Biomedical subjects

Jo Kitawaki

Publications and source records attributed to Jo Kitawaki.

18 recordsLinked to original sources

PubMed2006

Differential effects of progestogens, by type and regimen, on estrogen-metabolizing enzymes in human breast cancer cells.

OBJECTIVES: To investigate the in vitro effects of five progestogens commonly used in hormone replacement therapy (HRT) on estrogen-metabolizing enzymes in human breast cancer cells. METHODS: The human hormone-dependent breast cancer cell lines T47D, MCF-7, and MCF-7aro were cultured with estradiol (E(2)) and progestogens. The mRNA levels of estrogen-metabolizing enzymes were determined by RT-PCR or Northern blot, and enzyme activities by radiolabeled substrates. Cell proliferation was measured by bromodeoxyuridine incorporation. In vitro models for continuous combined regimen (CCR) and sequential combined regimen (SCR) were established to mimic the in vivo conditions of HRT. RESULTS: Medroxyprogesterone acetate (MPA) plus E(2) (10(-8)M) stimulated the mRNA levels and activities of estrogen-activating enzymes aromatase (at 10(-8)M MPA), 17beta-hydroxysteroid dehydrogenase type 1 (17betaHSD1) (at 10(-6)M), and sulfatase (at 10(-8) to 10(-6)M) compared to E(2) only. Progesterone also stimulated enzyme activity, but to a lower magnitude. Levonorgestrel, norethindrone, and dienogest showed no enzyme stimulation. The estrogen-inactivating enzymes 17beta-hydroxysteroid dehydrogenase type 2 and sulfotransferase were not affected by any of the progestogens tested. However, all the progestogens (at 10(-8) to 10(-6)M) inhibited E(2)-stimulated cell proliferation. While increased aromatase and 17betaHSD1 activities were observed in the CCR model, no significant enzyme stimulation was observed in the SCR model. CONCLUSIONS: The present study suggested that progestogens exert different actions on estrogen-metabolizing enzymes in breast cancer cells dependent on the specific progestogen and regimen used. Further studies are needed to elucidate whether MPA, a progestogen currently used in HRT, leads to a higher risk of breast cancer development than other progestogens.

17-Hydroxysteroid Dehydrogenases↗

PubMed2006

[Endometriosis].

Explore the source record for details and available documents.

Biomarkers↗

PubMed2006

Association of two polymorphisms in the peroxisome proliferator-activated receptor-gamma gene with adenomyosis, endometriosis, and leiomyomata in Japanese women.

OBJECTIVE: The peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a nuclear hormone receptor that plays an important role in many diseases. This study investigated whether two polymorphisms (Pro12Ala in exon B and C161T in exon 6) of the PPAR-gamma2 gene are related to adenomyosis, endometriosis, or leiomyomata. METHODS: A total of 390 patients with adenomyosis, endometriosis, and/or leiomyomata were classified into four groups: 103 patients with adenomyosis (21 adenomyosis only and 82 adenomyosis with endometriosis and/or leiomyomata), 95 patients with endometriosis only, 100 patients with leiomyomata only, and 92 patients with endometriosis and leiomyomata. RESULTS: There was no association between distribution of genotype or allele frequencies for the PPAR-gamma Pro12Ala polymorphism and the presence of adenomyosis, endometriosis, and/or leiomyomata. However, compared with results for controls, the PPAR-gamma 161CC genotype and 161C allele frequencies were significantly increased in patients with adenomyosis (genotype: chi2 = 8.185, corrected P value [Pc] = .0169; allele: chi2 = 8.337, Pc = .0155) and in patients with endometriosis (genotype: chi2 = 6.748, Pc = .0375; allele: chi2 = 6.413, Pc = .0453). CONCLUSION: The results suggest that the PPAR-gamma 161CC genotype could be a genetic risk factor for adenomyosis and endometriosis, whereas the Pro12Ala polymorphism was not associated with these estrogen-dependent benign uterine diseases in a Japanese population.

DNA↗

PubMed2006

Adenomyosis: the pathophysiology of an oestrogen-dependent disease.

