Microsatellite instability in childhood T cell acute lymphoblastic leukemia

Baccichet, A.; Benachenhou, Nadia; Couture, Françoise; Leclerc, Jean‐Marie; Sinnett, Daniel

doi:10.1038/sj.leu.2400650

Cited by 25 publications

(16 citation statements)

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“…The data for leukemias are contradictory, ranging from zero to 94% in different reports (5)(6)(7)(8)(9)(10)(11)(12)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32). Here we report a study on 43 patients with CML and AML.…”

Section: Resultsmentioning

confidence: 96%

Microsatellite instability and cytogenetic survey in myeloid leukemias

Ribeiro

Rodríguez

Cóser

et al. 2002

Braz J Med Biol Res

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Microsatellites are short tandem repeat sequences dispersed throughout the genome. Their instability at multiple genetic loci may result from mismatch repair errors and it occurs in hereditary nonpolyposis colorectal cancer. This instability is also found in many sporadic cancers. In order to evaluate the importance of this process in myeloid leukemias, we studied five loci in different chromosomes of 43 patients, 22 with chronic myelocytic leukemia (CML) in the chronic phase, 7 with CML in blast crisis, and 14 with acute myeloid leukemia (AML), by comparing leukemic DNA extracted from bone marrow and constitutional DNA obtained from buccal epithelial cells. Only one of the 43 patients (2.1%), with relapsed AML, showed an alteration in the allele length at a single locus. Cytogenetic analysis was performed in order to improve the characterization of leukemic subtypes and to determine if specific chromosome aberrations were associated with the presence of microsatellite instability. Several chromosome aberrations were observed, most of them detected at diagnosis and during follow-up of the patients, according to current literature. These findings suggest that microsatellite instability is an infrequent genetic event in myeloid leukemias, adding support to the current view that the mechanisms of genomic instability in solid tumors differ from those observed in leukemias, where specific chromosome aberrations seem to play a major role.

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Section: Resultsmentioning

confidence: 96%

Microsatellite instability and cytogenetic survey in myeloid leukemias

Ribeiro

Rodríguez

Cóser

et al. 2002

Braz J Med Biol Res

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“…Results from the genotyped cases are shown in Table 3 (26). In addition, recent analyses from atomic bomb survivors exposed in utero and as children younger than 6 years of age suggest a similar observation: although there were only 10 cancer deaths among those exposed in utero (n = 807), 9 occurred in females (24). Finally, females irradiated for retinoblastoma also seem at greater risk of a second cancer (28).…”

Section: Resultsmentioning

confidence: 63%

“…With this method, ASOs complementary to each of the variants distinguishing between the mutant and the normal alleles are used as probes to hybridize dot-blots containing PCR products (23). We extracted genomic DNA from cells derived either from mouth epithelium, peripheral blood, or bone marrow in remission, as previously described (24).…”

Section: Methodsmentioning

confidence: 99%

Risk of childhood leukemia associated with diagnostic irradiation and polymorphisms in DNA repair genes.

Infante‐Rivard

Mathonnet

Sinnett

2000

Environ Health Perspect

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114

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The purpose of the study was to measure risk ofchildhood acute lymphoblastic leukemia associated with reported postnatal diagostic X rays and to determine if it was modified in the presence of variants in genes involved i:n DNA repair. We conducted a population-based case-control study with 491 cases and 491 healthy controls among children 0-9 years of age at diagnosis. it is plausible that they would be associated with altered DNA repair capacity and with modified susceptibility to cancer. We can then hypothesize that postnatal irradiation in a child with certain forms of DNA repair genes would be at increased risk of cancer.The objectives of this study were to measure the effect of reported postnatal diagnostic irradiation on childhood acute lymphoblastic leukemia (ALL) and to carry out a preliminary study to assess whether this effect seems modified by DNA repair gene variants. Materials and MethodsGase ascertainment. The

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“…1995). and there has been onlv one documented case of childhood malignancy (Baccichet et al 1997). These obsernations suggest a tissue-specific relation between defects in mismatch-repair and tumorigenesis associated with the RER phenotype.…”

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confidence: 82%

Genomic loci susceptible to replication errors in cancer cells

Krajinović

Richer²,

Gorska‐Flipot³

et al. 1998

Br J Cancer

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Replication errors revealed by these four markers followed the same tumour specificity as observed in HNPCC patients. In particular, 24% (6/25) of colorectal. 33%0 (4/12) of endometrial and 17% (2/12) of ovarian cancers displayed the RER phenotype characterized by an increased allelic mobility, whereas none of the breast (n = 22) and the lung (n = 27) carcinomas were found to be unstable. Assaying RERs sensitive loci provides us with a useful diagnostic tool for HNPCC-like sporadic tumours.

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Microsatellite instability in childhood T cell acute lymphoblastic leukemia

Abstract: ted with the development of the disease. We examined 56

Cited by 25 publications

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Microsatellite instability and cytogenetic survey in myeloid leukemias

Microsatellite instability and cytogenetic survey in myeloid leukemias

Risk of childhood leukemia associated with diagnostic irradiation and polymorphisms in DNA repair genes.

Genomic loci susceptible to replication errors in cancer cells

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