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Received — 13 September 2026 ⏭

Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma

✇Omics in Hepatocellular
By: Nanbin Liu · Kun Li · Junqiao Feng · Shan Wang · Ji Li · Wenbin Yang · Senyang Li · Keping Feng
11 September 2026 at 18:00

Clin Exp Med. 2026 Jul 26;26(1):329. doi: 10.1007/s10238-026-02264-7.

ABSTRACT

KANSL2, a core component of the NSL histone acetyltransferase complex, has been implicated in tumorigenesis. However, its pan-cancer relevance and functional role in liver hepatocellular carcinoma (LIHC) remain unclear. Multi-omics data from TCGA, GEO, and HPA were integrated to systematically evaluate KANSL2 expression, clinical significance, genomic alterations, and immune associations across cancers. Functional enrichment, immune infiltration analyses, and single-cell transcriptomics were performed. In vitro assays were conducted to validate the biological effects of KANSL2 in LIHC cells. KANSL2 is broadly upregulated across cancers and exhibits strong diagnostic performance. Elevated KANSL2 expression correlates with unfavorable prognosis, particularly in LIHC. Mechanistically, KANSL2 and its co-expressed genes are enriched in cell-cycle progression. KANSL2 expression is also closely associated with immune infiltration and immunoregulatory signaling within the tumor microenvironment, with single-cell data indicating preferential expression in proliferative T-cell subsets. Functional experiments demonstrate that KANSL2 silencing suppresses proliferation, migration, and invasion, and induces G2/M phase arrest in LIHC cells. Notably, its effects on apoptosis are limited, suggesting that KANSL2 primarily drives tumor progression through cell-cycle-dependent mechanisms. This study identifies KANSL2 as a key regulator of tumor progression and immune remodeling in LIHC. By promoting malignancy predominantly via cell-cycle control, KANSL2 represents a promising biomarker for diagnosis and prognosis, and a potential therapeutic target.

PMID:42726304 | PMC:PMC13569553 | DOI:10.1007/s10238-026-02264-7

Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Nanbin Liu · Kun Li · Junqiao Feng · Shan Wang · Ji Li · Wenbin Yang · Senyang Li · Keping Feng
11 September 2026 at 18:00

Clin Exp Med. 2026 Jul 26;26(1):329. doi: 10.1007/s10238-026-02264-7.

ABSTRACT

KANSL2, a core component of the NSL histone acetyltransferase complex, has been implicated in tumorigenesis. However, its pan-cancer relevance and functional role in liver hepatocellular carcinoma (LIHC) remain unclear. Multi-omics data from TCGA, GEO, and HPA were integrated to systematically evaluate KANSL2 expression, clinical significance, genomic alterations, and immune associations across cancers. Functional enrichment, immune infiltration analyses, and single-cell transcriptomics were performed. In vitro assays were conducted to validate the biological effects of KANSL2 in LIHC cells. KANSL2 is broadly upregulated across cancers and exhibits strong diagnostic performance. Elevated KANSL2 expression correlates with unfavorable prognosis, particularly in LIHC. Mechanistically, KANSL2 and its co-expressed genes are enriched in cell-cycle progression. KANSL2 expression is also closely associated with immune infiltration and immunoregulatory signaling within the tumor microenvironment, with single-cell data indicating preferential expression in proliferative T-cell subsets. Functional experiments demonstrate that KANSL2 silencing suppresses proliferation, migration, and invasion, and induces G2/M phase arrest in LIHC cells. Notably, its effects on apoptosis are limited, suggesting that KANSL2 primarily drives tumor progression through cell-cycle-dependent mechanisms. This study identifies KANSL2 as a key regulator of tumor progression and immune remodeling in LIHC. By promoting malignancy predominantly via cell-cycle control, KANSL2 represents a promising biomarker for diagnosis and prognosis, and a potential therapeutic target.

PMID:42726304 | PMC:PMC13569553 | DOI:10.1007/s10238-026-02264-7

Received — 10 September 2026 ⏭

Instance-Aware Algorithm Selection for Maximum Clique via a Dual-Channel Graph Neural Architecture

