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CRC is heterogeneous with regard to molecular alterations and characterization of the molecular aetiology of sporadic CRC has identified different oncogenic pathways.
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Here, we review the main findings of these investigations as well as their possible biological and clinical implications, focusing on key findings obtained by genomic technologies, such as the expanded compendium of somatic gene alterations and the characterization of clonal evolution and of the epigenetic landscape of CLL.
The study produced a discovery-driven catalogue of protein-level alterations, and a functional characterization of the tumor biology of CRC.
Identification and characterization of genetic alterations are essential for diagnosis of multiple myeloma and may guide therapeutic decisions.
Identification and characterization of these alterations is of great relevance in understanding the underlying biology of cancer, as well as the design of clinically useful biomarkers of cancer relapse or metastases.
The application of multimodal MRI protocols is diagnostically relevant for the differentiation between schizophrenic patients and controls and provides a new strategy for the detection and characterization of subtle structural alterations in defined regions of the living brain.
Advances in microarray and RNA-seq technologies allow the systemic analysis and characterization of expression level alterations of genes during the disease process.
More recently, research emphasis has shifted toward the identification and characterization of causative genetic alterations that convey the associated risk linkages in human SLE [ 3], as well as mouse models of disease [ 4].
Therefore, identification and characterization of DNA copy number alteration regions in different racial groups helps to dissect the mechanism of tumorigenesis.
Better understanding and characterization of novel genetic and epigenetic alterations, which are important to hepatocarcinogenesis, may help understand the molecular pathogenesis of HCC, as well as providing novel therapeutic targets for HCC treatment.
Here, we report the design and characterization of a double-mutant p53 with alterations of residues at positions Met340 and Leu344.
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