PubMed · 13474545
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J LEDERER, R DE MEYER, F MEERESSEMAN. 1957. [Thyroid & corpus luteum].. https://pubmed.ncbi.nlm.nih.gov/13474545/
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Telomerase is a ribonuclear protein reverse transcriptase that maintains telomere length in eukaryotic cells. Activation of telomerase has been implicated in human cellular immortalization and carcinogenesis. Telomerase activity in ovarian neoplasm has been studied using polymerase chain reaction (PCR)-based methods and shown to be correlated with malignancy. However, we believe those results must be interpreted with caution because such studies used a heterogeneous mix of cells, including normal cell type known to express telomerase when activated. The present study used in situ hybridization that allows determination of the type of cells expressing telomerase, as well as the intensity of that expression, in ovarian neoplasms. A total of 75 specimens were studied. Epithelial telomerase reverse transcriptase mRNA expression was detected in 28 of 31 epithelial ovarian carcinomas, 1 of 1 malignant granulosa cell tumor, 7 of 9 serous borderline ovarian tumors, 11 of 11 mucinous borderline ovarian tumors, 4 of 5 serous cystadenofibromas, 2 of 4 serous cystadenomas, 8 of 8 mucinous cystadenomas, and 0 of 6 normal ovaries except the corpus luteum. Telomerase expression is heterogeneously found in both benign and malignant epithelial tissues. We conclude that human telomerase reverse transcriptase mRNA expression does not seem to be a reliable marker for clinical use in differentiating between benign and malignant tumors.
OBJECTIVE: To determine intrauterine levels of vascular endothelial growth factor (VEGF)-A during the menstrual cycle in the human female and to investigate the impact of decidualization and corpus luteum function. DESIGN: Prospective clinical study. SETTING: Tertiary university center. PATIENT(S): Fifty-four women with infertility problems. INTERVENTION(S): Intrauterine concentrations of VEGF-A were determined at various time points during the secretory phase using a novel intrauterine microdialysis device. Concomitantly, intrauterine insulin-like growth factor binding protein (IGFBP)-1 levels served as a paracrine parameter for decidualization. Serum progesterone (P) and E(2) levels were determined as markers for corpus luteum function. Intrauterine VEGF levels. RESULT(S): The VEGF levels in utero were clearly cycle dependent with increasing levels during the late secretory and premenstrual phases. There was a significant correlation with the decidualization marker IGFBP-1. In contrast, intrauterine VEGF levels showed a significant negative correlation with serum E(2) and P. CONCLUSION(S): Intrauterine VEGF levels are regulated in a cycle-dependent way. Increasing levels in the late secretory phase are clearly correlated with decidualization. In contrast, decreasing serum levels of steroids produced by the regressing corpus luteum are less likely to be responsible for increasing VEGF levels in the premenstrual phase.
PURPOSE: We describe a physiopathological model to the luteal insufficiency of infertile patients with mild/minimal endometriosis with normal hormone measurements in the early follicular phase. METHODS: We designed a case-control study with 24 patients, 14 fertile with in-phase endometrium (control group) and 10 infertile with mild/minimal endometriosis and luteal insufficiency (study group). The histologic dating of endometrium was performed during cycle days 23-25 and serum TSH, FSH, LH, prolactin, and estradiol levels were measured during the early follicular phase (cycle day 3). Progesterone serum levels were measured in three different occasions during the luteal phase. RESULTS: Patients with out-of-phase endometrium have lower estradiol levels (P = 0.031) and decreased progesterone secretion (P = 0.012) during the late luteal phase. Serum prolactin, TSH, FSH, and LH levels were similar between the groups (P > 0.05). CONCLUSIONS: The physiopathology of luteal phase defect in infertile patients with mild/minimal endometriosis is associated with a small and large luteal cells dysfunction, characterized by abnormal follicular phase (lower estradiol serum levels) and lower progesterone LH-dependent secretion.