Adenomyosis uteri is a common gynaecological disorder that is characterized by the presence of ectopic endometrial glands and stroma in the myometrium. Although adenomyosis and endometriosis are different diseases, both of them grow and regress in an oestrogen-dependent fashion. Polymorphisms in the oestrogen receptor alpha gene are associated with a risk of adenomyosis. Adenomyotic tissue contains steroid receptors as well as aromatase and sulphatase enzymes. Together with the circulating oestrogen, locally produced oestrogens stimulate the growth of tissue mediated by the oestrogen receptors. Oestrogen metabolism, including the expression pattern of aromatase and the regulation of 17beta-hydroxysteroid dehydrogenase type 2 is altered in the eutopic endometrium of women with endometriosis, adenomyosis, and/or leiomyomas compared to that in the eutopic endometrium of women without disease. In addition to the conventional hormonal treatment with gonadotropin-releasing hormone agonists and danazol, the use of steroid-releasing intrauterine devices may be applicable to clinics.

17-Hydroxysteroid Dehydrogenases↗

PubMed2006

Synergistic effect of interleukin-6 promoter (IL6 -634C/G) and intercellular adhesion molecule-1 (ICAM-1 469K/E) gene polymorphisms on the risk of endometriosis in Japanese women.

PROBLEM: Endometriosis is an immune-related, chronic inflammatory disease with a polygenic predisposition. The aim of this study was to investigate whether the interleukin-6 (IL-6) gene promoter region polymorphism (-634C/G) and the intercellular adhesion molecule-1 (ICAM-1) gene 469K/E polymorphism are responsible in part for the genetic susceptibility to endometriosis. METHODS OF STUDY: The IL-6 -634C/G and ICAM-1 469K/E genotypes were determined in 202 patients with endometriosis and 236 control women by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: There were no differences in the IL-6 -634C/G or the ICAM-1 469K/E genotypes and allele frequencies between control women and endometriosis patients collectively, or between control women and each clinical subgroup of endometriosis patients. Interestingly, the frequency of ICAM-1 EE homozygotes who concomitantly carried the IL-6 -634G allele was significantly higher in patients with endometriosis (chi(2) = 6.458, P = 0.0396, d.f. = 2). CONCLUSION: Our results suggest that the IL-6 -634C/G and ICAM-1 469K/E polymorphisms synergistically affect the susceptibility for endometriosis in the Japanese population.

Adult↗

PubMed2005

Usefulness and limits of CA-125 in diagnosis of endometriosis without associated ovarian endometriomas.

BACKGROUND: The aim of this study was to evaluate the diagnostic significance of CA-125 for endometriosis without ovarian endometriomas. METHODS: Preoperative serum CA-125 levels were measured in 775 consecutive women diagnosed by laparoscopy or laparotomy with endometriosis, adenomyosis, leiomyomas, or normal pelvis. RESULTS: Receiver operating characteristic curve analysis revealed that the area under the curve for endometriosis without endometriomas was 0.788, significantly smaller than that for endometriosis with endometriomas (0.935, P < 0.05). In diagnosis of endometriosis without endometriomas, both the maximal accuracy of 78.8% and the maximal diagnostic value of 61.2% were obtained at the cutoff value of 20 U/mL. Negative predictive value was 78.0% at the cutoff value of 20 U/mL, whereas positive predictive value was 92.9% at the cutoff value of 30 U/mL. This range is clearly superior to the empirical single cutoff of 35 U/mL. CONCLUSIONS: In the diagnosis of endometriosis without endometriomas, combined use of two cutoff values for CA-125, 20 and 30 U/mL, provides improved diagnostic performance. However, the accuracy of using only CA-125 testing for diagnosis is still limited. Serum CA-125 testing can be done during initial screenings of women with possible endometriosis.

Adult↗

PubMed2005

Progestins and estrogens and Alzheimer's disease.

