genotyping costs less than many clinical tests. We tested whether machine learning methods could provide a clinically-relevant genomic prediction of quantitative ultrasound speed of sound (SOS)--a risk factor for osteoporotic fracture.\n\nMethodsWe used 341,449 individuals from UK Biobank with SOS measures to develop genomically-predicted SOS (gSOS) using machine learning algorithms. We selected the optimal algorithm in 5,335 independent individuals and then validated it and its ability to predict incident fracture in an independent test dataset (N = 80,027). Finally, we explored whether genomic pre-screening could complement a UK-based osteoporosis screening strategy, based on the validated tool FRAX.\n\nResultsgSOS explained 4.8-fold more variance in SOS than FRAX clinical risk factors (CRF) alone (r2 = 23% vs. 4.8%). A standard deviation decrease in gSOS, adjusting for the CRF-FRAX score was associated with a higher increased odds of incident major osteoporotic fracture (1,491 cases / 78,536 controls, OR = 1.91 [1.70-2.14], P = 10-28) than that for measured SOS (OR = 1.60 [1.50-1.69], P = 10-52) and femoral neck bone mineral density (147 cases / 4,594 controls, OR = 1.53 [1.27-1.83], P = 10-6). Individuals in the bottom decile of the gSOS distribution had a 3.25-fold increased risk of major osteoporotic fracture (P = 10-18) compared to the top decile. A gSOS-based FRAX score, identified individuals at high risk for incident major osteoporotic fractures better than the CRF-FRAX score (P = 10-14). Introducing a genomic pre-screening step into osteoporosis screening in 4,741 individuals reduced the number of required clinical visits from 2,455 to 1,273 and the number of BMD tests from 1,013 to 473, while only reducing the sensitivity to identify individuals eligible for therapy from 99% to 95%.\n\nInterpretationThe use of genotypes in a machine learning algorithm resulted in a clinically-relevant prediction of SOS and fracture, with potential to impact healthcare resource utilization.\n\nResearch in ContextO_ST_ABSEvidence Before this StudyC_ST_ABSGenome-wide association studies have identified many loci associated with risk of clinically-relevant fracture risk factors, such as SOS. Yet, it is unclear if such information can be leveraged to identify those at risk for disease outcomes, such as osteoporotic fractures. Most previous attempts to predict disease risk from genotypes have used polygenic risk scores, which may not be optimal for genomic-prediction. Despite these obstacles, genomic-prediction could enable screening programs to be more efficient since most people screened in a population are not determined to have a level of risk that would prompt a change in clinical care. Genomic pre-screening could help identify individuals whose risk of disease is low enough that they are unlikely to benefit from screening.\n\nAdded Value of this StudyUsing a large dataset of 426,811 individuals we trained and tested a machine learning algorithm to genomically-predict SOS. This metric, gSOS, had performance characteristics for predicting fracture risk that were similar to measured SOS and femoral neck BMD. Implementing a gSOS-based pre-screening step into the UK-based osteoporosis treatment guidelines reduced the number of individuals who would require screening clinical visits and skeletal testing by approximately 50%, while having little impact on the sensitivity to identify individuals at high risk for osteoporotic fracture.\n\nImplications of all of the Available EvidenceClinically-relevant genomic prediction of heritable traits is feasible using the machine learning algorithm presented here in large sample sizes. Genome-wide genotyping is now less expensive than many clinical tests, needs to be performed once over a lifetime and could risk stratify for multiple heritable traits and diseases years prior to disease onset, providing an opportunity for prevention. The implementation of such algorithms could improve screening efficiency, yet their cost-effectiveness will need to be ascertained in subsequent analyses.

genomics↗

CAN NEUROPATHIC PAIN PREDICT RESPONSE TO ARTHROPLASTY IN KNEE OSTEOARTHRITIS? A PROSPECTIVE OBSERVATIONAL COHORT STUDY.

A significant proportion of patients with knee osteoarthritis (OA) continue to have severe ongoing pain following knee replacement surgery. Central sensitization and features suggestive of neuropathic pain before surgery may result in a poor outcome post-operatively. In this prospective observational study of patients undergoing primary knee arthroplasty (n=120), the modified PainDETECT score was used to divide patients, with primary knee OA, into nociceptive (<13), unclear (13-18) and neuropathic -like pain (>18) groups pre-operatively. Response to surgery was compared between groups using the Oxford Knee Score (OKS) and the presence of moderate to severe long-term pain 12 months after arthroplasty. The analyses were replicated in a larger independent cohort study (n=404). 120 patients were recruited to the main study cohort: 63 (52%) nociceptive pain; 32 (27%) unclear pain; 25 (21%) neuropathic-like pain. Patients with neuropathic-like pain had significantly worse OKS pre and post-operatively, compared to the nociceptive pain group, independent of age, sex and BMI. At 12-months post-operatively the mean OKS was 4 points lower in the neuropathic-like group compared with the nociceptive group in the study cohort (non-significant); with a difference of 5 points in the replication cohort (p<0.001). Moderate to severe long-term pain after arthroplasty at 12-months was present in 50% of the neuropathic-like pain group versus 24% in the nociceptive pain group, in the replication cohort (p<0.001). Neuropathic pain is common and targeted therapy pre, peri and post-operatively may improve treatment response.

