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Edge computing (EC) emerges as a novel computing paradigm to offload computing tasks from user equipments (UEs) to edge notes (ENs) in fifth-generation networks, which definitely breaks the resource limitation of UEs to a certain degree. However, it is troublesome to guarantee the overall operating performance of ENs due to the uneven distributed resource demands of UEs, the resulting transmission delay and the data loss for computation offloading between the covered EN and the deployed destination EN. In view of this challenge, a blockchain-based computation offloading method, named BCO, is proposed in this paper. Technically, since blockchain is a promising technique for the decentralized system, a blockchain-based EC framework is designed to degrade the data loss possibility by integrating blockchain and EC. Then, the nondominated sorting genetic algorithm, the third version (NSGA-III), is leveraged to acquire the balanced offloading strategies. Furthermore, by taking advantage of Simple Additive Weighting and Multiple Criteria Decision Making, the optimal offloading strategy is identified. Finally, systematic experiments and analyses on the comparative experiment are conducted to verify the efficiency of our proposed method BCO.

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Lung cancer is the leading cause of cancer death worldwide, with lung adenocarcinoma being the most common subtype. Many oncogenes and tumor suppressor genes are altered in this cancer type, and the discovery of oncogene mutations has led to the development of targeted therapies that have improved clinical outcomes. However, a large fraction of lung adenocarcinomas lacks mutations in known oncogenes, and the genesis and treatment of these oncogene-negative tumors remain enigmatic. Here, we perform iterative in vivo functional screens using quantitative autochthonous mouse model systems to uncover the genetic and biochemical changes that enable efficient lung tumor initiation in the absence of oncogene alterations. Generation of hundreds of diverse combinations of tumor suppressor alterations demonstrates that inactivation of suppressors of the RAS and PI3K pathways drives the development of oncogene-negative lung adenocarcinoma. Human genomic data and histology identified RAS/MAPK and PI3K pathway activation as a common feature of an event in oncogene-negative human lung adenocarcinomas. These Onc-negativeRAS/PI3K tumors and related cell lines are vulnerable to pharmacologic inhibition of these signaling axes. These results transform our understanding of this prevalent yet understudied subtype of lung adenocarcinoma. Significance: To address the large fraction of lung adenocarcinomas lacking mutations in proto-oncogenes for which targeted therapies are unavailable, this work uncovers driver pathways of oncogene-negative lung adenocarcinomas and demonstrates their therapeutic vulnerabilities.