Sex-specific incidence rates for Alzheimer's disease (AD) are higher in women than men. Many fundamental researches and some clinical investigations have reported therapeutic and preventive effects of estrogens on AD. But WHIMS [S.A. Shumaker, C. Legault, S.R. Rapp, L. Thal, R.B. Wallace, J.K. Ockene, S.L. Hendrix, B.N. Jones IIIrd, A.R. Assaf, R.D. Jackson, J.M. Kotchen, S. Wabertheil-Smoller, J. Wactawsk-Wende, WHIMS investigators, Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women. The women's health initiative memory study: a randomized controlled trial, JAMA 289 (2003) 2651-2662], which used daily continuous hormone replacement therapy (HRT), reported that the hazard ratio of the HRT for probable dementia was 2.05. Effect of progestins, and continuous (not cyclically) HRT, even only with estrogen should be reconsidered. In our clinical study, conjugated equine estrogen (CEE) alone showed good changes of psychiatric tests for AD on the 3rd week, but addition of medroxyprogesterone acetate (MPA) or norethindrone since 4th week suppressed these tests. Using human umbilical vein epithelial cell (HUVEC), levonorgestrel (LNG), norethindrone acetate (NETA), MPA increased intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-secretin but dienogest (DNG) showed no effect. In vitro flow system, estradiol (E2), suppressed adhesion of white cell, but LNG, NETA, MPA increased the adhesions. DNG showed less effect. Non-feminizing estrogen J 861, which has delta8,9 double bond and straight in its structure and has less effect on sexual organs. J 861 has shown ameliorative effects on central nervous system (CNS) (increasing of cholineacetyltransferase immunoreactive cells in substantia innominata (SI), etc.) like E2. More investigations about progestins and estrogens and AD should be done.

Alzheimer Disease↗

PubMed2004

Expression of allograft inflammatory factor-1 in human eutopic endometrium and endometriosis: possible association with progression of endometriosis.

Allograft inflammatory factor-1 (AIF-1) is a cytokine originally identified in rat cardiac allografts with chronic rejection. AIF-1 is expressed in various human immune-related tissues and is thought to play a role in inflammatory responses and the immune activation and function of macrophages. Expression has also been shown in human placentas and bovine embryos, suggesting that AIF-1 may be involved in reproductive function. Immune factors are thought to be involved in the pathogenesis of endometriosis. High concentrations of activated macrophages and various cytokines have been found in the peritoneal fluid of patients with endometriosis. In the current work we examined the expression of AIF-1 in human eutopic endometrium and endometriosis, and measured AIF-1 in peritoneal fluid samples from women with and without endometriosis. RT-PCR, Western blot analysis, and immunohistochemistry showed that AIF-1 mRNA and protein were expressed both in eutopic endometrium and in endometriotic tissue. In eutopic endometrium, expression was greater in the late secretory and menstrual phases than in other phases of the menstrual cycle (P < 0.01). AIF-1 protein was present in greater amounts in peritoneal fluid from patients with endometriosis than in women without it (P < 0.01), and its concentration correlated with the Revised American Society for Reproductive Medicine score (rs = 0.693; P < 0.0001). Peritoneal macrophages from endometriosis patients secreted more AIF-1 than those from unaffected women (P < 0.05). AIF-1 release from macrophages was stimulated by IL-1beta (P < 0.01) and interferon-gamma (P < 0.05). These results demonstrate for the first time that AIF-1 is expressed in eutopic endometrium and endometriotic tissue, suggesting that AIF-1 is one cytokine in the local network involved in the onset of menstruation. AIF-1 derived from peritoneal macrophages may also possibly play a significant role in the pathophysiology and progression of endometriosis.

Adult↗

PubMed2004

Interferon-gamma gene dinucleotide (CA) repeat and interleukin-4 promoter region (-590C/T) polymorphisms in Japanese patients with endometriosis.

BACKGROUND: Endometriosis is a multifactorial disease with possible genetic predisposition and involvement of environmental factors in its pathogenesis. Cytokines may play important roles in the pathogenesis of endometriosis. The aim of this study was to investigate whether the interferon-gamma gene (IFNG) CA-repeat and interleukin-4 (IL-4) promoter region (-590C/T) polymorphisms may be responsible in part for genetic susceptibility to endometriosis. METHODS: IFNG CA-repeat and IL-4 -590C/T polymorphisms were determined for 185 patients with endometriosis and 176 healthy fertile women by quantitative genescan technology and PCR-restriction fragment length polymorphism analysis, respectively. Patients with endometriosis were analysed further according to their stage of disease, the presence or absence of chocolate cysts and whether or not their disease was associated with adenomyosis and/or lyomyomata. RESULTS: The global IFNG allele frequencies in the patients with endometriosis were significantly different from those in the control women (chi2 = 12.964, 6 df, P = 0.0436). The difference was due to an increase of the a13 (114 bp) allele in patients with endometriosis (chi2 = 10.222, P = 0.0088, corrected P = 0.0352, odds ratio = 1.48, 95% confidence interval = 1.10-1.98). There were no differences in IL-4 -590C/T genotypes and allele frequencies between control women and all patients with endometriosis or between control women and each subgroup of patients with endometriosis. CONCLUSION: The results suggest that the IFNG CA-repeat polymorphism is associated with susceptibility to endometriosis in a Japanese population.

