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PubMed2004

Increased prevalence of p53 overexpression from typical endometriosis to atypical endometriosis and ovarian cancer associated with endometriosis.

OBJECTIVE: To evaluate the expression of p53, c-erb-B-2, MIB1 and Bcl-2 in normal endometrium, endometriosis, atypical endometriosis and ovarian cancer associated with endometriosis, looking for immunohistochemical markers that may help determine endometriosis with premalignant potential. STUDY DESIGN: Between 1948 and 1999, 410 epithelial ovarian cancers and 521 cases of endometriosis were surgically treated at Fundación Jiménez Díaz. Pathology reports and slides were reviewed. Four groups were defined: (1) endometriosis/cancer (n=17); (2) atypical endometriosis (n=6); (3) endometriosis (n=17); (4) endometrium (n=7). Tumors and controls were immunostained and evaluated for expression of p53, c-erb-B-2, MIB1 and Bcl-2. Statistical analysis was performed using Chi-square for linear trends, Fisher exact and Kruskal-Wallis tests. RESULTS: Of the 410 cancers, 17 (4.1%) had associated endometriosis and of the 521 endometriosis, 6 (1.2 %) had atypical changes. Fourteen of 17 (82.4%) cancers associated with endometriosis and all atypical endometriosis had p53 overexpression. Only 2 of 17 (11.8%) endometriosis and none of the endometriums had mutant p53 (P<0.01). We found a trend towards increased expression of MIB1 (0.073) in the cancer and atypical endometriosis groups, and no differences in expression of Bcl-2 or c-erb-B-2. The sensitivity and specificity of p53 as a marker for the diagnosis of atypical endometriosis and cancer associated with endometriosis were 87%; CI 95% (73.2-100%) and 92% (80.6-100%), respectively. When comparing all groups, the mean positive p53 and MIB1 cell count was statistically significant (P=0.01). CONCLUSIONS: Overexpression of p53 in atypical endometriosis and cancer associated with endometriosis is a common finding and may be used to identify endometriosis with premalignant potential.

Adult↗
PubMed2006

Patterns of loss of heterozygosity at 10q23.3 and microsatellite instability in endometriosis, atypical endometriosis, and ovarian carcinoma arising in association with endometriosis.

Genetic aberrations, such as loss of heterozygosity (LOH) and mutations leading to functional inactivation of the PTEN tumor suppressor gene, located on chromosome 10q23.3, have been shown to be associated with approximately one third of ovarian adenocarcinomas. In addition, microsatellite instability (MSI) leading to the functional inactivation of the PTEN gene has also been reported for ovarian adenocarcinomas with frequencies varying from 6 to 37%. However, the frequency of PTEN gene abnormalities has not been well studied or evaluated in lesions such as typical and atypical endometriosis. The aim of this study was to investigate a possible sequential progression from endometriosis through atypical endometriosis to ovarian carcinoma by assessing LOH at 10q23.3 and MSI in those entities. Genomic DNA was analyzed for LOH and MSI at 3 loci on chromosome 10, using polymerase chain reaction amplification. Significant differences in LOH were seen between endometriosis (4.3%) and ovarian carcinoma (23.5%) at D10S608. The differences at the other 2 loci were not significant. A high frequency of MSI was found in endometriosis (82.6%) and atypical endometriosis (75%); however, the differences were not significant. These results suggest that LOH at D105608 may possibly be an important molecular event in the progression of endometriosis to carcinoma. This study highlights that endometriosis and atypical endometriosis might act as precursor lesions that have the potential to progress into ovarian adenocarcinoma.

Adenocarcinoma↗
PubMed2000

Two Previously Unemphasized Features of Endometriosis: Micronodular Stromal Endometriosis and Endometriosis with Stromal Elastosis.

This report draws attention to two unusual features of the stromal component of endometriosis that can create problems in diagnosis. One of these is the exclusive presence of endometriotic stroma, so-called stromal endometriosis, that can occasionally take the form of microscopic nodules of endometriotic stroma on the pelvic peritoneum and other locations. This finding, which we refer to as a micronodular stromal endometriosis, can be overlooked entirely or lead to confusion with peritoneal involvement by low-grade endometrial stromal sarcoma. The other finding we describe is the presence of a prominent elastotic stromal response to endometriosis that can occasionally obscure or even focally obliterate the typical endometriotic stroma. This finding, although nonspecific, can be a diagnostic clue to the presence of endometriosis, especially when accompanied by the presence of the typical endometriod glands of that lesion. Int J Surg Pathol 8(3):223-227, 2000

Journal Article↗
PubMed1998

Biases in the endometriosis literature. Illustrated by 20 years of endometriosis research in Leuven.

