The occurrence of aneuploidy in human: lessons from the cytogenetic studies of human oocytes

Pellestor, Franck; Andréo, Brigitte; Anahory, T.; Hamamah, S.

doi:10.1016/j.ejmg.2005.08.001

Cited by 94 publications

(64 citation statements)

References 86 publications

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“…However, direct cytogenetic evidence for the increased incidence of chromosomal abnormalities with increased maternal age has been accumulating over recent years. Pellestor et al have studied 1397 human oocytes obtained from IVF treatment cycles and persuasively confirmed the positive association between maternal age and increased chromosomal abnormalities [117][118][119]. From the cytogenetic perspective, the occurrence of aneuploidy has been classically attributed to chromosomal non-disjunction during either meiosis I or II [120].…”

Section: Menopausementioning

confidence: 99%

Reproductive ageing in women

Djahanbakhch

Ezzati

Zosmer

2007

The Journal of Pathology

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The traditional view in respect to female reproduction is that the number of oocytes at birth is fixed and continuously declines towards the point when no more oocytes are available after menopause. In this review we briefly discuss the embryonic development of female germ cells and ovarian follicles. The ontogeny of the hypothalamic-pituitary-gonadal axis is then discussed, with a focus on pubertal transition and normal ovulatory menstrual cycles during female adult life. Biochemical markers of menopausal transition are briefly examined. We also examine the effects of age on female fertility, the contribution of chromosomal abnormalities of the oocyte to the observed decline in female fertility with age and the possible biological basis for the occurrence of such abnormalities. Finally, we consider the effects of maternal age on obstetric complications and perinatal outcome. New data that have the potential to revolutionize our understanding of mammalian oogenesis and follicular formation, and of the female reproductive ageing process, are also briefly considered.

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Section: Menopausementioning

confidence: 99%

Reproductive ageing in women

Djahanbakhch

Ezzati

Zosmer

2007

The Journal of Pathology

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“…23 In this regard, as such disomic oocytes can have various patterns of isodisomic and heterodisomic regions, it is impossible to discriminate between upd(15)mat through sister chromatid pre-division and that through conventional meiotic non-disjunction by microsatellite analysis. Thus, the patients classified as TR/GC (M1) group may have upd(15)mat due to maternal age-dependent conventional non-disjunction at M1 and maternal age-dependent sister chromatid pre-division, whereas those classified as TR/GC (M2) group may have upd(15)mat due to maternal age-independent conventional non-disjunction at M2 and maternal age-dependent sister chromatid pre-division.…”

Section: Maternal Age Effect On Tr/gc (M1) Type Upd(15)mat K Matsubarmentioning

confidence: 99%

Maternal age effect on the development of Prader–Willi syndrome resulting from upd(15)mat through meiosis 1 errors

et al. 2011

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Prader-Willi syndrome (PWS) is primarily caused by deletions involving the paternally derived imprinted region at chromosome 15q11.2-q13 and maternal uniparental disomy 15 (upd(15)mat). The underlying mechanisms for upd(15)mat include trisomy rescue (TR), gamete complementation (GC), monosomy rescue and post-fertilization mitotic error, and TR/GC is mediated by non-disjunction at maternal meiosis 1 (M1) or meiosis 2 (M2). Of these factors involved in the development of upd (15)mat, M1 non-disjunction is a maternal age-dependent phenomenon. We studied 117 Japanese patients with PWS and identified deletions in 84 patients (Deletion group) and TR/GC type upd(15)mat through M1 non-disjunction in 15 patients (TR/GC (M1) group), together with other types of abnormalities. Maternal age was significantly higher in TR/GC (M1) group than in Deletion group (median (range), 37 (35-45) versus 30 (19-42); P¼1.0Â10 À7 ). Furthermore, delayed childbearing age became obvious since the year 2003 in Japan, and relative frequency of TR/GC (M1) group was significantly larger in patients born since the year 2003 than in those born until the year 2002. The results imply that the advanced maternal age at childbirth is a predisposing factor for the development of upd(15)mat because of increased M1 errors.

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“…Når puberteten inntrer, vil sekresjonen av gonadotropiner fra hypofysen blant annet føre til at en kohort av follikler (ca. [15][16][17][18][19][20] utvikles hver måned. Av disse vil én dominant follikkel normalt gjennomgå eggløsning av ett modent egg, mens de andre gjennomgår programmert celledød (13,18).…”

Section: Antimüllerhormon Og Folliklerunclassified

Antimüllerhormon ved behandling av ufrivillig barnløshet

Kalra¹

2009

Tidsskriftet

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SammendragBakgrunn. Kvinner i Norge, som i mange andre utviklede land, venter lenger i dag med å få barn enn før. Fruktbarheten hos kvinner synker med alderen, spesielt etter 35 års alder. Det har lenge vaert behov for en bedre markør av ovarial reserve og ovarial respons ved behandling av ufrivillig barnløshet. Denne artikkelen gir en oversikt over fysiologisk utvikling av follikler i eggstokkene og den spesielle plassen antimüllerhormon har i denne prosessen.Materiale og metode. Det ble gjort ikke-systematisk litteratursøk for relevante artikler i PubMed, Athens og Embase.Resultater. Nivået av antimüllerhor-mon er relativt stabilt gjennom menstruasjonssyklusen, og hormonet synes å vaere en pålitelig markør for ovarial respons. Bestemmelse av hormonnivået vil kunne identifisere kvinner med høy risiko for avvikende respons ved ovarial stimulering.Fortolkning. Klinisk bruk av antimül-lerhormon er først og fremst aktuelt ved utredning og behandling av ufrivillig barnløshet.

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The occurrence of aneuploidy in human: lessons from the cytogenetic studies of human oocytes

Cited by 94 publications

References 86 publications

Reproductive ageing in women

Reproductive ageing in women

Maternal age effect on the development of Prader–Willi syndrome resulting from upd(15)mat through meiosis 1 errors

Antimüllerhormon ved behandling av ufrivillig barnløshet

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