Adult↗

PubMed2004

Aromatase cytochrome P450 and estrogen and progesterone receptors in uterine sarcomas: correlation with clinical parameters.

We examined the immunohistochemical expression of aromatase cytochrome P450 (P450arom), estrogen receptor (ER), progesterone receptor (PR), and Ki-67 in postoperative uterine sarcomas (n = 31) and the corresponding eutopic endometria (n = 20) to evaluate the relationships between the endocrine character of uterine sarcomas and the clinical features. In sarcoma tissues, P450arom was detected in 55% of cases, ER in 42%, PR in 42%, and Ki-67 in 90%. In eutopic endometria, P450arom was detected in 60% of cases, ER in 60%, and PR in 35%. There were correlations in the steroid-related proteins between the tumors and endometria (P = 0.001-0.026). The positivity of endometrial P450arom (P = 0.04) and ER (P = 0.006) was higher in surviving patients than dead patients regardless of the menstrual state. The results demonstrate correlation between the expression of P450arom, ER, and PR in tumors and eutopic endometria. Intense expression of the steroid-related proteins was associated with better survival.

Adult↗

PubMed2004

Genetic contribution of tumor necrosis factor (TNF)-alpha gene promoter (-1031, -863 and -857) and TNF receptor 2 gene polymorphisms in endometriosis susceptibility.

PROBLEM: Tumor necrosis factor (TNF)-alpha is a major cytokine involved in inflammatory and immune function. The aim of this study was to investigate whether polymorphisms at positions -1031, -863 and -857 in the TNF gene promoter region (TNFA) and TNF receptor type 2 gene (TNFR2) are responsible in part for genetic susceptibility to endometriosis. METHODS OF STUDY: TNFA and TNFR2 polymorphisms were determined in 123 patients with endometriosis and 165 fertile healthy women by the polymerase chain reaction (PCR) - preferential homoduplex formation assay and PCR-restriction fragment length polymorphism, respectively. RESULTS: The frequency of the TNFA-U01 haplotype was increased significantly in patients with endometriosis compared with controls (P = 0.045, OR = 1.45). The TNFA-U01 haplotype was strongly associated with HLA-B*0702. No difference was found in TNFR2 polymorphism between patients and controls. CONCLUSION: Our results indicated that TNFA promoter polymorphism was associated with susceptibility to endometriosis. However, this association was not independent of HLA-class I polymorphisms.

Adult↗

PubMed2003

Gonadotropin-releasing hormone agonist and danazol normalize aromatase cytochrome P450 expression in eutopic endometrium from women with endometriosis, adenomyosis, or leiomyomas.

OBJECTIVE: To investigate whether GnRH agonists or danazol therapy normalizes estrogen metabolism in the eutopic endometrium of women with endometriosis, adenomyosis, or leiomyomas. DESIGN: Prospective clinical study. SETTING: University hospital. PATIENT(S): Fifty-three women with endometriosis, adenomyosis, or leiomyomas. INTERVENTION(S): Patients received GnRH agonist or danazol. Biopsy samples of the endometrium were obtained before and after endocrine therapy. Nontreated endometrial explants were cultured in the presence of either drug. MAIN OUTCOME MEASURE(S): Reverse transcription polymerase chain reaction-Southern blot and immunohistochemical analyses of the endometrial expression of aromatase cytochrome P450, estrogen receptor, progesterone receptor, and Ki-67. Nontreated endometrial explants were cultured in the presence of either drug. RESULT(S): Messenger RNA and protein of aromatase cytochrome P450 were greatly reduced in the eutopic endometrium of patients treated with GnRH agonist for 2 months or more or with danazol for 1 month or more. Culture of endometrial explants with GnRH agonist (10(-9)-10(-7) M) did not change the amount of aromatase cytochrome P450, whereas danazol (10(-7)-10(-6) M) efficiently reduced aromatase cytochrome P450 expression. CONCLUSION(S): Therapy with GnRH agonist or danazol decreases expression of aromatase cytochrome P450 in diseased eutopic endometrium. Endocrine therapy normalized in part the impaired hormonal expression of the eutopic endometrium. GnRH agonist reduced aromatase cytochrome P450 expression mainly by promoting a hypoestrogenic state, whereas danazol reduced aromatase cytochrome P450 in part by direct action on the eutopic endometrium.