AIM: To review the Leuven data on endometriosis to demonstrate the shifts that occurred over the years in diagnosis of endometriosis, classification of women with endometriosis and thus in interpretation of results. RESULTS: The contributions to the LUF syndrome, to non-pigmented endometriosis, to cystic ovarian endometriosis, to deep endometriosis, to endometriosis as an immunologic disease and to the development of an animal model of endometriosis, illustrate the persistent interest in endometriosis over 20 years. Using these data it can be shown how progressively the recognition of endometriosis caused important shifts from women who in the beginning of this period were classified as normal, to women who later became classified as having minimal or mild endometriosis. This was caused initially by the active search for small typical lesions and later by the recognition of non-pigmented lesions as endometriosis. The second important shift was caused by the recognition that deep endometriosis is not only a frequent disease, but that these women are predominantly classified as having mild to moderate endometriosis and even as women without endometriosis. The third shift is still ongoing, since the deep lesions reported become progressively smaller, by the "enthusiasm" of the surgeons, and by the introduction of a menstrual clinical exam. A fourth bias in the literature concerns the diagnosis and treatment of cystic ovarian endometriosis. Together with these shifts in recognition and treatment of endometriosis, our understanding of the physiopathology of endometriosis has changed. This is illustrated by the new concepts which have emerged over this period. These are, the focal treatment of cystic ovarian endometriosis, the concept that mild endometriosis could be a normal physiological condition and the endometriotic disease theory. CONCLUSION: To interpret the data of the literature we should be aware of the shifts that have occurred in the classification of endometriosis over the past 20 years, and which still can hamper the comparison of results between research groups.

Animals↗
PubMed1997

Immunological factors in endometriosis-associated reproductive failure: studies in fertile and infertile women with and without endometriosis.

Immunopathophysiological mechanisms in endometriosis-associated reproductive failure were studied in appropriate populations: infertile and fertile women with and without endometriosis. The incidence of sera positive for any of the autoantibodies tested among infertile women with endometriosis (n = 25) was similar to that observed in the three control groups [unexplained infertility patients (n = 25) and fertile women with (n = 10) and without (n = 25) endometriosis]. The mean volume of peritoneal fluid was significantly elevated in women with endometriosis (both fertile and infertile) as compared with patients without endometriosis (fertile or infertile). The concentration of peritoneal fluid leukocytes and the percentage of cells positive for macrophage markers were significantly increased and the percentage of T lymphocytes significantly decreased in infertile women with endometriosis but not in patients with unexplained infertility and fertile women with endometriosis, as compared with fertile controls without endometriosis. Macrophages from infertile patients with endometriosis had higher sperm phagocytosis than did those from infertile women without endometriosis or fertile subjects with or without endometriosis. Incidences of serum and peritoneal fluid samples embryotoxic to the in-vitro development of 2-cell mouse embryos were significantly higher in infertile patients with endometriosis than in unexplained infertility patients and fertile women with or without endometriosis. It is concluded that immunological mechanisms of endometriosis-associated infertility exist but that these peritoneal immunological factors in infertile women with endometriosis are related to their subfertility rather than to the presence of ectopic endometrial implants. This is supported by the lack of immunological abnormalities observed among fertile women with endometriosis. These immunological abnormalities are lacking in patients with unexplained infertility.

Adult↗
PubMed1994

Deeply infiltrating endometriosis is a disease whereas mild endometriosis could be considered a non-disease.

