Michalides R
J Pathol. 1999 Aug;188(4):341-3. doi: 10.1002/(SICI)1096-9896(199908)188:4<341::AID-PATH384>3.0.CO;2-1.
Cancer cells arise from an increasing genetic disarray affecting control over proliferation, self-defence, and senescence. Multiple mechanisms with a multitude of players are invoked in the genetic distortion which leads to tumour progression in different tissues. Tumour pathology is in need of a clear, distinctive classification of tumour samples for assessment of risk and treatment. What for, and how should these two fields be combined? Markers which indicate the overall genetic disorder in cancer cells may be sufficient, in addition to a morphological description, to assess risk of cancer patients, in particular in cases with lymph node-negative disease. However, a refinement of risk is at hand when a better evaluation of genetic alterations is achieved. The status of genetic malfunctioning may also provide target(s) for therapy as well. In this editorial, the genetic alterations implicated in disturbed regulation of the G1 phase of the cell cycle by the Rb/cyclin D1/p16/cdk4 pathway are considered to provide relevant information to assess risk as well as to target therapy.
癌细胞源自日益严重的基因紊乱,这种紊乱影响了对细胞增殖、自我防御和衰老的控制。在导致不同组织肿瘤进展的基因畸变过程中,涉及多种机制和众多参与者。肿瘤病理学需要对肿瘤样本进行清晰、独特的分类,以评估风险和制定治疗方案。这两个领域为何要结合以及应如何结合?除了形态学描述外,能够指示癌细胞整体基因紊乱的标志物可能足以评估癌症患者的风险,特别是在淋巴结阴性疾病的情况下。然而,当能够更好地评估基因改变时,风险评估将得到进一步完善。基因功能失调的状态也可能为治疗提供靶点。在这篇社论中,Rb/细胞周期蛋白D1/p16/细胞周期蛋白依赖性激酶4途径对细胞周期G1期调控的干扰所涉及的基因改变,被认为可为评估风险和靶向治疗提供相关信息。