Apoptosis and Ki-67 Expression in Adenomyotic Lesions and in the Corresponding Eutopic Endometrium

Matsumoto, Yumi; Iwasaka, Tsuyoshi; Yamasaki, Fumio; Sugimori, Hajime

doi:10.1097/00006250-199907000-00014

Cited by 13 publications

(19 citation statements)

References 17 publications

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“…To the best of our knowledge, no study has yet evaluated the proliferation rate and steroid hormone receptor levels in parallel with apoptosis assessment. Proliferative properties have been determined in combination with apoptosis in adenomyosis but not in endometriosis (21).…”

Section: Discussionmentioning

confidence: 99%

Reduction of apoptosis and proliferation in endometriosis

Béliard

Noël

Foidart

2004

Fertility and Sterility

151

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Objective: To evaluate whether endometriosis could be related to an impaired balance between apoptosis and proliferation, two processes which could be modulated by hormonal status.Design: Immunohistochemical study.Setting: Academic research laboratory. Intervention(s):Endometriotic samples obtained from peritoneum of women aged 26-40 years who were undergoing laparoscopy for pain or infertility. Main Outcome Measure(s):Apoptotic cells were detected with the use of the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. The production of p53 and bcl-2, estrogen and Progesterone (P) receptors, and cellular proliferation were assessed by immunohistochemistry in eutopic and ectopic endometria from 30 patients with endometriosis throughout the menstrual cycle. Results were compared with those from normal endometria from 15 fertile patients. Result(s):Endometriotic lesions were characterized by reduced TUNEL and p53 stainings and by enhanced bcl-2 staining. No correlation between apoptosis and estrogen receptor or P receptor levels was found. A lower amount of steroid receptor was found in endometriotic tissues, without cyclic modulation, compared with the eutopic endometrium. Conclusion(s):Our results suggest that when endometrial tissue is located at ectopic locations, it differs from eutopic endometrium by its proliferation rate, steroid hormone levels, and markers of apoptosis. A reduced sensitivity of endometriotic cells to apoptosis could promote the dissemination and implantation of these cells to ectopic sites.

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Section: Discussionmentioning

confidence: 99%

Reduction of apoptosis and proliferation in endometriosis

Béliard

Noël

Foidart

2004

Fertility and Sterility

151

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“…The adenomyotic tissue did not have the same cyclic changes as eutopic endometrium and was rarely influenced by hormonal change, which suggests that adenomyotic lesions do not originate in the basal endometrium. 33 Growth factors such as basic fibroblast growth factor and angiogenic growth factor have been found to be different between ectopic and eutopic endometrium, which may contribute to the pathogenesis of abnormal uterine bleeding as seen in some patients with adenomyosis. 34…”

Section: Iv2 De Novo From Embryologic Misplaced Pleuripotent Müllerimentioning

confidence: 99%

Adenomyosis: A Clinical Review of a Challenging Gynecologic Condition

Struble

Reid

Bedaiwy

2016

Journal of Minimally Invasive Gynecology

248

225

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“…Only very few apoptotic stromal cells were detected at any stage of the menstrual cycle [1,2]. However, a large number of apoptotic stromal cells was reported to be found during the late secretory phase [3,4]. Another study [5] showed that apoptotic stromal cells were almost equally detected during early proliferative and late secretory phases.…”

Section: Introductionmentioning

confidence: 99%

The Role of c-Jun Protein in Proliferation and Apoptosis of the Endometrium throughout the Menstrual Cycle

Udou

Hachisuga

Tsujioka

et al. 2004

Gynecol Obstet Invest

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Proliferation and apoptosis of the endometrium throughout the menstrual cycle were evaluated. Sections from 30 premenopausal women were examined using antibodies of c-jun protein, c-fos protein, estrogen receptors alpha and beta (ER-α and ER-β), progesterone receptor (PR), and Ki-67. Apoptotic cells were identified using a modified terminal deoxynucleotidyl-transferase-mediated biotinylated deoxyuridine triphosphate nick-end labeling (TUNEL) method. The cyclic changes of c-jun protein, c-fos protein, ER-α, PR, and Ki-67 were shown in glandular epithelial cells. Although the stromal expression of ER-α decreased during the secretory phase, a high stromal expression of c-jun protein and PR was still observed during the late secretory phase. The expression of ER-β appeared lower as compared with that of ER-α, without a cyclic change. The apoptotic index was significantly elevated in the glandular epithelial cells of the late secretory phase, whereas a few apoptotic cells were detected in the stromal cells at any stage of the cycle. The cyclic change of c-jun protein probably plays an important role in proliferation and apoptosis of glandular epithelial cells. The persistent stromal expression of c-jun protein and PR is thus considered to prevent stromal cells from entering into apoptosis during the late secretory phase.

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Apoptosis and Ki-67 Expression in Adenomyotic Lesions and in the Corresponding Eutopic Endometrium

Cited by 13 publications

References 17 publications

Reduction of apoptosis and proliferation in endometriosis

Reduction of apoptosis and proliferation in endometriosis

Adenomyosis: A Clinical Review of a Challenging Gynecologic Condition

The Role of c-Jun Protein in Proliferation and Apoptosis of the Endometrium throughout the Menstrual Cycle

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