Female gamete preservation

Davis, Victoria

doi:10.1002/cncr.22105

Cited by 25 publications

(16 citation statements)

References 63 publications

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“…One of the commonly recognized side effects of cancer treatment in women is ovarian failure as a result of depletion of follicles (257, 258). For example, alkylating agents that are used for treatment of breast cancers are toxic to the ovary-particularly to primordial follicles, which constitute the ovarian reserve (259,260). Studies have also shown that women treated with both radiation below the diaphragm and alkylating agent chemotherapy are at greatest risk of having an accelerated menopause.…”

Section: Suggested Clinical Applications Of Our Current Knowledge mentioning

confidence: 99%

Molecular Mechanisms Underlying the Activation of Mammalian Primordial Follicles

2009

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In humans and other mammalian species, the pool of resting primordial follicles serves as the source of developing follicles and fertilizable ova for the entire length of female reproductive life. One question that has intrigued biologists is: what are the mechanisms controlling the activation of dormant primordial follicles. Studies from previous decades have laid a solid, but yet incomplete, foundation. In recent years, molecular mechanisms underlying follicular activation have become more evident, mainly through the use of genetically modified mouse models. As hypothesized in the 1990s, the pool of primordial follicles is now known to be maintained in a dormant state by various forms of inhibitory machinery, which are provided by several inhibitory signals and molecules. Several recently reported mutant mouse models have shown that a synergistic and coordinated suppression of follicular activation provided by multiple inhibitory molecules is necessary to preserve the dormant follicular pool. Loss of function of any of the inhibitory molecules for follicular activation, including PTEN (phosphatase and tensin homolog deleted on chromosome 10), Foxo3a, p27, and Foxl2, leads to premature and irreversible activation of the primordial follicle pool. Such global activation of the primordial follicle pool leads to the exhaustion of the resting follicle reserve, resulting in premature ovarian failure in mice. In this review, we summarize both historical and recent results on mammalian primordial follicular activation and focus on the up-to-date knowledge of molecular networks controlling this important physiological event. We believe that information obtained from mutant mouse models may also reflect the molecular machinery responsible for follicular activation in humans. These advances may provide a better understanding of human ovarian physiology and pathophysiology for future clinical applications.

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Section: Suggested Clinical Applications Of Our Current Knowledge mentioning

confidence: 99%

Molecular Mechanisms Underlying the Activation of Mammalian Primordial Follicles

2009

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“…Irradiation of the ovaries will induce ovarian failure in almost 90% of women, as observed in childhood abdominal radiation [5]. Ovarian transposition, shielding, or transplantation can be offered to try and reduce the risk of radiation-induced ovarian damage but the efficacy of this intervention is variable and not well established [9]. With the wider availability of assisted reproductive technology, there are commonly opportunities for ovarian stimulation and oocyte or embryo cryopreservation prior to chemoradiation.…”

Section: Introductionmentioning

confidence: 99%

The Impact of Uterine Radiation on Subsequent Fertility and Pregnancy Outcomes

Teh

Stern

Chander

et al. 2014

BioMed Research International

112

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Future fertility is of paramount importance to younger cancer survivors. Advances in assisted reproductive technology mean that young women treated with radiation involving the uterus may require clinical guidance regarding whether to attempt a pregnancy themselves. We performed a review of the literature regarding radiation involving uterus (total body irradiation (TBI) and pelvic radiation), fertility, and pregnancy outcomes to come up with a recommendation for our patients. Limited evidence suggests lower fecundity and an increased incidence of pregnancy complications after uterine radiation. Higher radiation doses and direct uterine radiation both significantly increase the risk of an adverse pregnancy outcome. Uterine radiation doses of <4 Gy do not appear to impair uterine function. Adult TBI data (usually 12 Gy) suggest pregnancy is possible but with lower fecundity and more complications. Although there is no clear data indicating the dose of radiation to the uterus, above which a pregnancy would not be sustainable, we suggest patients receiving >45 Gy during adulthood and >25 Gy in childhood be counselled to avoid attempting pregnancy. There is preliminary evidence that menopausal hormone therapy and a combination of pentoxifylline and tocopherol may improve uterine function following irradiation.

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“…Some anticancer drugs are well known to induce ovarian damage in addition to cancer cell death (1)(2)(3)(4)(5). Anticancer drugs may increase the apoptotic susceptibilities of normal ovarian follicles and cause granulosa cell apoptosis in ovarian follicles.…”

Section: Discussionmentioning

confidence: 99%

“…Advances in reproductive technology may provide help toward the preservation of fertility in such patients. Several studies have already evaluated the feasibilities of ovarian protection with concurrent hormone therapy, such as oral contraceptives (OCs) or gonadotropin-releasing hormone agonists (GnRHa), and clinical applications of assisted reproductive technology (ART), including embryo cryopreservation, oocyte cryopreservation, ovarian tissue cryopreservation and in vitro oocyte maturation (3)(4)(5). However, ovarian protection with OCs or GnRHa has not been completely established and its effects are currently insufficient.…”

Section: Introductionmentioning

confidence: 99%

“…However, ovarian protection with OCs or GnRHa has not been completely established and its effects are currently insufficient. The ART strategies mentioned above are developing technologies and successful pregnancy rates in patients treated with intensive chemotherapy have been low to date (4,5). Although ovarian damage is the main long-term adverse effect following chemotherapy, its molecular mechanisms have not yet been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Irinotecan-induced ovarian follicular apoptosis is attenuated by deleting the kinase domain of death-associated protein kinase

Tanaka²,

Yukawa³

et al. 2009

Int J Oncol

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Abstract. Although death-associated protein kinase (DAPK) is a Ca2+ /calmodulin-regulated serine/threonine kinase that plays important roles in various types of apoptotic cell death, there have been no reports of its tissue distributions and functions in female reproductive organs. By comparing C57BL/6 wild-type mice with DAPK-mutant mice lacking the 74-amino acid catalytic kinase domain of DAPK, the cellular distributions and biological functions of DAPK in murine ovaries were investigated. In situ hybridization analyses with sense and antisense riboprobes revealed that DAPK mRNA was selectively and highly expressed in granulosa cells in the ovaries of both types of mice. There were no significant differences in the body weights, ovarian weights and unstimulated ovarian follicular numbers between the wild-type and DAPK-mutant mice. Intraperitoneal injection of CPT-11, an anticancer topoisomerase I inhibitor that causes granulosa cell-specific apoptosis partly through Fas-Fas ligand (FasL) interactions in MCH mice, induced follicular apoptosis in both the wild-type and DAPK-mutant mice. However, the numbers of apoptotic follicles were significantly reduced in the DAPK-mutant mice. The Fas and FasL expression levels in the CPT-11-injected mice did not differ significantly between the wild-type and DAPK-mutant mice. These results indicate that DAPK positively regulates intracellular signaling pathways for CPT-11-induced granulosa cell apoptosis.

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Female gamete preservation

Cited by 25 publications

References 63 publications

Molecular Mechanisms Underlying the Activation of Mammalian Primordial Follicles

Molecular Mechanisms Underlying the Activation of Mammalian Primordial Follicles

The Impact of Uterine Radiation on Subsequent Fertility and Pregnancy Outcomes

Irinotecan-induced ovarian follicular apoptosis is attenuated by deleting the kinase domain of death-associated protein kinase

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