Centre for Cancer Research and Cell Biology, Queen's University of Belfast, Belfast, United Kingdom; Belfast Health and Social Care Trust, Belfast, United Kingdom.
Centre for Cancer Research and Cell Biology, Queen's University of Belfast, Belfast, United Kingdom; Belfast Health and Social Care Trust, Belfast, United Kingdom; Northern Ireland Molecular Pathology Laboratory, Belfast, United Kingdom.
Am J Pathol. 2018 Sep;188(9):1936-1948. doi: 10.1016/j.ajpath.2018.05.021. Epub 2018 Jul 18.
Colorectal cancer (CRC) diagnosis and prognostic stratification are based on histopathologic assessment of cell or nuclear pleomorphism, aberrant mitotic figures, altered glandular architecture, and other phenomic abnormalities. This complexity is driven by oncogenic perturbation of tightly coordinated spatiotemporal signaling to disrupt multiple scales of tissue organization. This review clarifies molecular and cellular mechanisms underlying common CRC histologic features and helps understand how the CRC genome controls core aspects of tumor aggressiveness. It further explores a spatiotemporal framework for CRC phenomics based on regulation of living cells in fundamental and organotypic model systems. The review also discusses tissue homeostasis, considers distinct classes of oncogenic perturbations, and evolution of cellular or multicellular cancer phenotypes. It further explores the molecular controls of cribriform, micropapillary, and high-grade CRC morphology in organotypic culture models and assesses relevant translational studies. In addition, the review delves into complexities of morphologic plasticity whereby a single molecular signature generates heterogeneous cancer phenotypes, and, conversely, morphologically homogeneous tumors show substantive molecular diversity. Principles outlined may aid mechanistic interpretation of omics data in a setting of cancer pathology, provide insight into CRC consensus molecular subtypes, and better define principles for CRC prognostic stratification.
结直肠癌(CRC)的诊断和预后分层基于对细胞或核多形性、异常有丝分裂象、腺体结构改变和其他表型异常的组织病理学评估。这种复杂性是由致癌基因对时空信号的紧密协调的扰动驱动的,从而破坏了多个组织尺度的组织。本综述阐明了常见 CRC 组织学特征背后的分子和细胞机制,有助于了解 CRC 基因组如何控制肿瘤侵袭性的核心方面。它进一步探讨了基于基本和器官型模型系统中活细胞调控的 CRC 表型的时空框架。该综述还讨论了组织稳态、不同类别的致癌扰动以及细胞或多细胞癌症表型的进化。它进一步探讨了在器官型培养模型中筛状、微乳头状和高级 CRC 形态的分子控制,并评估了相关的转化研究。此外,该综述深入探讨了形态可塑性的复杂性,即单一分子特征产生异质的癌症表型,相反,形态上同质的肿瘤显示出实质性的分子多样性。概述的原则可能有助于在癌症病理学背景下对组学数据进行机制解释,深入了解 CRC 共识分子亚型,并更好地定义 CRC 预后分层的原则。