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Received — 2 April 2026 ⏭

Multi-Agent Memory from a Computer Architecture Perspective: Visions and Challenges Ahead

✇cs.AI, q-bio.NC updates on arXiv.org
By: Zhongming Yu · Naicheng Yu · Hejia Zhang · Wentao Ni · Mingrui Yin · Jiaying Yang · Yujie Zhao · Jishen Zhao
1 April 2026 at 12:00
arXiv:2603.10062v2 Announce Type: replace-cross Abstract: As LLM agents evolve into collaborative multi-agent systems, their memory requirements grow rapidly in complexity. This position paper frames multi-agent memory as a computer architecture problem. We distinguish shared and distributed memory paradigms, propose a three-layer memory hierarchy (I/O, cache, and memory), and identify two critical protocol gaps: cache sharing across agents and structured memory access control. We argue that the most pressing open challenge is multi-agent memory consistency. Our architectural framing provides a foundation for building reliable, scalable multi-agent systems.

HOX code-based stratification reveals RUNX1T1-HDAC reprogramming as a targetable driver of lineage plasticity across cancers

✇Omics In Lung
By: Yuyin Jiang · Siyuan Cheng · Catherine Yijia Zhang · Xiao Jin · Longjun Li · Ha Eun Shin · Assma Alrefai · Anfeng Luo · Yaru Xu · Isaac Yi Kim · Ping Mu
30 March 2026 at 18:00

Cancer Lett. 2026 Mar 28;648:218465. doi: 10.1016/j.canlet.2026.218465. Online ahead of print.

ABSTRACT

Cancer remains a leading cause of death worldwide, with lineage plasticity emerging as a hallmark that drives therapy resistance and tumor progression by enabling cancer cells to alter identity and evade targeted therapies. Although genomic and transcriptomic aberrations correlate with lineage plasticity, the absence of scalable cross-cancer markers to rapidly identify plastic subtypes has limited predictive utility. Homeobox (HOX) genes encode transcription factors that define tissue identity through distinct expression patterns, or HOX codes, within specific lineages. By analyzing multi-omics data encompassing 39 HOX genes across more than 80,000 RNA-seq samples across 23 cancer types spanning 114 cancer subtypes, we found that HOX code expression robustly stratifies lineage-constrained and lineage-plastic states at a cross-cancer level. This framework revealed previously unrecognized lineage-plastic subtypes in prostate cancer, lung cancer, and acute myeloid leukemia (AML), each displaying distinct HOX code divergence compared to non-plastic counterparts. Differential expression analysis across these representative malignancies identified RUNX1T1 as a consistent regulator associated with HOX-defined plastic states. We validated RUNX1T1 upregulation in bulk and single-cell RNA-seq from extensive preclinical and clinical cohorts and demonstrated that RUNX1T1 is functionally required for lineage-plastic programs in prostate cancer models. AI-based structural modeling and co-immunoprecipitation established the NCOR/HDAC3 complex as a critical binding partner of RUNX1T1. CUT&RUN profiling revealed that RUNX1T1 remodels chromatin by globally reducing active enhancer marks, thereby repressing lineage-defining differentiation programs and reshaping HOX positional identity. Selective pharmacologic inhibition of HDAC3 or targeted gene silencing via lipid nanoparticles suppressed the growth of lineage-plastic cancer cells, uncovering a therapeutically actionable vulnerability. Together, these findings establish RUNX1T1 as a cross-lineage regulator of HOX code-defined plasticity and identify the RUNX1T1-HDAC axis as a targetable mechanism underlying cancer lineage plasticity.

PMID:41912135 | DOI:10.1016/j.canlet.2026.218465

HOX Code-Based Stratification Reveals RUNX1T1-HDAC Reprogramming as a Targetable Driver of Lineage Plasticity Across Cancers

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Yuyin Jiang · Siyuan Cheng · Catherine Yijia Zhang · Xiao Jin · Longjun Li · Ha Eun Shin · Assma Alrefai · Anfeng Luo · Yaru Xu · Isaac Yi Kim · Ping Mu
30 March 2026 at 18:00

Cancer Lett. 2026 Mar 28:218465. doi: 10.1016/j.canlet.2026.218465. Online ahead of print.