Adult↗

PubMed2003

Relationships between the serum levels of soluble leptin receptor and free and bound leptin in non-pregnant women of reproductive age and women undergoing controlled ovarian hyperstimulation.

BACKGROUND: The aim of this study was to investigate the relationships between the serum levels of soluble leptin receptor (SLEPR), and total, free and bound leptin, and the change in the serum SLEPR level during an IVF cycle. METHODS: Serum concentrations of leptin and SLEPR were measured in 50 Japanese women of reproductive age, and 20 patients participating in an IVF programme. The total leptin was fractionated into free and bound portions by gel filtration chromatography. RESULTS: The SLEPR level was negatively correlated with the body mass index (BMI) (r = -0.548, P < 0.0001), total leptin (r = -0.433, P < 0.0001), the percentage of free leptin (r = -0.732, P < 0.0001) and the absolute free leptin concentration (r = -0.506, P < 0.0001). The SLEPR level was positively correlated with the percentage of bound leptin (r = 0.730, P < 0.0001), whereas there was little variation in the absolute bound leptin concentration, regardless of the BMI or SLEPR concentration. During the IVF cycle, total and free leptin elevated during maximal ovarian stimulation, whereas there was no significant difference in the SLEPR concentration. CONCLUSIONS: The results demonstrate a skillful mechanism where a change in the serum SLEPR level regulates, in part, the biological activity of leptin in the circulation.

Adult↗

PubMed2003

Giant ovarian tumor removed after preoperative drainage, with abdominoplasty. A case report.

BACKGROUND: Giant ovarian tumors are rarely seen in modern surgical practice. Cardiopulmonary complications associated with the removal of such tumors are serious problems. CASE: An ovarian tumor weighing 55 kg was removed from a 33-year-old woman without cardiorespiratory complications using preoperative drainage and abdominoplasty by excision of the excess skin. CONCLUSION: Preoperative drainage before and abdominoplasty after removal of giant ovarian tumors are effective.

Abdomen↗

PubMed2002

Lack of stimulatory effect of dienogest on the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 by endothelial cell as compared with other synthetic progestins.

OBJECTIVES: Monocyte adhesion to endothelial cells is an important initial event at the onset of atherosclerosis. It is partially mediated by the expression of adhesion molecules on the endothelial cell surface. While estrogens inhibit the development of atherosclerosis, the effect of co-administered progestin remains controversial. We examined the effect of progestins on cytokine-stimulated human umbilical venous endothelial cell (HUVEC) expression of adhesion molecules. METHODS: In HUVECs, mRNA expression of progesterone receptors (PRs) and androgen receptors (AR) was determined by RT-PCR. HUVECs were stimulated by interleukin-1beta (IL-1beta) for 24 h with or without various steroids, and then the cell-surface expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was semiquantified by ELISA. RESULTS: In all preparations of HUVECs used in this study, RT-PCR confirmed mRNA expression of both isoforms of PR, PR-A and PR-B, as well as AR. Addition of progesterone (10(-10)-10(-7) M) or dienogest (DNG) (10(-10)-10(-8) M) did not affect IL-1beta-stimulated ICAM-1 or VCAM-1 expression. In contrast, medroxyprogesterone acetate, norethindrone acetate and levonorgestrel (10(-10)-10(-8) M) dose-dependently increased cell adhesion molecules. The progestin-induced increase was blocked by the concomitant addition of mifepristone, a PR antagonist, but not by hydroxyflutamide, an AR antagonist, indicating that the progestin stimulation was mediated predominantly via PR. CONCLUSIONS: These results suggest that DNG, unlike other synthetic progestins, lacks stimulation of cell adhesion molecules. For the prevention of atherosclerosis, estrogen in combination with DNG may be a suitable regimen in hormone replacement therapy in postmenopausal women.

