Germline Stem Cells and Follicular Renewal in the Postnatal Mammalian Ovary

Johnson, Joshua; Canning, Jacqueline; Kanedo, Tomoko; Pru, James K.; Tilly, Jonathan L.

doi:10.1097/00006254-200407000-00017

Cited by 238 publications

(438 citation statements)

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“…Furthermore, preliminary observations indicate the existence of proliferative germ cells sustaining oocyte-and folliculogenesis in the post-natal ovary in the mouse [82], and the surface epithelium of adult women is a source of oocyte and granulosa cells in vitro [87], further indicating that the ovarian tunica albuginea contains stem cells. Ovarian somatic stem cells within this epithelial layer are expected to divide asymmetrically, yielding both a daughter cell that proceeds to terminal differentiation and an undifferentiated self-copy.…”

Section: Ovarian Cancer: Pluripotency and Putative Cscsmentioning

confidence: 97%

Cancer stem cells as targets for cancer therapy: selected cancers as examples

Hombach‐Klonisch

Paranjothy

Wiecheć

et al. 2008

Arch. Immunol. Ther. Exp.

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It is becoming increasingly evident that cancer constitutes a group of diseases involving altered stem-cell maturation/differentiation and the disturbance of regenerative processes. The observed malignant transformation is merely a symptom of normal differentiation processes gone astray rather than the primary event. This review focuses on the role of cancer stem cells (CSCs) in three common but also relatively under-investigated cancers: head and neck, ovarian, and testicular cancer. For didactic purpose, the physiology of stem cells is first introduced using hematopoietic and mesenchymal stem cells as examples. This is followed by a discussion of the (possible) role of CSCs in head and neck, ovarian, and testicular cancer. Aside from basic information about the pathophysiology of these cancers, current research results focused on the discovery of molecular markers specific to these cancers are also discussed. The last part of the review is largely dedicated to signaling pathways active within various normal and CSC types (e.g. Nanog, Nestin, Notch1, Notch2, Oct3 and 4, Wnt). Different elements of these pathways are also discussed in the context

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Section: Ovarian Cancer: Pluripotency and Putative Cscsmentioning

confidence: 97%

Cancer stem cells as targets for cancer therapy: selected cancers as examples

Hombach‐Klonisch

Paranjothy

Wiecheć

et al. 2008

Arch. Immunol. Ther. Exp.

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“…They suggested that Tsc/Mtorc1 signaling pathway and PTEN/PI3K signaling pathway regulate the on-and-off of primordial follicles activation collaboratively, ensuring a normal reproductive lifespan. Meanwhile, novel concept has arisen to challenge traditional understanding of ovarian functions, stating that ovarian germ cells are capable of self-renewal over time [19]. Further studies are required to support such optimistic concept.…”

Section: Etiologic Mechanisms Of Primary Ovarian Insufficiencymentioning

confidence: 99%

An update on primary ovarian insufficiency

Jin

Huang

2012

Sci. China Life Sci.

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Primary ovarian insufficiency (POI) occurs in about 1% of female population under the age of 40, leading to reproductive problems, an earlier encounter with menopausal symptoms, and complicated diseases. There are three presumable mechanisms involved in the development of POI, namely apoptosis acceleration, follicular maturation blocking and premature follicle activation, through the following studied causes: (i) chromosomal abnormalities or gene mutations: mostly involve X chromosome, such as FMR1 premutation; more and more potentially causal genes have been screened recently; (ii) metabolic disorders such as classic galactosaemia and 17-OH deficiency; (iii) autoimmune mediated ovarian damage: observed alone or with some certain autoimmune disorders and syndromes; but the specificity and sensitivity of antibodies towards ovary are still questionable; (iv) iatrogenic: radiotherapy or chemotherapy used in cancer treatment, as well as pelvic surgery with potential threat to ovaries' blood supply can directly damage ovarian function; (v) virus infection such as HIV and mumps; (vi) toxins and other environmental/lifestyle factors: cigarette smoking, toxins (e.g., 4-vinylcyclohexene diepoxide), and other environmental factors are associated with the development of POI. The etiology of a majority of POI cases is not identified, and is believed to be multifactorial. Strategies to POI include hormone replacement and infertility treatment. Assisted conception with donated oocytes has been proven to achieve pregnancy in POI women. Embryo cryopreservation, ovarian tissue cryopreservation and oocyte cryopreservation have been used to preserve ovarian reserve in women undergoing cancer treatments. Primary ovarian insufficiency (POI), commonly referred to as premature ovarian failure (POF), is defined as the occurrence of amenorrhea (for 4 months or more) before the age of 40 in women, accompanied with an increase of serum FSH to menopausal level (usually over 40 IU L 1 , obtained at least 1 month apart), and estradiol levels less than 50 pg mL 1 (which indicate hypoestrogenism) [1]. Primary ovarian insufficiency is first brought to light by Fuller Albright in 1942, who emphasized that the end stage of ovarian function is the primary defect rather than abnormality in gonadotropin secretion [2], and avoided the discomforting and inaccurate stressing on "failure", like death-sentence for ovarian function and conception.Menopause is a destined phase of women, which is expected to occur at around the age of (50±4) years in US women [3]. The age of 40 is two standard deviations below this average [4]. With an incidence of 1% in women under the age of 40, and 0.1% in women under the age of 30 [5], POI renders patients estrogen deficiency and anovulation, resulting in vasomotor symptoms (hot flashes and night sweats), atrophic vaginitis, dyspareunia, primary or secondary amenorrhea, and infertility. 76% of POI cases developed after normal puberty and establishment of regular menses [6]. Some of such conditions occur after stopping...

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“…They maintain their self-renewal and differentiation potentials and persist throughout the life of the mouse. Adult GSCs are thought to exist only in the testes, although the existence of GSCs in the ovary is still a subject of considerable debate (Eggan et al, 2006;Gosden, 2004;Johnson et al, 2004;Telfer et al, 2005;Zou et al, 2009).…”

Section: Developmentmentioning

confidence: 99%