PO.BCS01.12 · 生物信息与计算
迈向用于预测癌细胞动力学的精准量子支持向量模块
Towards an accurate quantum support vector module for predicting cancer cell dynamics
作者与单位 Authors & Affiliations
摘要 Abstract
中文摘要
高维癌症组学数据集捕获了对肿瘤进展和治疗耐药至关重要的分子异质性,然而经典方法在面对非线性变异时往往会压缩或掩盖这种结构。识别既能保留致癌信号又能区分细微表型状态的计算框架,仍是一项重大挑战。为解决这一问题,我们引入了 QomiKS(Quantum Oncological Kernel Suite,量子肿瘤学核套件),旨在研究量子增强的特征空间如何恢复癌症表型之间具有生物学意义的分离。利用基于保真度的量子核、经典 Gram 矩阵以及轻量级 NumPy 角度编码流程,我们评估了肿瘤来源样本之间的可分性在不同编码方案下如何变化。早期基于 PCA 的量子模型带来了适度的改进,但需要大量计算资源。相比之下,角度编码的 QSVM 在恶性与非恶性状态之间产生了更清晰的区分,同时降低了计算成本,表明量子核即使在特征极少的情况下也能保留高价值的致癌结构。使用 ZZFeatureMap 和 PauliFeatureMap 的实现揭示了对与增殖、免疫逃逸或代谢改变相关的通路级非线性的互补敏感性。在多样化的数据集中,我们观察到一致的模式。由于经典 SVM 在致癌信号稀疏时具有稳定性,它们在数据极少的情形下占据优势。随着训练规模的增加,QSVM 越来越多地恢复出经典核无法解析的潜在生物学结构,最终以具有统计学意义的增益超越经典基线。这反映了从受噪声限制到受结构限制的学习转变,其中量子特征空间充当几何投影器,放大致癌程序、谱系状态或微环境适应中的细微差异。这些发现表明,经典模型和量子模型以根本不同的方式编码癌症特异性生物学。QomiKS 提供了一个理解这些差异的框架,并识别出量子核能更清晰地区分恶性表型的条件。随着量子硬件的发展和多组学队列的扩大,量子核学习或将为解码支配肿瘤行为的复杂分子景观、以及支持更精确的分类和治疗分层提供一条有前景的途径。
查看英文原文 English abstract
High dimensional cancer omics datasets capture molecular heterogeneity central to tumor progression and treatment resistance, yet classical methods often compress or obscure this structure when faced with nonlinear variation. Identifying computational frameworks that preserve oncogenic signals while distinguishing subtle phenotypic states remains a major challenge. To address this, we introduce QomiKS, a Quantum Oncological Kernel Suite designed to examine how quantum enhanced feature spaces recover biologically meaningful separation among cancer phenotypes.Using fidelity based quantum kernels, classical Gram matrices, and a lightweight NumPy angle encoding pipeline, we evaluate how separability among tumor derived samples shifts under different encoding schemes. Early PCA driven quantum models provided modest improvements but required substantial computational resources. In contrast, angle encoded QSVMs produced sharper discrimination among malignant and nonmalignant states while lowering computational cost, showing that quantum kernels can preserve high value oncogenic structure even with minimal features. Implementations using ZZFeatureMap and PauliFeatureMap revealed complementary sensitivities to pathway level nonlinearities linked to proliferation, immune evasion, or metabolic change.Across diverse datasets, we observe a consistent pattern. Classical SVMs dominate in extremely low data regimes due to their stability when oncogenic signal is sparse. As training sizes increase, QSVMs increasingly recover latent biological structures that classical kernels fail to resolve, ultimately surpassing classical baselines with statistically significant gains. This reflects a shift from noise limited to structure limited learning in which quantum feature spaces act as geometric projectors that amplify subtle differences in oncogenic programs, lineage states, or microenvironmental adaptation.These findings show that classical and quantum models encode cancer specific biology in fundamentally different ways. QomiKS provides a framework for understanding these differences and identifies conditions in which quantum kernels yield clearer discrimination of malignant phenotypes. As quantum hardware develops and multi omics cohorts grow, quantum kernel learning may offer a promising route for decoding complex molecular landscapes that govern tumor behavior and for supporting more precise classification and therapeutic stratification.
利益披露 Disclosure
A. Prakash, None.