Prehn R T
Department of Pathology, School of Medicine, University of Washington, Seattle, USA.
Cancer Res. 1996 Mar 1;56(5):937-940.
Partial regression in cutaneous malignant melanoma has been reported by a number of observers, albeit not all, to be associated with a relatively poor prognosis; in contrast, a keratoacanthoma, which eventually regresses, does not metastasize. The Hammond effect could explain the possibly poor prognosis of the thin regressing melanoma. Hammond(W.G. Hammond et al., Cancer J., 8: 130-138, 1995) showed that the speed of biological progression to less differentiated phenotypes is directly related to the immunocompetences of the tumor hosts. If partial regression is a sign of an unusually strong immune reaction, then the melanoma that partially regresses might have a relatively poor prognosis because of the greater risk of biological progression among the surviving tumor clones. A Hammond effect is not associated with regression of a keratoacanthoma. I postulate that the growth of this tumor is accelerated, rather than restrained, by the immune reaction and that the ultimate regression of the tumor is the result, not of immune cytotoxicity, but of a rapid terminal differentiation (a reverse Hammond effect); alternatively, very rapid growth might lead to an exhaustion of growth potential before progression to clonal immortality could occur.
许多观察者报告称，皮肤恶性黑色素瘤的部分消退与相对较差的预后相关，尽管并非所有观察者都这么认为；相比之下，最终会消退的角化棘皮瘤不会发生转移。哈蒙德效应可以解释消退型薄黑色素瘤可能预后较差的原因。哈蒙德（W.G. Hammond等人，《癌症杂志》，8: 130 - 138，1995）表明，生物进展到低分化表型的速度与肿瘤宿主的免疫能力直接相关。如果部分消退是异常强烈免疫反应的标志，那么部分消退的黑色素瘤可能预后相对较差，因为存活的肿瘤克隆中生物进展的风险更大。哈蒙德效应与角化棘皮瘤的消退无关。我推测这种肿瘤的生长是由免疫反应加速的，而不是受到抑制，并且肿瘤最终的消退不是免疫细胞毒性的结果，而是快速终末分化（反向哈蒙德效应）的结果；或者，非常快速的生长可能导致在进展到克隆永生之前生长潜力耗尽。
