The incidence of lymphoma in first-degree relatives of patients with Hodgkin disease and non-Hodgkin lymphoma

Paltiel, Ora; Schmit, Tal; Adler, Bella; Rachmilevitz, Eliezer A.; Polliack, Aaron; Cohen, Amos; Haim, Nissim; Shachar, Menachem Ben; Epelbaum, Ron; Barchana, Micha; Cohen, Rinat; Yehuda, Dina Ben

doi:10.1002/(sici)1097-0142(20000515)88:10<2357::aid-cncr21>3.0.co;2-3

Cited by 62 publications

(28 citation statements)

References 25 publications

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“…Razis criticized Peacocke's much earlier Hodgkin's twins study from 1905 [47] because '[in some families] the proband had Hodgkin's disease but the relative had another form of lymphoma' [30]. Evaluating the Population Registry, Israel's national disease database, Paltiel et al [36] demonstrated anticipation in first degree relatives of patients with HD and NHL. She found that probands with another lymphoma case in the family were younger on average than the entire group of HD and NHL cases.…”

Section: Discussionmentioning

confidence: 99%

Anticipation in families with Hodgkin's and non-Hodgkin's lymphoma in their pedigree

Alexandrescu

Garino

Brown-Balem

et al. 2006

Leukemia & Lymphoma

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Anticipation is an earlier onset and/or increasing severity in successive generations. This study was conducted to determine whether anticipation occurs in families that exhibit both Hodgkin's (HD) and non-Hodgkin's (NHL) lymphoma in their pedigrees. Nine published reports of multi-generational lymphoma and 33 previously unreported families with both lymphomas were analysed for evidence of anticipation. The difference between age at onset for each affected related pair was tested against the null hypothesis that there is no difference in age at onset. Differences between disease-free survival in affected generations were determined. These analyses were also conducted separately using only parent -child pairs with an age of onset above 25 years in an effort to avoid ascertainment bias. Age at onset in studied cases was also compared with the HD and NHL series from the Surveillance Epidemiology and End Results (SEER) Program of the US National Cancer Institute. The mean age at onset in the child and parent generations of all case families (60.2 and 35.7 years, respectively) and in the selected pairs (61.5 and 45.6, years) were significantly different (mean difference 724.5 years; P 5 0.00001, and 715.9 years, P 5 0.00001, respectively). Mean anticipation for parents with HD and children with NHL was 76.8 years (P ¼ 0.01) for the unpublished and 714.4 years (P ¼ 0.002) for the published families (overall anticipation 710.1 years). Mean anticipation for parents with NHL and children with HD was 734.4 years (P 5 0.0001) for the unpublished and 732.7 years (P 5 0.0001) for the published families (overall anticipation 734.2 years, P 5 0.0001). The signed rank test rejected the null hypothesis which stated that there was no difference in age at onset between parents and children for overall, as well as selected pairs (P 5 0.00001). The null hypothesis was also rejected for both the parents with HD/children with NHL group and the parents with NHL/children with HD group pairs (P 5 0.0001). Age at onset distributions were significantly different for all generations with HD or NHL when compared to the SEER population (P 5 0.00001), except for the parents with NHL, which showed no difference. In addition, this study reports four previously unpublished families with three generations of lymphoma in their pedigrees. These data suggest that anticipation occurs in families that exhibit both HL and NHL and that both neoplasms may have a common genetic basis.

