Cytogenetic and molecular analysis of chromosome 11q23 abnormalities in leukaemia

Young, Bryan D.

doi:10.1016/s0950-3536(11)80050-8

Cited by 26 publications

(13 citation statements)

References 99 publications

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“…131, and one I have consulted upon) with a similar phenotype, however, do have some evidence of variable mild to moderate mental retardation. There is some evidence for CBL2 mutation in sporadic leukemia, 168 and leuanticipation.…”

Section: Cbl2mentioning

confidence: 99%

The genetics of familial leukemia

Horwitz

1997

Leukemia

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mechanisms operating in the common, sporadic cases. AnticiKeywords: leukemia; familial; anticipation pation occurs in Huntington disease, myotonic dystrophy, and other inherited neurodegenerative illness where it results from the expansion of unstable trinucleotide repeat sequences. IntroductionSince this remains as the only molecularly defined instrument for anticipation, I weigh the possibility that an analogous situ-A family history of leukemia in a first degree relative increases ation holds for leukemia genes. I also review evidence that the risk for leukemia by approximately three-to five-fold. 1,2anticipation may be present in other types of familial cancer, The magnitude of this risk elevation is equivalent to or even including those in which the gene has been characterized and greater than that exhibited for malignancies well known to does not contain trinucleotide repeat tracts, but is involved have a substantial proportion of cases resulting from autosoin maintaining genome integrity. Here I propose a novel and mal dominant inheritance of a mutant tumor suppressor gene, alternative hypothesis for anticipation in familial cancer based such as breast cancer 3 and colorectal carcinoma. 4 On the on the inheritance of a cascade of de novo mutations in secother hand, familial leukemia is exceptionally rare, and only a ondary tumor suppressor genes resulting from a primary defect few pedigrees obviously transmitting leukemia have ever been in a gene responsible for DNA fidelity. recognized. This paradox and other observations suggest that the fraction of leukemia attributable to heritable factors could be markedly under appreciated. First, acute lymphocytic leuLeukemia as part of a syndrome kemia (ALL) is predominately a disease of childhood. 5 In other childhood malignancy, such as retinoblastoma and Wilm's Several syndromic illnesses have leukemia as a component tumor, a large proportion of cases are the result of germline feature (Table 1) Since M7 AML is relatively rare in the general population, the

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Section: Cbl2mentioning

confidence: 99%

The genetics of familial leukemia

Horwitz

1997

Leukemia

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“…Rearrangements and/or interstitial deletions involving chromosome band llq23 are a relatively common cytogenetic alteration in human acute leukemias (Heim and Mitelman, 1987;Pui et al, 1990;Mitelman, 1991;Young, 1992;Raimondi, 1993). A gene coding for a putative nuclear transcription factor, and variably designated MLL, ALL-1, or HTRX-1, was recently cloned and found to be consistently disrupted by the llq23 breakpoints (Ziemin-van der Poel et al, 1991; Djabali et al, 1992;Gu et al, 1992;Tkachuk et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Distribution ofTP53 mutations among acute leukemias withMLL rearrangements

Lucchesi

Gaïdano

Cimino

et al. 1996

Genes Chromosom. Cancer

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“…[1][2][3][4] At least 40 different partner chromosomes have been involved in 11q23 translocations. [5][6][7][8][9][10][11][12] To date, 13 genes involved in translocations with MLL have been cloned. [13][14][15][16][17][18][19][20][21][22][23][24][25] It has been suggested that alteration of the MLL protein is the critical event in oncogenesis and that fusion partners may not play an important role in the oncogenic process.…”

Section: Introductionmentioning

confidence: 99%

True

1999

Leukemia

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Cytogenetic and molecular analysis of chromosome 11q23 abnormalities in leukaemia

Cited by 26 publications

References 99 publications

The genetics of familial leukemia

The genetics of familial leukemia

Distribution ofTP53 mutations among acute leukemias withMLL rearrangements

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