Familial Chronic Lymphatic Leukemia

Reilly, Emmett B.; Rapaport, Samuel I.; Karr, Norman W.; Mills, Harold; Carpenter, Gurth

doi:10.1001/archinte.1952.00240070093009

Cited by 23 publications

(4 citation statements)

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“…However, one of these mutations represents a polymorphism (Vorechovsky et al, 1999) and hence the observation is at most of borderline significance. Furthermore, a recent study of 28 families with Rosenow (1925) Parent F71, offspring M42 Hirschfeld (1925) Siblings M67, M70 Schereschewsky (1926) Siblings M61, F54 Vercelotti (1926) Siblings F55, M59 Riccitelli & Ragnotti (1927) Parent M65, offspring F43 Dameshek et al (1929); Gunz & Damashek (1957) MZ twins M54, M55, and offspring M53 Morawitz (1933) Siblings M57, M59 Petri (1933) Siblings M51, M52 Ardashnikov (1934) Cousins M45,?54 Curschmann (1936) Parent M50, offspring M59 Ardashnikov (1937) Cousins M57, M46 Decastello (1939) Siblings M, F; 2 offspring M, F Maack (1940) Siblings M46, M63 Hornbaker (1942) Siblings F39, F55 Additional sibling with CML Rohr (1945) Siblings F58, F62 Offspring of younger sibling with CML Videbaek (1947) Aunt 70, nephew 48 Thiersch (1947) Siblings M49, F48 Frech (1948) Siblings M50, M56 Portmann & Robinson (1951) Siblings M40, F41 Reilly et al (1952) Siblings M36, M54, M56 Stobbe & Taeschner (1952) MZ twins M56, M69 Guasch ( Brem & Morton (1955) Siblings M54, M56 Third sibling M35 with leukaemia Videbaek (1958) Uncle 69, nephew 50 Hudson & Wilson (1960) Siblings M64, M74 Siblings M63, M68 Gunz et al (1962); Siblings F67, M56, M79 Fitzgerald & Hamer (1969) Furbetta & Solinas (1963 Grandparent M69; parent F53; offspring F56 Wisniewski & Weinreich (1966) Parent M71; offspring M44 Rigby et al (1966) 2 half-siblings Ardizzone et al (1968) Siblings M56,…”

Section: Discussionmentioning

confidence: 99%

Familial chronic lymphocytic leukaemia: a survey and review of published studies

Yuille¹,

Matutes²,

Marossy³

et al. 2000

Br J Haematol

110

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B-cell chronic lymphocytic leukaemia (CLL) is the most common form of leukaemia. To gain insight into the role of inherited factors in the disease, we have conducted a survey of the family histories of 268 CLL patients and have reviewed published familial cases and epidemiological studies. The results of our survey and published studies strongly support the hypothesis that a subset of the disease can be ascribed to a genetic predisposition. The most likely genetic model for inherited predisposition appears to be dominantly acting genes with pleiotropic effects because in many families CLL appears to be associated with other lymphoproliferative disorders.

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Section: Discussionmentioning

confidence: 99%

Familial chronic lymphocytic leukaemia: a survey and review of published studies

Yuille¹,

Matutes²,

Marossy³

et al. 2000

Br J Haematol

110

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“…Chronic lymphocytic leukemia (CLL) is a lymphoproliferative malignancy characterized by a proliferation of small, mature lyrnphocytes, usually of B cell origin (Rundles 1983). A possible genetic component to its origins is suggested by clinical reports of familial aggregation and data from population-based epidemiologic studies (Reilly et al 1952, Gunz & Dameshek 1957, Fraumeni et al 1969, Blattner et al 1976, Gunz & Veale 1969, Gunz et al 1976).…”

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confidence: 99%

HLA antigens in chronic lymphocytic leukemia

et al. 1988

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HLA-A, B, and C phenotypes of 88 white and 14 black patients with chronic lymphocytic leukemia (CLL) were compared with those of 3761 white and 660 black laboratory population controls, and HLA-DR phenotypes were compared with 742 white and 236 black controls from the same population. Several statistically significant associations were found, one of which (a strongly positive association with Cw6 for whites) persisted after correction for the number of antigens tested.

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“…In an earlier publication (Videbaek, 1947) he described an increased incidence of cancer, leukaemia and pernicious anaemia among the families of leukaemic patients. Anderson (1951) reported five cases of leukaemia among eight children; Reilly, Rapaport, Karr, Mills and Carpenter (1952) Bieber (1951) and Revol, Millet and Thivollet (1954). Guasch (1954), reporting the replies received from 64 haematologists, listed 39 familial cases of leukaemia among a total of 8,586 cases, including grandparents, parents, uncles and aunts as well as siblings, and among these were 14 pairs of uniovular twins, in eight of which both twins were affected, in six only one twin, and in three pairs of binovular twins both were affected in two and only one in the other pair.…”

Section: Discussionmentioning

confidence: 99%