Deeply infiltrating endometriosis can be defined as endometriosis infiltrating deeper than 5 mm under the peritoneal surface. Type I is a conical lesion suggested to be caused by infiltration; type II is mainly caused by retraction of the bowel over the lesion; type III is the most severe lesion suggested to be caused by adenomyosis externa. Severe cases are clinically apparent by nodularities in the pouch of Douglas, whereas mild and subtle forms of deep endometriosis are easily missed. Clinical examination during menstruation and scrutiny at laparoscopy for indurations, followed, preferably, by CO2-laser-excision are the key features for diagnosis and treatment. It is important to realize that depth of infiltration and lateral spread cannot be evaluated by laparoscopic inspection but only during excision, that CA125 concentration but not ultrasound or nuclear magnetic resonance can be helpful in the diagnosis, and that in the most severe cases medical pretreatment is advocated. Results of excision, as evaluated by disappearance of pain in some 80% of women, by a cumulative pregnancy of some 70% and a low recurrence rate, are excellent. The peritoneal fluid is thought to play a key role in the physiopathology of deep endometriosis which is considered to be endometriosis which has escaped from the influence of the peritoneal fluid. This concept is clinically important for the medical treatment of endometriosis, which is suggested to shrink deep lesions and to bring them back under peritoneal fluid control. A model of endometriosis is proposed and discussed. Subtle lesions are considered a natural condition occurring intermittently in all women, whereas we question whether mild endometriosis is a disease. In some women endometriosis has an aggressive behavior and develops into cystic ovarian endometriosis or into deeply infiltrating endometriosis. In this model subtle and mild forms would be called "endometriosis," whereas deep and cystic ovarian forms could be called "endometriotic disease." It is stressed that deep and cystic ovarian endometriosis are two distinct entities, which is important for our understanding of endometriosis, for classification and for treatment of endometriosis.

Endometriosis↗
PubMed2000

Danazol for pelvic pain associated with endometriosis.

BACKGROUND: Endometriosis is defined as the presence of endometrial tissue (stromal and glandular) outside the normal uterine cavity. Conventional medical and surgical treatments for endometriosis aim to remove or decrease deposits of ectopic endometrium. The observation that hyperandrogenic states (an excess of male hormone) induce atrophy of the endometrium has led to the use of androgens in the treatment of endometriosis. Danazol is one of these treatments used. The efficacy of danazol is based on its ability to produce a high androgen/low estrogen environment (a pseudo menopause) which results in the atrophy of endometriotic implants and thus an improvement in painful symptoms. OBJECTIVES: To determine the effectiveness of danazol compared to placebo or no treatment in the treatment of the symptoms and signs, other than infertility, of endometriosis in women of reproductive age. SEARCH STRATEGY: The Menstrual Disorders Group search strategy was used to identify randomised controlled trials of the use of danazol in endometriosis. In addition, all reference lists of included trials were searched, and relevant drug companies were contacted for details of unpublished trials SELECTION CRITERIA: Randomised controlled trials in which danazol (alone or as adjunctive therapy) was compared to placebo or no therapy. Trials which only reported infertility outcomes were excluded. DATA COLLECTION AND ANALYSIS: Only four trials met the inclusion criteria and two authors extracted data independently from these trials. All four trials compared danazol to placebo. Two trials used danazol as sole therapy and two trials used danazol as an adjunct to surgery. Although the main outcome was pain improvement other data relating to laparoscopic scores and hormonal parameters were also collected. MAIN RESULTS: Treatment with danazol (including adjunctive surgical therapy) was effective in relieving painful symptoms related to endometriosis when compared to placebo. Laparoscopic scores were improved with danazol treatment (including adjunctive therapy) when compared with either placebo or no treatment. Side effects were more commonly reported in those patients receiving danazol than placebo. REVIEWER'S CONCLUSIONS: Danazol is effective in treating the symptoms and signs of endometriosis. However, its use is limited by the occurrence of androgenic side effects.

Danazol↗
PubMed2006

Higher frequency of chromosomal aberrations in ovarian endometriosis compared to extragonadal endometriosis: A possible link to endometrioid adenocarcinoma.

Endometriosis may progress to invasive endometrioid adenocarcinoma, particularly in the ovary. Up to now, little is known of the molecular mechanisms possibly involved in the malignant transformation of endometriosis. Therefore, in this study, extragonadal endometriosis (n = 10), ovarian endometriosis without malignancy (n = 10), ovarian endometriosis with direct transition into endometrioid adenocarcinoma (n = 8), and normal endometrium (n = 12) were investigated for numerical chromosomal aberrations by fluorescence in situ hybridization using centromere enumeration probes. The proportions of cells with aneusomies were semiquantitatively assessed. Trisomies 1 and 7, and monosomies 9 and 17 were found in endometriosis, ovarian endometrioid adenocarcinoma, and normal endometrium. The proportions of aneusomic cells were significantly higher in ovarian endometrioid carcinoma compared with ovarian endometriosis (P < 0.001), and in ovarian endometriosis compared with extragonadal endometriosis and normal endometrium (P < 0.001). The data provide new evidence of a common lineage of endometriosis and ovarian endometrioid carcinoma. The higher frequency of chromosomal aberrations in endometrioid carcinoma than in endometriosis may reflect an expansion of aberrant cell clones already present in endometriosis during the progression to cancer. The higher frequency of chromosomal aberrations in ovarian endometriosis than in extragonadal endometriosis suggests a role of the ovarian stromal milieu in the induction of genetic changes, which may eventually lead to invasive cancer.

