Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD 20892, USA.
J Clin Oncol. 2010 Nov 20;28(33):4935-44. doi: 10.1200/JCO.2010.29.1112. Epub 2010 Oct 12.
Previous studies have shown increased risks of second malignancies after non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL); however, no earlier investigation has quantified differences in risk of new malignancy by lymphoma subtype.
We evaluated second cancer and leukemia risks among 43,145 1-year survivors of CLL/small lymphocytic lymphoma (SLL), diffuse large B-cell lymphoma (DLBCL), or follicular lymphoma (FL) from 11 Surveillance, Epidemiology, and End Results (SEER) population-based registries during 1992 to 2006.
Among patients without HIV/AIDS-related lymphoma, lung cancer risks were significantly elevated after CLL/SLL and FL but not after DLBCL (standardized incidence ratio [SIR], CLL/SLL = 1.42, FL = 1.28, DLBCL = 1.00; Poisson regression P for difference among subtypes, P(Diff) = .001). A similar pattern was observed for risk of cutaneous melanoma (SIR: CLL/SLL = 1.92, FL = 1.60, DLBCL = 1.06; P(Diff) = .004). Acute nonlymphocytic leukemia risks were significantly elevated after FL and DLBCL, particularly among patients receiving initial chemotherapy, but not after CLL/SLL (SIR: CLL/SLL = 1.13, FL = 5.96, DLBCL = 4.96; P(Diff) < .001). Patients with HIV/AIDS-related lymphoma (n = 932) were predominantly diagnosed with DLBCL and had significantly and substantially elevated risks for second anal cancer (SIR = 120.50) and Kaposi's sarcoma (SIR = 138.90).
Our findings suggest that differing immunologic alterations, treatments (eg, alkylating agent chemotherapy), genetic susceptibilities, and other risk factors (eg, viral infections, tobacco use) among lymphoma subtypes contribute to the patterns of second malignancy risk. Elucidating these patterns may provide etiologic clues to lymphoma as well as to the second malignancies.
既往研究表明,非霍奇金淋巴瘤(NHL)和慢性淋巴细胞白血病(CLL)患者发生第二恶性肿瘤的风险增加;然而,尚无研究量化淋巴瘤亚型与新恶性肿瘤风险之间的差异。
我们评估了 1992 年至 2006 年期间来自 11 个监测、流行病学和最终结果(SEER)人群登记处的 43145 名 CLL/小淋巴细胞淋巴瘤(SLL)、弥漫性大 B 细胞淋巴瘤(DLBCL)或滤泡性淋巴瘤(FL)1 年幸存者的第二癌症和白血病风险。
在无 HIV/AIDS 相关淋巴瘤的患者中,CLL/SLL 和 FL 后肺癌风险显著升高,但 DLBCL 后无此风险(标准化发病比 [SIR],CLL/SLL = 1.42,FL = 1.28,DLBCL = 1.00;亚组间差异的泊松回归 P 值,P(差异)=.001)。皮肤黑色素瘤的风险也观察到类似的模式(SIR:CLL/SLL = 1.92,FL = 1.60,DLBCL = 1.06;P(差异)=.004)。FL 和 DLBCL 后急性非淋巴细胞白血病风险显著升高,尤其是接受初始化疗的患者,但 CLL/SLL 后无此风险(SIR:CLL/SLL = 1.13,FL = 5.96,DLBCL = 4.96;P(差异)<.001)。患有 HIV/AIDS 相关淋巴瘤的患者(n = 932)主要被诊断为 DLBCL,第二肛门癌(SIR = 120.50)和卡波西肉瘤(SIR = 138.90)的风险显著且显著升高。
我们的研究结果表明,不同的免疫改变、治疗方法(如烷化剂化疗)、遗传易感性和其他危险因素(如病毒感染、吸烟)在淋巴瘤亚型中导致了第二恶性肿瘤风险的模式。阐明这些模式可能为淋巴瘤以及第二恶性肿瘤提供病因线索。