Scardino P T
Scott Department of Urology, Baylor College of Medicine, Houston, Texas.
Urol Clin North Am. 1989 Nov;16(4):635-55.
Many important features of the biology of prostate cancer have not been discussed in this review, which has emphasized the traditional criteria for characterizing the biologic behavior of the disease: volume, grade, and invasiveness. Studies of the pathology of prostate cancer found at autopsy or in the clinic, the natural history of the disease, and the results of treatment trials leave little room for doubt that large cancers, particularly those that are not well differentiated or that invade outside of the prostate, will prove lethal if not effectively treated. We do not know whether some small prostate cancers are potentially dangerous. Perhaps studies of nuclear features, DNA content, or oncogene expression will be able to distinguish the potentially lethal small cancers from the truly "latent" small cancers. We do, however, have strong evidence that every big cancer is dangerous. Autopsy studies have established that there are not two forms of prostate cancer, but one. Initial malignant transformation in the prostate produces an adenocarcinoma histologically indistinguishable from any other prostate cancer. However, a promoter seems to be necessary to activate the tumor and allow it to express its malignant potential. The strong correlation between the prevalence of large, proliferative cancers found at autopsy and the clinical incidence and mortality rate of prostate cancer in populations around the world strongly supports the concept of a multistep process in the pathogenesis of the disease. If McNeal's detailed volumetric studies are accurate, then we can estimate the proportion of "autopsy" cancers that are large enough to threaten the life and well-being of their host. This proportion appears to be about 20 per cent, and these are the undetected but "clinically important" cancers. The dilemma of prostate cancer becomes less puzzling when viewed in this light. In a daunting display of the power of the paradox of prostate cancer, Chodak estimated that if every cancer present in American men were to be found and treated, 75,000 men would die from the treatment, whereas less than 30,000 are expected to die of the disease this year! But this paradox can be explained by introducing time into the analysis, basing estimates on the lifetime risks rather than the annual incidence. For a 50-year-old man, the lifetime risk of developing cancer in the prostate is about 42 per cent, the risk of developing the disease clinically is 9.5 per cent, and the risk of dying from the disease is 2.9 per cent.(ABSTRACT TRUNCATED AT 400 WORDS)
本综述未讨论前列腺癌生物学的许多重要特征，而是着重强调了用于描述该疾病生物学行为的传统标准：体积、分级和侵袭性。对尸检或临床中发现的前列腺癌病理学、疾病自然史以及治疗试验结果的研究，毫无疑问地表明，大的癌症，尤其是那些分化不良或侵犯前列腺外的癌症，如果不进行有效治疗，将被证明是致命的。我们不知道一些小的前列腺癌是否具有潜在危险性。或许对细胞核特征、DNA含量或癌基因表达的研究将能够区分潜在致命的小癌症与真正“潜伏”的小癌症。然而，我们确实有充分的证据表明，每一个大的癌症都是危险的。尸检研究已证实，前列腺癌不存在两种形式，而是一种。前列腺的初始恶性转化产生的腺癌在组织学上与其他任何前列腺癌并无区别。然而，似乎需要一个启动子来激活肿瘤并使其发挥恶性潜能。尸检中发现的大的、增殖性癌症的患病率与世界各地人群中前列腺癌的临床发病率和死亡率之间的强烈相关性，有力地支持了该疾病发病机制中多步骤过程的概念。如果麦克尼尔详细的体积研究是准确的，那么我们可以估算出“尸检”癌症中足以威胁宿主生命和健康的比例。这个比例似乎约为20%，而这些就是未被发现但“临床上重要”的癌症。从这个角度来看，前列腺癌的困境就不那么令人困惑了。乔达克令人畏惧地展示了前列腺癌悖论的力量，他估计，如果美国男性体内存在的每一个癌症都能被发现并治疗，7.5万名男性将死于治疗，而预计今年死于该疾病的人数不到3万！但通过在分析中引入时间，以终生风险而非年发病率为基础进行估算，这个悖论是可以解释的。对于一名50岁的男性来说，一生中患前列腺癌的风险约为42%，临床上患该病的风险为9.5%，死于该病的风险为2.9%。（摘要截选至400字）