Aneuploidy↗
PubMed2005

Initial endometriosis showing direct morphologic evidence of metaplasia in the pathogenesis of ovarian endometriosis.

It is believed that ovarian endometriosis may be generated by a celomic metaplastic process from existing epithelium in the ovary. However, no morphologic evidence of metaplastic process has been described. In this study, we intended to identify the earliest morphologic changes of endometriosis within the ovary to examine if evidence of metaplasia exists. Included in this study were 110 ovarian endometriosis cases and 30 benign ovaries without endometriosis but with ovarian epithelial inclusions (OEIs). Among the 110 well-established ovarian endometriosis cases, 34 cases showed areas of initial endometriosis (IE), which is defined as lesions showing direct transitions from normal-looking ovarian tissue to areas of minimal formation of endometriosis and/or to areas of full-blown endometriosis. We further divided IE into two types: type I IE was present on the ovarian surface, which was associated with ovarian surface epithelia; type II was located within the ovarian cortex, which was associated with OEIs. Sections containing IE, OEIs, and well-formed endometriosis were subject to CD10 and aromatase immunostaining. In IE lesions, the number of CD10-positive cells were significantly higher than the number of that in OEIs, but lower than that of well-formed endometriosis areas (p < 0.05). Aromatase expression was detected in both epithelial and stromal components of the IE lesions, indicating that estrogen local production may be involved in this initial process of endometriosis. Microvessel density was higher in IE lesions than in areas of OEI (p < 0.05). Based on the morphologic characteristics of IE, we believe that IE represent a spectrum of the earliest morphologic changes of endometriosis identifiable by routine microscopy. The morphologic transitions from ovarian surface epithelium or OEI to IE lesions provide direct metaplastic evidence for the pathogenesis of ovarian endometriosis. This metaplastic process may not only involve the ovarian epithelial cells, but also stromal components. Local production of estrogen, probably in high-levels, may be related to the initial process of endometriosis, although detailed mechanisms remain to be clarified.

Adult↗
PubMed2000

Ovulation suppression for endometriosis.

BACKGROUND: Although the etiology of endometriosis is unknown, several theories exist, the most popular of which is retrograde menstruation. As endometriosis can only be diagnosed by laparoscopy, neither the incidence (annual occurrence) nor the prevalence (proportion of the population affected) of endometriosis is known. The association between endometriosis and infertility isn't clear in Stage I (minimal) and Stage II (mild) endometriosis. Endometriosis appears to be an estrogen dependent condition. At the time of menopause, most endometriosis becomes quiescent. This hormonal dependency prompted researchers to seek agents which would suppress ovarian activity. OBJECTIVES: To determine effectiveness of a) ovulation suppression with danazol, medroxy progesterone acetate, gestrinone, combined oral contraceptive pills and GnRH analogues versus placebo or no treatment and b) any of the above agents versus danazol, for the treatment of endometriosis explained infertility in terms of clinical pregnancy rate. SEARCH STRATEGY: The Cochrane Subfertility Review Group specialised register of controlled trials was searched. SELECTION CRITERIA: Four RCTs with five treatment arms compared an ovulation suppression agent with placebo or no treatment. Eight trials were identified comparing a suppressive agent with danazol. DATA COLLECTION AND ANALYSIS DATA EXTRACTION: A diverse search strategy was employed, including hand-search of 43 core journals from 1966 to the present, bibliographies of relevant trials, MEDLINE database, abstracts from North American and European meetings and contact with authors of relevant papers. Relevant data were extracted independently by two reviewers using the standardised data extraction sheet. Validity was assessed in terms of method of randomisation, completeness of follow-up, presence or absence of crossover and co-intervention. DATA SYNTHESIS: 2x2 tables were generated for all relevant outcomes. Odds ratios were generated using the Peto modified Mantel-Haenszel technique. Statistical heterogeneity was assessed using x2. MAIN RESULTS: The common odds ratio for pregnancy following ovulation suppression versus placebo or no treatment was 0.83 (95% CI 0.5-1.39). These data were statistically homogeneous although clinical heterogeneity was present. Their consistency in showing no treatment benefit suggests that this group of interventions is ineffective. Common odds ratio for pregnancy following all agents versus danazol was 1.20 (95% CI 0. 85-1.68). Again these data were homogeneous and suggest no significant treatment benefit in terms of pregnancy rate. REVIEWER'S CONCLUSIONS: Given the significant period of amenorrhea associated with ovulation suppression, the lack of treatment benefit demonstrated and the adverse effects commonly associated with these treatments, ovulation suppression cannot be recommended as a standard therapy for endometriosis-associated infertility.

