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Static robust optimization has played an important role in radiotherapy, where the decisions aim to safeguard against all possible realizations of uncertainty. However, it may lead to overly conservative decisions or too expensive treatment plans, such as delivering significantly more dose than necessary. Motivated by the success of adjustable robust optimization in reducing highly conservative decision-making of static robust optimization in applications, in this paper, we present an affinely adjustable robust optimization (AARO) model for hypoxia-based radiation treatment planning in the face of evolving data uncertainty. We establish an exact semi-definite program reformulation of the model under a so-called affine decision rule and evaluate our model and approach on a liver cancer case as a proof-of-concept. Our AARO model incorporates uncertainties both in dose influence matrix and re-oxygenation data as well as inexactness of the revealed (re-oxygenation) data. Our numerical experiments demonstrate that the adjustable model successfully handles uncertainty in both re-oxygenation and the dose matrix. They also show that, by utilizing information halfway through the treatment plan, the adjustable solutions of the AARO model outperform a static method while maintaining a similar total dose. [ABSTRACT FROM AUTHOR]

Metabolic reprogramming plays a critical role in hepatocarcinogenesis. However, the mechanisms regulating metabolic reprogramming in primary liver cancer (PLC) are unknown. Differentially expressed miRNAs between PLC and normal tissues were identified using bioinformatic analysis. RT-qPCR was used to determine miR-10b-5p and SCL38A2 expression levels. IHC, WB, and TUNEL assays were used to assess the proliferation and apoptosis of the tissues. The proliferation, migration, invasion, and apoptosis of PLC cells were determined using the CCK-8 assay, Transwell assay, and flow cytometry. The interaction between miR-10b-5p and SLC38A2 was determined using dual-luciferase reporter assay. A PLC xenograft model in BALB/c nude mice was established, and tumorigenicity and SLC38A2 expression were estimated. Finally, liquid chromatography - mass spectrometry (LC-MS) untargeted metabolomics was used to analyze the metabolic profiles of xenograft PLC tissues in nude mice. miR-10b-5p was a key molecule in the regulation of PLC. Compared with para-carcinoma tissues, miR-10b-5p expression was increased in tumor tissues. miR-10b-5p facilitated proliferation, migration, and invasion of PLC cells. Mechanistically, miR-10b-5p targeted SLC38A2 to promote PLC tumor growth. Additionally, miR-10b-5p altered the metabolic features of PLC in vivo. Overexpression of miR-10b-5p resulted in remarkably higher amounts of lumichrome, folic acid, octanoylcarnitine, and Beta-Nicotinamide adenine dinucleotide, but lower levels of 2-methylpropanal, glycyl-leucine, and 2-hydroxycaproic acid. miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment. [ABSTRACT FROM AUTHOR]