Familial non‐Hodgkin lymphoma: Histologic diversity and relation to other cancers

Greene, Mark H.; Miller, Robert W.; Herrmann, Julia

doi:10.1002/ajmg.1320010406

Cited by 16 publications

(3 citation statements)

References 21 publications

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“…Familial non‐Hodgkin's lymphoma (NHL) cases were collected from two sources: the published medical literature ( Camino, 1975; Greene & Miller, 1978; Shelley, 1980; Greene et al , 1982 ; Haim et al , 1982 ; Veltri et al , 1983 ; Kato et al , 1989 ; Lynch et al , 1992 ; Hayoz et al , 1993 ; Donadieu et al , 1996 ; James et al , 1998 ) from 1926 to the present; and our series of unpublished families with multigenerational NHL. Additional information on one of the published families was obtained by personal communication with the author ( James et al , 1998 ).…”

Section: Methodsmentioning

confidence: 99%

Age of onset evidence for anticipation in familial non‐Hodgkin's lymphoma

Wiernik

Wang

et al. 2000

Br J Haematol

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Summary. Anticipation, a phenomenon in which an inherited disease is diagnosed at an earlier age in each successive generation of a family, has been demonstrated in certain neurological and haematological disorders. This study was conducted to determine whether anticipation occurs in familial non-Hodgkin's lymphoma (NHL). Eleven published reports of multigenerational familial NHL were analysed for evidence of anticipation, together with 18 previously unreported families with familial NHL. Differences in disease-free survival between generations were determined. The difference between age at onset for each affected parent±child pair was tested against the null hypothesis that there was no difference in age at onset. These analyses were also performed separately using only parent± child pairs with age of onset > 25 years to avoid ascertainment bias. In addition, the age at onset distribution of the studied cases was compared with that of the Surveillance Epidemiology and End Results (SEER) Program using data for 1973±98. The median ages at onset in the child and parent generations of all families (48´5 and 71´3 years respectively) and in the selected pairs (52´5 and 71´5 years respectively) were signi®cantly different (P < 0´000002 and P < 0´000001 respectively). The null hypothesis was rejected for all (P < 0´000001) as well as selected pairs (P < 0´000003). A signi®cant difference was observed between the ages of onset of the child generation and the SEER population (P < 0´009), but not between the parent generation and the SEER population. Anticipation occurs in familial NHL, which suggests a genetic basis for it.

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Section: Methodsmentioning

confidence: 99%

Age of onset evidence for anticipation in familial non‐Hodgkin's lymphoma

Wiernik

Wang

et al. 2000

Br J Haematol

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“…1) accounted for the significantly elevated risk of developing these neoplasms in the first‐degree relatives of the 33 probands aged 15–25 years with lymphomas. Families 189, 215 and 263 show some similarities with those described by Greene and Miller 22. Each of the probands with Hodgkin's disease from families 189 and 263 had a parent affected by B‐cell lymphoma.…”

Section: Discussionmentioning

confidence: 53%

Malignant tumors in first‐degree relatives of cancer patients aged 0–25 years (province of Trieste, Italy)