Danazol↗
PubMed1998

The use of serum CA-125 as a marker for endometriosis in patients with dysmenorrhea for monitoring therapy and for recurrence of endometriosis.

BACKGROUND: To estimate the value of CA-125 for the diagnosis of endometriosis in women with dysmenorrhea, as well as its significance in monitoring therapy and follow-up. METHODS: One hundred and fifty-seven women undergoing laparoscopy for dysmenorrhea were prospectively studied for serum CA-125 concentration. For those with advanced endometriosis receiving danazol treatment after conservative surgery, CA-125 was also determined every month during medication and once every 12 months after treatment. RESULTS: The sensitivity and specificity of serum CA-125 for the diagnosis of endometriosis were 61.1% and 87.5% respectively. Elevated CA-125 (>35 U/ml) was noted in 65/75 cases (86.70%) with advanced endometriosis, but in only 15/56 patients (26.8%) with minimal and mild endometriosis. Although there were significantly higher CA-125 levels in unmarried women, and a negative correlation (r=-0.1970, p=0.0284) between CA-125 and parity, there was no statistical difference in incidence of endometriosis by the status of marriage or parity. Ten women with advanced endometriosis were found with persistent endometriosis by laparoscopy during danazol treatment, even though they tested with normal CA-125 levels (<35 U/ml) at that time. Fifteen patients had elevated CA-125 levels before and one year after therapy, and were confirmed with recurrence of endometriosis by laparoscopy. Nine women with elevated CA-125 levels before treatment, were found without recurrence of endometriosis and had normal CA-125 levels one year after therapy. CONCLUSION: For endometriosis, CA-125 is a valuable adjuvant in the follow-up of recurrence in patients with advanced endometriosis and initially elevated CA-125 levels. It is not an effective screening tool for patients with dysmenorrhea, or for monitoring therapy. There was no significant correlation between the development of endometriosis and reproductive factors.

Adolescent↗
PubMed2005

Endometrium from women with and without endometriosis, and peritoneal, ovarian and bowel endometriosis, show different c-kit protein expression.

BACKGROUND: Endometriosis is defined by the presence of endometrium outside the uterus. Changes in the expression of the proto-oncogene c-kit are associated with aggressive behaviour of both benign and malignant tumours, but there are few data on its c-kit expression in endometriosis. Here we examined c-kit expression in endometrium and endometriotic tissue. METHODS: Immunohistochemistry was used for qualitative and semi-quantitative (mean+/-S.D. positive cells) analysis of c-kit expression in endometrium from women with (n=9) and without endometriosis (n=18), and in peritoneal (n=20), ovarian (n=20) and colorectal endometriosis (n=20). RESULTS: Semi-quantitative c-kit expression was higher in endometrial glandular cells from women with endometriosis than from women without endometriosis (15.0+/-14.6% versus 3.9+/-7.4%, p=0.01). No difference in c-kit expression was found in qualitative analysis and according to the phase of the menstrual cycle. C-kit expression values in peritoneal, ovarian and colorectal endometriosis were 2.0+/-3.8%, 2.0+/-4.1% and 21.7+/-18.4%, respectively. Qualitative and semi-quantitative c-kit expression was higher in colorectal endometriosis than in peritoneal and ovarian endometriosis (p<0.001); no difference was found between ovarian and peritoneal endometriosis. No c-kit expression was detected in stromal cells of either endometrium or endometriotic tissue. CONCLUSION: These results suggest that the c-kit/stem cell factor axis is involved in the pathogenesis of endometriosis. Strong c-kit protein expression was associated with invasive endometriotic lesions.

