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Cell autonomous cancer dependencies are now routinely identified using CRISPR loss-of-function viability screens. However, a bias exists that makes it difficult to assess the true essentiality of genes located in amplicons, since the entire amplified region can exhibit lethal scores. These false-positive hits can either be discarded from further analysis, which in cancer models can represent a significant number of hits, or methods can be developed to rescue the true-positives within amplified regions. We propose two methods to rescue true positive hits in amplified regions by correcting for this copy number artefact. The Local Drop Out (LDO) method uses the relative lethality scores within genomic regions to assess true essentiality and does not require additional orthogonal data (e.g. copy number value). LDO is meant to be used in screens covering a dense region of the genome (e.g. a whole chromosome or the whole genome). The General Additive Model (GAM) method models the screening data as a function of the known copy number values and removes the systematic effect from the measured lethality. GAM does not require the same density as LDO, but does require prior knowledge of the copy number values. Both methods have been developed with single sample experiments in mind so that the correction can be applied even in smaller screens. Here we demonstrate the efficacy of both methods at removing the copy number effect and rescuing hits from some of the amplified regions. We estimate a 70-80% decrease of false positive hits with either method in regions of high copy number compared to no correction.
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http://dx.doi.org/10.1371/journal.pcbi.1006279 | DOI Listing |
Front Genet
August 2025
Department of Medical Genetics, Jiangxi Maternal and Child Health Hospital, Nanchang, China.
Objective: The aim of this study was to determine the diagnostic value of prenatal chromosomal microarray analysis (CMA) for fetuses at high risk for various conditions on chromosomal abnormalities.
Methods: In the study, 8,560 clinical samples were collected from pregnant women between February 2018 and June 2022, including 75 villus, 7,642 amniotic fluid, and 843 umbilical cord blood samples. All samples were screening for chromosomal abnormalities using both CMA and karyotyping.
J Med Case Rep
September 2025
Department of Anesthesiology, LMU University Hospital Munich LMU, Marchioninistrasse 15, 81377, Munich, Germany.
Background: The treatment of critically ill patients in intensive care units is becoming increasingly complex. For example, organ transplants are regularly carried out, the recipients are seriously ill, and the postoperative course can be complicated. This is why organ replacement and hemadsorption procedures are becoming increasingly important.
View Article and Find Full Text PDFGenome Biol
September 2025
Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, 100101, Beijing, China.
Background: Centromeres are crucial for precise chromosome segregation and maintaining genome stability during cell division. However, their evolutionary dynamics, particularly in polyploid organisms with complex genomic architectures, remain largely enigmatic. Allopolyploid wheat, with its well-defined hierarchical ploidy series and recent polyploidization history, serves as an excellent model to explore centromere evolution.
View Article and Find Full Text PDFMol Genet Genomic Med
September 2025
Department of Maternal-Fetal Medicine, Augusta University, Augusta, Georgia, USA.
Introduction: Spinal muscular atrophy (SMA), caused by pathogenic variants in the survival motor neuron (SMN) gene, is the most common genetic cause of mortality in children under the age of two. Prior reports of obstetric sonograms performed in pregnancies with severe forms of fetal SMA have discrepant findings that may stem from a failure to account for the SMN2 copy number.
Methods: We present a neonate diagnosed with SMA type 0 postnatally (0SMN1/1SMN2 genotype).
JDS Commun
September 2025
Livestock Improvement Corporation Ltd., Newstead, Hamilton 3240, New Zealand.
SLICK1 is an allelic variant of the prolactin receptor () that is found in Senepol beef cattle. The presence of a single copy of this allele produces a short hair coat and confers heat tolerance. We aimed to determine the effect of 2 copies of this allele on milking performance of dairy cattle.
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