Arteriosclerosis↗

PubMed2002

Association of HLA class I and class II alleles with susceptibility to endometriosis.

Although the exact etiology of endometriosis is unclear, several lines of evidence support roles for both cell-mediated and humoral immunity in its pathogenesis. To assess the association between HLA genotypes and endometriosis, we investigated the frequencies of HLA-A, -B, -C, and -DRB1 antigens or alleles in 123 Japanese patients with endometriosis and 165 healthy women as controls. Significant positive association with endometriosis was observed for HLA-B7 (OR = 2.7, 95% CI = 1.5-5.1, p(u) = 0.0022, p(c) = 0.0440) and for Cw*0702 (OR = 2.1, 95% CI = 1.2-3.3, p(u) = 0.0026, p(c) = 0.0398). An increased frequency of DRB1*0101 was observed in endometriosis patients compared with control subjects (OR = 2.3, 95% CI = 1.2-4.4, p(u) = 0.0143), but was not statistically significant after correction for multiple comparisons. Two-locus analysis indicated that the susceptibility to endometriosis was primarily associated with B7, and that the increased frequencies of Cw*0702 and DRB1*0101 in patients reflected the linkage disequilibrium between B7 and Cw*0702 and DRB1*0101. Most of the B7 antigens were encoded by the B*0702 allele, which was in complete linkage disequilibrium with A24, Cw*0702, and DRB1*0101. Therefore, our results indicated that the HLA-A24-B*0702-Cw*0702-DRB1*0101 haplotype was associated with endometriosis susceptibility. Our findings may provide an important clue to elucidating the pathogenesis of endometriosis.

Adult↗

PubMed2002

Genetic contribution of the interleukin-10 promoter polymorphism in endometriosis susceptibility.

PROBLEM: Interleukin-10 (IL-10) is an important immunomodulatory cytokine. The aim of this study was to investigate whether polymorphisms of the IL-10 gene promoter polymorphisms may be responsible in part for genetic susceptibility to endometriosis. METHODS OF STUDY: Polymorphisms at position -1082 and -592 in the IL-10 promoter region were determined in 196 patients with endometriosis and 160 fertile healthy women by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). RESULTS: There were no statistically significant differences in the genotype and allele frequencies of IL-10 promoter polymorphism between the endometriosis and control groups. However, when subgrouped according to clinical features, the frequencies of the -592*CC genotype and -592*C allele were significantly increased in patients with autoantibodies to carbonic anhydrase II (anti-CA II ab) compared with controls. CONCLUSION: IL-10 promoter polymorphisms were associated with the production of anti-CA II ab in patients with endometriosis, suggesting a role in the genetic susceptibility for endometriosis.

Adult↗

PubMed2002

Association of the CYP17 gene and CYP19 gene polymorphisms with risk of endometriosis in Japanese women.

BACKGROUND: To investigate whether polymorphisms of CYP17 and CYP19 genes are associated with the risk of endometriosis, we analysed the frequency and distribution of a single nucleotide polymorphism at the 5' untranslated region of the CYP17 gene, and a tetranucleotide (TTTA) tandem repeat polymorphism and a 3 bp insertion (I)/deletion (D) polymorphism in intron 4 of the CYP19 gene. METHODS: We studied 140 patients with endometriosis, 67 with adenomyosis and/or leiomyomas and 177 healthy control women. RESULTS: The distribution of the genotypes of CYP17 and alleles of the TTTA repeat polymorphism of CYP19 were not significantly different between the groups. In contrast, an increased frequency of the D/D genotype was observed in the endometriosis group as compared with the control group (D/D genotype versus I/I plus I/D genotypes; corrected P = 0.024). This was more evident in the endometriosis subgroups with chocolate cysts (corrected P = 0.043) and at severe clinical stages (corrected P = 0.035). CONCLUSIONS: The results suggest that the 3 bp I/D polymorphism of the CYP19 gene may be weakly associated with the susceptibility of endometriosis in a Japanese population.

Adult↗