ABSTRACT

Cancer remains a leading cause of death worldwide, with lineage plasticity emerging as a hallmark that drives therapy resistance and tumor progression by enabling cancer cells to alter identity and evade targeted therapies. Although genomic and transcriptomic aberrations correlate with lineage plasticity, the absence of scalable cross-cancer markers to rapidly identify plastic subtypes has limited predictive utility. Homeobox (HOX) genes encode transcription factors that define tissue identity through distinct expression patterns, or HOX codes, within specific lineages. By analyzing multi-omics data encompassing 39 HOX genes across more than 80,000 RNA-seq samples across 23 cancer types spanning 114 cancer subtypes, we found that HOX code expression robustly stratifies lineage-constrained and lineage-plastic states at a cross-cancer level. This framework revealed previously unrecognized lineage-plastic subtypes in prostate cancer, lung cancer, and acute myeloid leukemia (AML), each displaying distinct HOX code divergence compared to non-plastic counterparts. Differential expression analysis across these representative malignancies identified RUNX1T1 as a consistent regulator associated with HOX-defined plastic states. We validated RUNX1T1 upregulation in bulk and single-cell RNA-seq from extensive preclinical and clinical cohorts and demonstrated that RUNX1T1 is functionally required for lineage-plastic programs in prostate cancer models. AI-based structural modeling and co-immunoprecipitation established the NCOR/HDAC3 complex as a critical binding partner of RUNX1T1. CUT&RUN profiling revealed that RUNX1T1 remodels chromatin by globally reducing active enhancer marks, thereby repressing lineage-defining differentiation programs and reshaping HOX positional identity. Selective pharmacologic inhibition of HDAC3 or targeted gene silencing via lipid nanoparticles suppressed the growth of lineage-plastic cancer cells, uncovering a therapeutically actionable vulnerability. Together, these findings establish RUNX1T1 as a cross-lineage regulator of HOX code-defined plasticity and identify the RUNX1T1-HDAC axis as a targetable mechanism underlying cancer lineage plasticity.

PMID:41912135 | DOI:10.1016/j.canlet.2026.218465

Received — 17 March 2026 ⏭

LR-SGS: Robust LiDAR-Reflectance-Guided Salient Gaussian Splatting for Self-Driving Scene Reconstruction

✇cs.AI, q-bio.NC updates on arXiv.org
By: Ziyu Chen · Fan Zhu · Hui Zhu · Deyi Kong · Xinkai Kuang · Yujia Zhang · Chunmao Jiang
16 March 2026 at 12:00
arXiv:2603.12647v1 Announce Type: cross Abstract: Recent 3D Gaussian Splatting (3DGS) methods have demonstrated the feasibility of self-driving scene reconstruction and novel view synthesis. However, most existing methods either rely solely on cameras or use LiDAR only for Gaussian initialization or depth supervision, while the rich scene information contained in point clouds, such as reflectance, and the complementarity between LiDAR and RGB have not been fully exploited, leading to degradation in challenging self-driving scenes, such as those with high ego-motion and complex lighting. To address these issues, we propose a robust and efficient LiDAR-reflectance-guided Salient Gaussian Splatting method (LR-SGS) for self-driving scenes, which introduces a structure-aware Salient Gaussian representation, initialized from geometric and reflectance feature points extracted from LiDAR and refined through a salient transform and improved density control to capture edge and planar structures. Furthermore, we calibrate LiDAR intensity into reflectance and attach it to each Gaussian as a lighting-invariant material channel, jointly aligned with RGB to enforce boundary consistency. Extensive experiments on the Waymo Open Dataset demonstrate that LR-SGS achieves superior reconstruction performance with fewer Gaussians and shorter training time. In particular, on Complex Lighting scenes, our method surpasses OmniRe by 1.18 dB PSNR.

LatentChem: From Textual CoT to Latent Thinking in Chemical Reasoning

✇cs.AI, q-bio.NC updates on arXiv.org
By: Xinwu Ye · Yicheng Mao · Jia Zhang · Yimeng Liu · Li Hao · Fang Wu · Zhiwei Li · Yuxuan Liao · Zehong Wang · Yingcheng Wu · Zhiyuan Liu · Zhenfei Yin · Li Yuan · Philip Torr · Huan Sun · Xiangxiang Zeng · Mengdi Wang · Le Cong · Shenghua Gao · Xiangru Tang
16 March 2026 at 12:00
arXiv:2602.07075v4 Announce Type: replace-cross Abstract: Chemical large language models (LLMs) predominantly rely on explicit Chain-of-Thought (CoT) in natural language to perform complex reasoning. However, chemical reasoning is inherently continuous and structural, and forcing it into discrete linguistic tokens introduces a fundamental representation mismatch that constrains both efficiency and performance. We introduce LatentChem, a latent reasoning interface that decouples chemical computation from textual generation, enabling models to perform multi-step reasoning directly in continuous latent space while emitting language only for final outputs. Remarkably, we observe a consistent emergent behavior: when optimized solely for task success, models spontaneously internalize reasoning, progressively abandoning verbose textual derivations in favor of implicit latent computation. This shift is not merely stylistic but computationally advantageous. Across diverse chemical reasoning benchmarks, LatentChem achieves a 59.88\% non-tie win rate over strong CoT-based baselines on ChemCoTBench, while delivering a 10.84$\times$ average reduction in reasoning overhead. Our results provide empirical evidence that chemical reasoning is more naturally and effectively realized as continuous latent dynamics rather than discretized linguistic trajectories.
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