epidemiology↗

An essential mycolate remodeling program for mycobacterial adaptation in host cells

The success of Mycobacterium tuberculosis (MTB) stems from its ability to remain hidden from the immune system within macrophages. Here, we report a new technology (Path-seq) to sequence miniscule amounts of MTB transcripts within up to million-fold excess host RNA. Using Path-seq we have discovered a novel transcriptional program for in vivo mycobacterial cell wall remodeling when the pathogen infects alveolar macrophages in mice. We have discovered that MadR transcriptionally modulates two mycolic acid desaturases desA1/A2 to initially promote cell wall remodeling upon in vitro macrophage infection and, subsequently, reduces mycolate biosynthesis upon entering dormancy. We demonstrate that disrupting MadR program is lethal to diverse mycobacteria making this evolutionarily conserved regulator a prime antitubercular target for both early and late stages of infection.\n\nOne Sentence SummaryNovel technology (Path-seq) discovers cell wall remodeling program during Mycobacterium tuberculosis infection of macrophages

microbiology↗

An Atlas of Human and Murine Genetic Influences on Osteoporosis

Osteoporosis is a common debilitating chronic disease diagnosed primarily using bone mineral density (BMD). We undertook a comprehensive assessment of human genetic determinants of bone density in 426,824 individuals, identifying a total of 518 genome-wide significant loci, (301 novel), explaining 20% of the total variance in BMD--as estimated by heel quantitative ultrasound (eBMD). Next, meta-analysis identified 13 bone fracture loci in ~1.2M individuals, which were also associated with BMD. We then identified target genes from cell-specific genomic landscape features, including chromatin conformation and accessible chromatin sites, that were strongly enriched for genes known to influence bone density and strength (maximum odds ratio = 58, P = 10-75). We next performed rapid throughput skeletal phenotyping of 126 knockout mice lacking eBMD Target Genes and showed that these mice had an increased frequency of abnormal skeletal phenotypes compared to 526 unselected lines (P < 0.0001). In-depth analysis of one such Target Gene, DAAM2, showed a disproportionate decrease in bone strength relative to mineralization. This comprehensive human and murine genetic atlas provides empirical evidence testing how to link associated SNPs to causal genes, offers new insights into osteoporosis pathophysiology and highlights opportunities for drug development.

genomics↗

Targeting stromal remodeling and cancer stem cell plasticity to overcome chemoresistance in triple negative breast cancer

The cellular and molecular basis of stromal cell recruitment, activation and crosstalk in carcinomas is poorly understood, limiting the development of targeted anti-stromal therapies. In mouse models of triple negative breast cancer (TNBC), Hh ligand produced by neoplastic cells reprogrammed cancer-associated fibroblast (CAF) gene expression, driving tumor growth and metastasis. Hh-activated CAFs upregulated expression of FGF5 and production of fibrillar collagen, leading to FGFR and FAK activation in adjacent neoplastic cells, which then acquired a stem-like, drug-resistant phenotype. Treatment with smoothened inhibitors (SMOi) reversed these phenotypes. Stromal treatment of TNBC patient-derived xenograft (PDX) models with SMOi downregulated the expression of cancer stem cell markers and sensitized tumors to docetaxel, leading to markedly improved survival and reduced metastatic burden. In the phase I clinical trial EDALINE, 3 of 12 patients with metastatic TNBC derived clinical benefit from combination therapy with the SMOi Sonidegib and docetaxel chemotherapy, with one patient experiencing a complete response. Markers of pathway activity correlated with response. These studies identify Hh signaling to CAFs as a novel mediator of cancer stem cell plasticity and an exciting new therapeutic target in TNBC.\n\nSIGNIFICANCECompared to other breast cancer subtypes, TNBCs are associated with significantly worse patient outcomes. Standard of care systemic treatment for patients with non-BRCA1/2 positive TNBC is cytotoxic chemotherapy. However, the failure of 70% of treated TNBCs to attain complete pathological response reflects the relative chemoresistance of these tumors. New therapeutic strategies are needed to improve patient survival and quality of life. Here, we provide new insights into the dynamic interactions between heterotypic cells within a tumor. Specifically, we establish the mechanisms by which CAFs define cancer cell phenotype and demonstrate that the bidirectional CAF-cancer cell crosstalk can be successfully targeted in mice and humans using anti-stromal therapy.

cancer biology↗

Harmonization of cortical thickness measurements across scanners and sites

With the proliferation of multi-site neuroimaging studies, there is a greater need for handling non-biological variance introduced by differences in MRI scanners and acquisition protocols. Such unwanted sources of variation, which we refer to as \"scanner effects\", can hinder the detection of imaging features associated with clinical covariates of interest and cause spurious findings. In this paper, we investigate scanner effects in two large multi-site studies on cortical thickness measurements, across a total of 11 scanners. We propose a set of general tools for visualizing and identifying scanner effects that are generalizable to other modalities. We then propose to use ComBat, a technique adopted from the genomics literature and recently applied to diffusion tensor imaging data, to combine and harmonize cortical thickness values across scanners. We show that ComBat removes unwanted sources of scan variability while simultaneously increasing the power and reproducibility of subsequent statistical analyses. We also show that ComBat is useful for combining imaging data with the goal of studying life-span trajectories in the brain.

neuroscience↗