Optimizing hormone therapy for future reproductive performance in women with premature ovarian failure

Gelbaya, Tarek A.; Vitthala, S.; Nardo, Luciano G.; Seif, M

doi:10.3109/09513590.2010.501875

Cited by 14 publications

(10 citation statements)

References 76 publications

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“…To our knowledge, no cases of hemangioma related to the antineoplastic treatment have been reported in literature whereas they are typically reported in female young adults with history of oral contraceptive therapy (12). The use of oral contraceptives is indicated in the treatment of young women with premature ovarian failure caused by antineoplastic treatment (14,15). Maybe our findings have to be interpreted considering that all of the patients with hemangiomas were girls with a median age of 18.3 years, half of which were receiving oral contraceptive therapy.…”

Section: Discussionmentioning

confidence: 99%

Benign Hepatic Nodular Lesions After Treatment for Childhood Cancer

Masetti¹,

Colecchia²,

Rondelli³

et al. 2013

J. pediatr. gastroenterol. nutr.

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Section: Discussionmentioning

confidence: 99%

Benign Hepatic Nodular Lesions After Treatment for Childhood Cancer

Masetti¹,

Colecchia²,

Rondelli³

et al. 2013

J. pediatr. gastroenterol. nutr.

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“…Studies have also implicated the involvement of the mTOR pathway in the development of leiomyomas. Makker et al, (36) showed that mTOR signaling is increased in leiomyomas, while Yin et al (37), revealed that estrogen requires mTOR to drive G1 cell cycle progression in leiomyomas. Elongation factor 2 (EF2), a gene that functions in protein synthesis and a downstream mediator of the mTOR pathway, is involved in control of global translation.…”

Section: Discussionmentioning

confidence: 99%

Role of microRNA-21 and programmed cell death 4 in the pathogenesis of human uterine leiomyomas

Fitzgerald

Chennathukuzhi

Koohestani

et al. 2012

Fertility and Sterility

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Objective To determine if programmed cell death 4 (PDCD-4) is altered in autologous leiomyoma and myometrial tissues and microRNA-21's (miR-21) role in PDCD-4 expression, apoptosis and translation. Design Laboratory research. Setting Academic medical center. Patient(s) Myometrial and leiomyoma tissues from patients with symptomatic leiomyomata. Interventions(s) Tissue analysis and miR-21 knockdown in cultured immortalized myometrial (UtM) and leiomyoma (UtLM) cells. Main Outcome Measure(s) MiR-21 and PDCD-4 mRNA and protein expression. Result(s) Leiomyoma tissues robustly expressed the full-length 51kDA isoform of PDCD-4, while normal myometrial tissue had negligible expression Consistent with autologous tissues, UtLM cells expressed elevated miR-21 and a similar pattern of PDCD-4 compared to UtM cells. Knockdown of miR-21 increased PDCD-4 levels in UtM cells and UtLM cells, indicating that it can regulate PDCD-4 expression. Loss of miR-21 also increased cleavage of caspase-3 (apoptosis marker) and increased phosphorylation of elongation factor -2 (marker of reduced translation) in both cell lines. Conclusions Elevated leiomyoma miR-21 levels are predicted to decrease PDCD-4 levels, thus leiomyomas differ from other tumors where loss of PDCD-4 is associated with tumor progression. Our studies indicate regulation of PDCD-4 expression is not a primary miR-21 function in leiomyomas, but instead miR-21 is able to impact cellular apoptosis and translation, through unknown targets, in a manner consistent with its involvement in the pathophysiology of uterine fibroids.

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“…HRT currently represent the mainstay therapy for women with POI and plays a pivotal role in reducing long-term comorbidities (e.g. osteoporosis and cardiovascular disease) and improving sexual health by restoring normal serum estrogen concentrations according to age (3,8,31).…”

Section: Discussionmentioning

confidence: 99%

A Long contiguous stretches of homozygosity disclosed a novel biallelic pathogenic variant in STAG3 causing Primary Ovarian Insufficiency

Mellone¹,

Zavattaro²,

Vurchio³

et al. 2021

Preprint

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Background: Primary ovarian insufficiency (POI) refers to an etiologically heterogeneous disorder characterized by hypergonadotropic hypogonadism that represents a major cause of infertility in women under 40 years. Most cases of isolated POI still appear sporadically, but ∼10–15% have an affected first-degree relative, indicating a significant genetic etiology. Several genes implicated in development, meiosis, hormonal signaling and metabolism are involved in the genetic form of the disorder in both syndromic and isolated POI. However, most cases of POI remain unsolved even after exhaustive investigation. Results: Here is reported a 19-year-old Senegalese female affected by non-syndromic POI showing primary amenorrhoea, who well answered to the hormonal induction of puberty reaching a complete sexual maturation in two years. In order to investigate the presence of a genetic defect, aCGH-SNP analysis was performed. A 13.5 Mb long contiguous stretch of homozygosity (LCSH) region on chromosome 7q21.13-q22.1 was identified where the exome sequencing revealed a novel homozygous 4-bp deletion (c.3381_3384delAGAA) in STAG3 . Pathogenic variants in this gene, encoding for a meiosis-specific protein, have been previously reported as cause POI in only seven families and recently as cause of infertility in a male. The here identified mutation leads to the truncation of the last 55 aminoacids, confirming the important role in meiosis of the STAG3 C-terminal domain. Conclusions: In conclusion we identified a loss of function variant in STAG3 in a Senegalese woman with POI reinforcing the role the cohesin complex in the genetic etiology of this disorder. This gene should be included in the screening of POI to offer a better genetic counseling and long term follow-up considering the risk of ovarian tumor in woman carrying pathogenic variants in genes involved in germ cell differentiation.

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Optimizing hormone therapy for future reproductive performance in women with premature ovarian failure

Cited by 14 publications

References 76 publications

Benign Hepatic Nodular Lesions After Treatment for Childhood Cancer

Benign Hepatic Nodular Lesions After Treatment for Childhood Cancer

Role of microRNA-21 and programmed cell death 4 in the pathogenesis of human uterine leiomyomas

A Long contiguous stretches of homozygosity disclosed a novel biallelic pathogenic variant in STAG3 causing Primary Ovarian Insufficiency

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