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首页> 外文期刊>Cell cycle >Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.
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Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.

机译：再次回顾c-myc和Ras的合作：在细胞周期蛋白D1-CDK4复合体上融合并挑战癌症生物学的基本概念。

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摘要

The c-myc is a proto-oncogene that manifests aberrant expression at high frequencies in most types of human cancer. C-myc gene amplifications are often observed in various cancers as well. Ample studies have also proved that c-myc has a potent oncogenicity, which can be further enhanced by collaborations with other oncogenes such as Bcl-2 and activated Ras. Studies on the collaborations of c-myc with Ras or other genes in oncogenicity have established several basic concepts and have disclosed their underlying mechanisms of tumor biology, including "immortalization" and "transformation". In many cases, these collaborations may converge at the cyclin D1-CDK4 complex. In the meantime, however, many results from studies on the c-myc, Ras and cyclin D1-CDK4 also challenge these basic concepts of tumor biology and suggest to us that the immortalized status of cells should be emphasized. Stricter criteria and definitions for a malignantly transformed status and a benign status of cells in culture also need to be established to facilitate our study of the mechanisms for tumor formation and to better link up in vitro data with animal results and eventually with human cancer pathology.
机译：c-myc是一种原癌基因，可在大多数类型的人类癌症中高频率显示异常表达。在各种癌症中也经常观察到C-myc基因扩增。大量研究还证明c-myc具有强致癌性，可通过与其他癌基因（如Bcl-2和活化的Ras）合作进一步增强其致癌性。关于c-myc与Ras或其他基因在致癌性方面的合作研究已经建立了几个基本概念，并揭示了其潜在的肿瘤生物学机制，包括“永生化”和“转化”。在许多情况下，这些合作可能会融合到细胞周期蛋白D1-CDK4复合体上。然而，与此同时，有关c-myc，Ras和细胞周期蛋白D1-CDK4的许多研究结果也挑战了肿瘤生物学的这些基本概念，并向我们建议应强调细胞的永生状态。还需要建立用于培养细胞的恶性转化状态和良性状态的更严格的标准和定义，以促进我们对肿瘤形成机制的研究，并更好地将体外数据与动物结果以及最终与人类癌症病理联系起来。

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