Adolescent acne includes a familial genetic predisposition. Additional environmental factors of psychological stress, skin oiliness and high caloric diets may also contribute to the onset of acne in Chinese adolescents.

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Our results of this study strongly indicated that a shorter CAG repeat length and specific haplotypes of AR attributed to the risk of acne development and thus could serve as a susceptibility marker.

Vulnerabilities need to be detected and removed from software. Although previous studies demonstrated the usefulness of employing prediction techniques in deciding about vulnerabilities of software components, the accuracy and improvement of effectiveness of these prediction techniques is still a grand challenging research question. This paper proposes a hybrid technique based on combining N-gram analysis and feature selection algorithms for predicting vulnerable software components where features are defined as continuous sequences of token in source code files, i.e., Java class file. Machine learning-based feature selection algorithms are then employed to reduce the feature and search space. We evaluated the proposed technique based on some Java Android applications, and the results demonstrated that the proposed technique could predict vulnerable classes, i.e., software components, with high precision, accuracy and recall.

Oncogenic KIT or PDGFRA receptor tyrosine kinase mutations are compelling therapeutic targets in gastrointestinal stromal tumor (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with advanced GIST. Polyclonal emergence of KIT/PDGFRA secondary mutations is the main mechanism of imatinib progression, making it challenging to overcome KIT/PDGFRA-inhibitor resistance. It is unclear whether there are other therapeutic targets in advanced GIST. Using genome-wide transcriptomic profiling of advanced versus early-stage GIST and CRISPR knockout functional screens, we demonstrate that CDK1 is frequently highly expressed in advanced GIST but not in early-stage GIST across three patient cohorts. High expression of CDK1 was associated with malignancy in GIST. CDK1 was critically required for advanced GIST, including imatinib-resistant GIST. CDK1 ablation led to robust proliferation inhibition. A mass spectrometry-based proteomics screen further revealed that AKT is a novel substrate of CDK1 kinase in GIST. CDK1 bound AKT and regulated its phosphorylation, thereby promoting GIST proliferation and progression. Importantly, a pharmacologic inhibitor of CDK1, RO-3306, disrupted GIST cell proliferation in CDK1 highly expressed GIST but not in CDK1-negative GIST cells and nontransformed fibroblast cells. Treatment with RO-3306 reduced tumor growth in both imatinib-resistant and imatinib-sensitive GIST xenograft mouse models. Our findings suggest that CDK1 represents a druggable therapeutic target in GIST and warrants further testing in clinical trials. Significance: These findings propose CDK1 as a novel cell-cycle–independent vulnerability in gastrointestinal stromal tumors, representing a new therapeutic opportunity for patients with advanced disease.

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