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Section: Discussionmentioning

confidence: 99%

Anticipation in families with Hodgkin's and non-Hodgkin's lymphoma in their pedigree

Alexandrescu

Garino

Brown-Balem

et al. 2006

Leukemia & Lymphoma

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“…Familial clusters of haematopoietic malignancies have been reported, pointing to the involvement of genetic factors, and the risk of NHL is increased by about 2- to 3-fold in first-degree relatives of patients with LDs and other haematopoietic malignancies 24 25. The role of infectious agents in lymphomagenesis is increasingly recognised.…”

Section: Lymphomagenesismentioning

confidence: 99%

Inflammatory bowel disease and lymphoproliferative disorders: the dust is starting to settle

Sokol

Beaugerie

2009

Gut

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The risk of lymphoproliferative disorders (LDs) has become a major concern for clinicians managing patients with inflammatory bowel disease (IBD). Yet it is difficult to distinguish the possible responsibility of immunosuppressive therapy from the background risk due to the inflammatory disorder itself. LDs are clonal B or T cell proliferation showing considerable heterogeneity and the incidence has increased since the 1970s. The strongest and best-established risk factors for LDs are primary and acquired immunodeficiency (HIV, immunosuppressant), notably via defective immune surveillance of Epstein-Barr virus. In many auto-immune diseases (eg, Sjögren's syndrome), inflammatory diseases (eg, rheumatoid arthritis) or chronic suppuration (chronic pyothorax), the risk of LD is increased. In IBD patients, in general, the risk of LD seems to be similar to or very slightly higher than in the general population. The role of immunosuppressants in lymphomagenesis is difficult to individualise because other factors potentially involved are inter-linked. Concordant data suggest that thiopurine therapy is associated with a moderately increased risk of LD. Data regarding methotrexate are scarce and come from diseases other than IBD but the risk seems low. Data regarding risk of LD in IBD patients receiving anti-tumour necrosis factor alpha (TNFalpha) agents are insufficient at this time, mainly because most of the patients are co-treated with thiopurines. The recently individualised risks of hepatosplenic T cell lymphoma and fatal post-mononucleosis LD, in young male patients with IBD who are co-treated with anti-TNFalpha and thiopurines, and EBV-seronegative IBD males, respectively, are probably low but remain to be better quantified.

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“…[12][13][14][15][16][17] Our group recently analyzed data from registries in Scandinavia and found significant familial aggregation of HL (RR ϭ 3.1) and other lymphoproliferative tumors. 13 Relative risks were higher in men compared with women, and in siblings of cases compared with parents and offspring.…”

Section: Genetic Factorsmentioning

confidence: 99%

“…11 A role for genetic factors is unequivocal based on evidence from multiply-affected families from case series, a twin study, a case-control study, and population-based registry studies. [12][13][14][15][16][17] Emerging data from Eastern Asia and among Chinese immigrants in North America indicate increasing incidence trends for HL associated with westernization, which emphasizes the importance of lifestyle and environmental risk factors even in a short-term perspective. 18,19 …”

mentioning

confidence: 99%

Current Insight on Trends, Causes, and Mechanisms of Hodgkin’s Lymphoma

et al. 2009

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Hodgkin's lymphoma (HL) has a unique and distinct history, epidemiology, treatment, and biology. A viral agent or infectious agent has long been considered as the etiologic agent and Epstein-Barr virus is the main candidate for the infectious agent causing HL; however, Epstein-Barr virus genome is found within the tumor in only about 20% to 40% of HL cases with a prior diagnosis of infectious mononucleosis. Recently, autoimmune and related conditions have drawn attention to a potential role for immune-related and inflammatory conditions in the etiology and pathogenesis of the malignancy. Evidence from multiply-affected families, a twin study, a case-control study, and population-based registry studies implicate genetic factors. Data from Eastern Asia and among Chinese immigrants in North America indicate increasing incidence trends for HL being associated with westernization. These results emphasize an interaction between environmental and genetic risk factors in HL.

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The incidence of lymphoma in first-degree relatives of patients with Hodgkin disease and non-Hodgkin lymphoma

Cited by 62 publications

References 25 publications

Anticipation in families with Hodgkin's and non-Hodgkin's lymphoma in their pedigree

Anticipation in families with Hodgkin's and non-Hodgkin's lymphoma in their pedigree

Inflammatory bowel disease and lymphoproliferative disorders: the dust is starting to settle

Current Insight on Trends, Causes, and Mechanisms of Hodgkin’s Lymphoma

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