✇cs.AI, q-bio.NC updates on arXiv.org
By: Xiang Li · Shanshan Wang · Chenglong Xiao
10 September 2026 at 12:00
arXiv:2508.08005v5 Announce Type: replace-cross Abstract: Although the Maximum Clique Problem (MCP) has been extensively studied and features a rich ecosystem of exact solvers, empirical evidence shows that solver performance varies substantially across graph families. Consequently, selecting an appropriate algorithm for a given instance remains an open and practically important challenge that has received little systematic attention. We address this gap by developing an instance-aware selection framework that systematically combines global statistical descriptors with learned topological representations. We construct a comprehensive benchmark by evaluating four state-of-the-art exact solvers on a diverse collection of graph instances and deriving both global statistical and local structural features. An evaluation of conventional classifiers establishes Random Forest as a strong baseline and reveals that connectivity and topological features are key predictors of performance. Motivated by these observations, we introduce a dual-channel architecture that jointly leverages a Graph Attention Network for capturing local neighborhood patterns and a Multilayer Perceptron for modeling global statistical features. Extensive experiments show that the proposed dual-channel model consistently surpasses classical baselines and the single-best solver, achieving 90.43% test accuracy. These findings demonstrate the value of integrating local topological encoding with global statistical cues for combinatorial algorithm selection. Code and models are available at: https://anonymous.4open.science/r/GAT-MLP-7E5F.
Received — 8 April 2026 ⏭

Representation learning to advance multi-institutional studies with electronic health record data from US and France

✇cs.AI, q-bio.NC updates on arXiv.org
By: Doudou Zhou · Han Tong · Linshanshan Wang · Suqi Liu · Xin Xiong · Ziming Gan · Romain Griffier · Boris Hejblum · Yun-Chung Liu · Chuan Hong · Clara-Lea Bonzel · Tianrun Cai · Kevin Pan · Yuk-Lam Ho · Lauren Costa · Vidul A. Panickan · J. Michael Gaziano · Kenneth Mandl · Vianney Jouhet · Rodolphe Thiebaut · Zongqi Xia · Kelly Cho · Katherine Liao · Tianxi Cai
7 April 2026 at 12:00
arXiv:2502.08547v2 Announce Type: replace Abstract: The widespread adoption of electronic health records has created new opportunities for translational clinical research, yet this promise remains constrained by fragmented data across privacy-siloed institutions and substantial heterogeneity in local coding practices. While privacy-preserving collaborative learning allows institutions to work together without sharing patient-level data, it does not address inconsistencies in how clinical concepts are represented across sites. We introduce a graph-based framework that addresses this gap by treating data harmonization as a scalable representation learning problem. Rather than relying on fixed standards or manual mappings, the framework integrates institution-specific summary statistics from health records, curated biomedical knowledge graphs, and semantic information derived from large language models to learn a shared semantic space. This joint learning approach aligns diverse, site-specific vocabularies while preserving patient privacy. Evaluated across seven institutions and two languages, the framework provides a robust, data-centric foundation for training and deploying clinical models across heterogeneous healthcare systems.

SETDB2 induces abnormal SHP-1 splicing and promotes immunosuppression in hepatocellular carcinoma

✇Oncogene - Issue - nature.com science feeds
By: Qinlian Jiao · Yidan Ren · Xin Su · Zigan Li · Yuxuan Cai · Tangbin Hu · Yunshan Wang · Guangyong Zhang · Miaoqing Zhao · Maoxiao Feng
7 April 2026 at 08:00

Oncogene, Published online: 07 April 2026; doi:10.1038/s41388-026-03759-z

SETDB2 induces abnormal SHP-1 splicing and promotes immunosuppression in hepatocellular carcinoma
Received — 17 February 2026 ⏭

InnoEval: On Research Idea Evaluation as a Knowledge-Grounded, Multi-Perspective Reasoning Problem

✇cs.AI, q-bio.NC updates on arXiv.org
By: Shuofei Qiao · Yunxiang Wei · Xuehai Wang · Bin Wu · Boyang Xue · Ningyu Zhang · Hossein A. Rahmani · Yanshan Wang · Qiang Zhang · Keyan Ding · Jeff Z. Pan · Huajun Chen · Emine Yilmaz
17 February 2026 at 13:00
arXiv:2602.14367v1 Announce Type: cross Abstract: The rapid evolution of Large Language Models has catalyzed a surge in scientific idea production, yet this leap has not been accompanied by a matching advance in idea evaluation. The fundamental nature of scientific evaluation needs knowledgeable grounding, collective deliberation, and multi-criteria decision-making. However, existing idea evaluation methods often suffer from narrow knowledge horizons, flattened evaluation dimensions, and the inherent bias in LLM-as-a-Judge. To address these, we regard idea evaluation as a knowledge-grounded, multi-perspective reasoning problem and introduce InnoEval, a deep innovation evaluation framework designed to emulate human-level idea assessment. We apply a heterogeneous deep knowledge search engine that retrieves and grounds dynamic evidence from diverse online sources. We further achieve review consensus with an innovation review board containing reviewers with distinct academic backgrounds, enabling a multi-dimensional decoupled evaluation across multiple metrics. We construct comprehensive datasets derived from authoritative peer-reviewed submissions to benchmark InnoEval. Experiments demonstrate that InnoEval can consistently outperform baselines in point-wise, pair-wise, and group-wise evaluation tasks, exhibiting judgment patterns and consensus highly aligned with human experts.
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