Preimplantation aneuploid embryos undergo self-correction in correlation with their developmental potential

Purpose To investigate chromosomal characteristics in the same embryos at cleavage and blastocyst stage. Methods Six PGD/PGS cycles were retrospective studied, including five chromosomal translocation PGD cycles and one recurrent abortion PGS cycle. The cleavage embryos were biopsied one blastomere at day 3, followed by blastocyst culture. Trophectoderm cell biopsy was performed when embryos developed into the blastocyst stage. Whole genome amplification and 24-chromosomal analysis by CGH/SNP microarray was performed on each blastomere and trophectoderm cells. Results After PGD/PGS, only one couple had no euploid embryos to transfer. Five couples delivered a healthy, balancedkaryotype baby. A total of 18 embryos had both blastomere and trophectoderm cell reliable results available. Of the 18 embryos, eleven embryos contained identical chromosomes from cleavage stage to blastocyst stage and six embryos contained almost identical chromosomes . Only one embryo presented opposite chromosomal results for the cleavage and blastocyst stage, with abnormal chromosomes in the blastomere but normal chromosomes in trophectoderm cells. Conclusions Most embryos maintain chromosomal stability during embryonic development. Compared to cleavage stage, blastocyst stage may provide more reliable aneuploidy results.

Section: Discussionsupporting

confidence: 60%

Chromosomal characteristics at cleavage and blastocyst stages from the same embryos

Huang

Zhao

Wang

et al. 2015

“…2009 and 2010, while TE biopsy accounted for less than 1 % [6]. The same data referring to years 2012-2013 revealed a shift toward trophectoderm biopsies for PGD as cleavagestage biopsies decreased to approximately 75 % of all embryo biopsy cycles [reviewed by [8]].…”

Section: % Of All Biopsy Procedures Performed In Europe Betweenmentioning

confidence: 98%

“…Both PGD and PGS require access to the DNA of the preimplanted embryos, which is provided by either polar body biopsy, blastomere biopsy of cleavagestage embryos, or trophectoderm biopsy of blastocysts. PGS is mainly performed on trophectodermal cells biopsied from blastocysts to allow a better representation of the embryo ploidity [3][4][5][6][7]. In contrast, PGD for severe monogenic disorders is usually performed on blastomeres biopsied from day 3 embryos.…”

Section: Introductionmentioning

confidence: 99%

Blastomere biopsy for PGD delays embryo compaction and blastulation: a time-lapse microscopic analysis

Bar-El

Kalma

Malcov

et al. 2016

Self Cite

Purpose The purpose of the study was to explore the effect of blastomere biopsy for preimplantation genetic diagnosis (PGD) on the embryos' dynamics, further cleavage, development, and implantation. Methods The study group included 366 embryos from all PGD treatments (September 2012 to June 2014) cultured in the EmbryoScope™ time-lapse monitoring system. The control group included all intracytoplasmic sperm injection (ICSI) embryos cultured in EmbryoScope™ until day 5 during the same time period (385 embryos). Time points of key embryonic events were analyzed with an EmbryoViewer™. Results Most (88 %) of the embryos were biopsied at ≥8 cells. These results summarize the further dynamic development of the largest cohort of biopsied embryos and demonstrate that blastomere biopsy of cleavage-stage embryos significantly delayed compaction and blastulation compared to the control non-biopsied embryos. This delay in preimplanation developmental events also affected postimplantation development as observed when the dynamics of non-implanted embryos (known implantation data (KID) negative) were compared to those of implanted embryos (KID positive). Conclusion Analysis of morphokinetic parameters enabled us to explore how blastomere biopsy interferes with the dynamic sequence of developmental events. Our results show that biopsy delays the compaction and the blastulation of the embryos, leading to a decrease in implantation.

“…Mosaicism is postulated to originate from improper expression of cell cycle checkpoint genes during the primary mitotic cell divisions in the early embryo when maternal transcripts control the cell cycle [9]. At later cleavage stages, the embryonic genome takes over and may be able to overcome mosaicism by allowing the proliferation of normal cells and the inhibition of mitotic activity in abnormal ones [11][12][13]. Such a process is supported by data showing that chromosomal mosaicism is far lower at the blastocyst stage (days 5-6) as compared to the cleavage stage (day 3).…”

Section: Introductionmentioning

confidence: 99%

Human embryo mosaicism: did we drop the ball on chromosomal testing?

Esfandiari

Bunnell

Casper

2016