Brunetti¹,

Tamaro²,

Cavallieri³

et al. 2003

Intl Journal of Cancer

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To determine whether the occurrence of first and second primary malignancies in first-degree relatives of cancer patients aged 0 -25 years (probands) differed from that in the general population, a cohort study was carried out on 860 relatives of 265 probands living in the province of Trieste, Italy. During the follow-up period (median duration ‫؍‬ 28 years, 25th-75th percentile ‫؍‬ 20 -34), the relatives developed 103 first primary cancers vs. 88.9 expected for a standardized incidence ratio ( The causes of most malignant tumors of childhood remain little understood. Few environmental factors are consistently associated with cancers affecting children, and Mendelian disorders play a role in the etiology of only a small proportion of them. 1 Epidemiologic studies of familial aggregation are carried out to determine whether clustering is real or due to chance association, and constitute the first of the 3 sequential steps 2 aimed at clarifying genetic-environmental interaction in disease etiology. They have failed to provide strong evidence that the most frequent childhood malignancies cluster in families and have not reported an overall increased risk of cancer among the close relatives of children with tumors. 1 However, we observed a statistically significant excess of first primary malignancies in the first-degree relatives of childhood cancer patients and, in particular, among the relatives of children affected by brain tumors, through a population-based cohort study conducted in the northeastern Italian province of Trieste. 3 The data presented here update those in Brunetti et al. 3 Furthermore, we estimate the likelihood of developing a second primary neoplasm in those relatives, and the risk of first and second primaries among the first-degree relatives of the individuals who had cancer between 15 and 25 years of age, because tumors in adolescents and young adults were found to have several epidemiologic features in common with those occurring in childhood. 4 SUBJECTS AND METHODSAll resident males and females aged 0 -25 years with a first primary cancer diagnosed between 1 January 1971 and 31 December 1993 (probands) were sorted out from the file of the Cancer Registry of the Province of Trieste (CRPT). 5 Their tumors were grouped according to the International Classification of Childhood Cancer, 6 a histology-based scheme that also proved suitable for the descriptive analysis of neoplasms among adolescents and young adults. 4 No cancer was diagnosed incidentally, registered on the basis of information on the death certificate only (DCO) or recorded with an unknown or ill-defined primary site. 7 The proportion of tumors with microscopic verification of diagnosis was 95%, because 1 glioma of the optic chiasma, 1 supratentorial brain tumor, 2 craniopharyngiomas, 3 brainstem neoplasms and 7 pituitary microadenomas were detected by means of imaging techniques. At the date of study termination (31 December 1999) 1 proband (0.4%) was lost to follow-up because she had emigrated abroad.Information found in medic...

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“…Family C (290). Of nine sibs, four had malignancies (melanoma and cancers of colon, breast, and endometrium); a tumor-free sister had a daughter with breast cancer, whose daughter had breast and skin cancers and son had colon cancer; of seven children of the woman with colon cancer, one daughter had squamous-cell carcinoma of unknown primary site and three others had non-Hodgkin lymphoma (Greene and Miller, 1978). Family D (323).…”

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confidence: 99%

Sister chromatid exchanges and chromosomes in chronic myelogenous leukemia and cancer families

Cheng¹,

Mulvihill

Greene

et al. 1979

Intl Journal of Cancer

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Spontaneous sister chromatid exchanges and banded karyotypes were studied in blood lymphocytes from 96 individuals: seven patients with chronic myelogenous leukemia, 15 normal controls, and five "cancer families" comprising 12 cancer patients, 40 tumor-free blood relatives and 22 spouses. The families had: malignant melanoma; Epstein-Barr virus-associated malignancies and a birth defect syndrome; non-Hodgkin lymphoma and diverse carcinomas; Hodgkin's lymphoma and adenocarcinomas; and acute myelogenous leukemia. In addition to the Philadelphia chromosome in chronic myelogenous leukemia patients, karyotypic abnormalities, especially breaks and fragments, were found in 29% of cancer family members, but were inconsistent and usually attributable to radiotherapy. Mean sister chromatid exchange values were normal in chronic myelogenous leukemia, but low (by t-test) in tumor patients and their blood relatives in cancer-prone families. In tumor patients, mean sister chromatid exchange levels fell as age increased. After adjusting for this age effect, no significant differences remained among groups. In patients at high risk of cancer (because they have chronic myelogenous leukemia or a strong family history of cancer), spontaneous sister chromatid exchange rates were not a marker of cancer risk.

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Familial non‐Hodgkin lymphoma: Histologic diversity and relation to other cancers

Cited by 16 publications

References 21 publications

Age of onset evidence for anticipation in familial non‐Hodgkin's lymphoma

Age of onset evidence for anticipation in familial non‐Hodgkin's lymphoma

Malignant tumors in first‐degree relatives of cancer patients aged 0–25 years (province of Trieste, Italy)

Sister chromatid exchanges and chromosomes in chronic myelogenous leukemia and cancer families

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