Munker R, Hiller E, Melnyk A, Gutjahr P
UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. UNIV MUNICH,KLINIKUM GROSSHADERN,MED KLIN 3,D-8000 MUNICH,GERMANY. UNIV MAINZ,KINDERKLIN,D-6500 MAINZ,GERMANY.
Int J Oncol. 1996 Oct;9(4):763-76. doi: 10.3892/ijo.9.4.763.
The secondary development of malignant tumors after the treatment of Hodgkin's disease has been termed the price of success, but is relevant also to other types of cancer and gives an opportunity to study mechanisms of carcinogenesis and tumor induction. The authors review here their experience with second malignant neoplasms (SMN) as well as the result of an extensive search of the recent literature. The primary malignancies discussed in this article include Hodgkin's disease, pediatric cancer, breast cancer, lung cancer and other types of tumors. The international literature was searched (Medline 1989-1995) for reports of SMN with special emphasis on risk factors and the molecular mechanisms of tumor induction. In Hodgkin's disease, a 3 to 5-fold elevated risk for SMN was recognized, with a 15-year cumulative incidence in the range of 11-18%. All types of malignancies have a statistically increased risk (leukemias, non-Hodgkin's lymphomas, solid tumors). The risk for leukemia is related to the intensity of treatment with alkylating agents. Some solid tumors like lung cancer or breast cancer are related to radiation therapy. Present-day treatments may carry a lower risk of inducing secondary malignancies than treatments in the past. For non-Hodgkin's lymphoma as primary malignancy, fewer data exist on SMN. In pediatric cancer, no general risk estimate can be given and the genetic influence is greater as a cause of SMN. The improved prognosis for acute lymphoblastic leukemia has led to a changing pattern of pediatric SMN. In head and neck- and in lung cancer, the same etiologic factors which cause the primary tumor may also cause SMN. SMN occur as part of familial cancer syndromes. Two types of treatment related leukemias (mostly AMLs) exist and can be recognized by cytogenetic and molecular analysis. A complete follow-up is necessary to fully appreciate the risk of second malignancy. The goal to prevent SMN must be reached without decreasing the cure rates of the primary tumor. New treatment approaches need to be carefully monitored for SMN. Improved tests of mutagenesis and molecular screening may help to recognize patients prone to develop SMN and permit to estimate certain types of risk. Screening and prevention strategies are useful in high-risk situations.
霍奇金病治疗后发生的恶性肿瘤二次发展被称为成功的代价，但这也与其他类型的癌症相关，并且为研究致癌机制和肿瘤诱发提供了机会。作者在此回顾了他们关于第二原发性恶性肿瘤（SMN）的经验以及对近期文献广泛检索的结果。本文讨论的原发性恶性肿瘤包括霍奇金病、儿童癌症、乳腺癌、肺癌和其他类型的肿瘤。检索了国际文献（1989 - 1995年的Medline）中关于SMN的报告，特别强调了危险因素和肿瘤诱发的分子机制。在霍奇金病中，SMN的风险升高了3至5倍，15年累积发病率在11% - 18%范围内。所有类型的恶性肿瘤在统计学上都有增加的风险（白血病、非霍奇金淋巴瘤、实体瘤）。白血病的风险与烷化剂治疗强度有关。一些实体瘤如肺癌或乳腺癌与放射治疗有关。与过去的治疗相比，当今的治疗引发二次恶性肿瘤的风险可能更低。对于作为原发性恶性肿瘤的非霍奇金淋巴瘤，关于SMN的数据较少。在儿童癌症中，无法给出总体风险估计，遗传影响作为SMN的病因更大。急性淋巴细胞白血病预后的改善导致了儿童SMN模式的变化。在头颈癌和肺癌中，导致原发性肿瘤的相同病因因素也可能导致SMN。SMN作为家族性癌症综合征的一部分出现。存在两种与治疗相关的白血病（主要是急性髓细胞白血病），可通过细胞遗传学和分子分析识别。需要进行完整的随访以充分了解二次恶性肿瘤的风险。必须在不降低原发性肿瘤治愈率的情况下实现预防SMN的目标。新的治疗方法需要仔细监测是否发生SMN。改进的诱变测试和分子筛查可能有助于识别易发生SMN的患者，并允许估计某些类型的风险。筛查和预防策略在高风险情况下是有用的。
