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DeGRe: Dense-supervised Generative Reranking for Recommendation

arXiv:2605.25749v1 Announce Type: cross Abstract: In multi-stage recommender systems, reranking optimizes overall utility by capturing intra-list contextual dependencies, yet its central challenge lies in exploring optimal sequences within an exponentially large permutation space. Recent studies have shifted towards end-to-end generative frameworks, which typically leverage list-wise rewards or preference alignment to guide generator training. However, these methods still face two critical issues. First is the heuristic label bias. Existing methods often construct training targets based on simple rules, such as promoting clicked items to the top, while ignoring causal dependencies within the list context. Second is the credit assignment problem. Sparse list-level posterior rewards fail to directly guide intermediate steps in sequence generation, leading to ambiguous optimization directions. To address these issues, we propose DeGRe (Dense-supervised Generative Reranking), a generative reranking framework that bridges the gap between offline exploration and online efficiency through dense supervision. The core of DeGRe lies in its offline-online decoupled design. During the offline phase, we introduce a Lookahead Evaluator based on cumulative regression, which leverages beam search to actively mine high-value lookahead sequences in the unexposed space. During training, we transform the step-wise value estimations from the evaluator into dense supervision signals and distill them into a lightweight Online Generator. This mechanism enables the generator to internalize lookahead planning capabilities, requiring only a single efficient greedy decoding pass during online inference to approximate the global optimum. Experiments demonstrate that DeGRe outperforms baseline models on public benchmarks and industrial datasets. We have successfully deployed DeGRe on Taobao Flash Shopping, significantly improving online recommendations.

ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming

14 April 2026 at 18:00

Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.

ABSTRACT

Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3Ξ² phosphorylation. Combined with ANP32E-mediated GSK3Ξ² suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-Ξ²-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3Ξ² inactivation, representing a prognostic biomarker and therapeutic target validated by PGG.

PMID:41980942 | DOI:10.1038/s41419-026-08712-2

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