Adult↗
PubMedDate not supplied

Somatic DNA alterations in endometriosis: high frequency of chromosome 17 and p53 loss in late-stage endometriosis.

PROBLEM: Genetic predisposition to endometriosis is well established, but the gene(s) involved largely remain unknown. Although endometriosis is considered a benign disease, it displays several features similar to malignancy: altered morphology, disregulated growth, invasion. We hypothesize endometriosis arises as result of somatic DNA alterations occurring in a multi-step process, analogous to origin of neoplasia. Since chromosome 17 and TP53 tumor suppressor gene (TSG) alterations occur frequently in premalignant and malignant tissues, including endometrial and ovarian epithelial carcinomas, we sought to determine if similar somatic changes occur in late stage endometriosis. METHOD OF STUDY: To determine the frequencies of monosomy for chromosome 17, as well as for perturbations of p53 and other loci on 17, two different approaches were used. Fluorescent in situ hybridization (FISH) analysis was used to detect monosomy for the 17 centromere and for the p53 locus. For FISH, archival tissue (n=6) and fresh endometriotic touch preparations were prepared from women (n=8) undergoing extirpation of advanced stage endometriosis. Direct-labeled probes specific for p53 (17p13.1) and for the chromosome 17 alpha-satellite centromere region (1711.1-q11.1) were used to compare single glandular and stromal cells from endometriosis and normal tissue. DNA analysis of polymorphic DNA loci were used to detect loss of heterozygosity (LoH) for other loci on 17. We assessed matched endometriotic and normal DNA (peripheral blood) from women with severe/late stage disease (n=15), studying these dinucleotide markers: HGH (located on 17q22-24), D17S250 (17q11.2-q12) and CHRNB1 (17p13.1). RESULTS: Loss of the chromosome 17 centromere (monosomy) was shown by FISH in some cells from all 14 endometriosis specimens, although in no case did every cell show monosomy 17. In 12 of 14 specimens, significant proportions of cells not only were monosomic for the chromosome 17-centromere (8 to 42% of cells) but also showed loss of p53 locus. In the two remaining cases, p53 loss alone was observed in 8 and 14%. LoH for other alleles on chromosome 17 was observed less often, namely only 3 of 15 specimens for HGH, 1 of 15 for D17S250, and 0 of 15 for CHRNB1. CONCLUSIONS: Our study indicates that perturbations of chromosome 17 in general and the p53 locus in particular occur frequently in severe/late stage endometriosis. That not all cells show loss of whole chromosome 17 or the p53 locus suggests somatic mutation, perhaps occurring late in the pathogenesis of endometriosis. Clonal evolution of endometriosis must depend not only on somatic mutations for p53 but also on other oncogenes or TSG. Alternatively, the clone could begin with a germline or somatic mutation involving a nonneoplastic process, followed by one or more somatic mutations involving an oncogene or TSG like p53. Additional candidate genes clearly must be evaluated in order to determine the precise role chromosome 17 and p53 alterations play in endometriosis; however, additional genes seem unlikely to involve region connoted by HGH, D17S250 or CHRNB1.

Chromosomes, Human, Pair 17↗
PubMed1996

Effect of surgically induced endometriosis on pregnancy and effect of pregnancy and lactation on endometriosis in mice.

Endometriosis, a disease of women and nonhuman primates in which endometrial tissue grows outside the uterus, can be mimicked surgically in rats and mice. The disease is related to infertility in women, and surgical induction of endometriotic lesions reduces fertility in rats according to some studies. Conversely, pregnancy appears to have a beneficial effect on endometriosis in women and some rat studies. Our objective was to evaluate a new mouse model of surgically induced endometriosis with respect to the effects of pregnancy on endometriosis and the effects of endometriosis on pregnancy. Female B6C3F1 mice were divided into four groups. Those in Group A and B underwent induction surgery for endometriosis and hemi-ovariectomy, those in Group C underwent sham surgery and hemi-ovariectomy, and animals in Group D received no surgery at all. Three weeks later, Group A, C, and D were bred. Eighteen days later one half of the dams in Groups A, B, and C only were sacrificed, and evaluations included endometriotic lesion diameter, number of pups, fetal weight, and various organ weights. The remaining dams delivered, and, 18 days after parturition, dams and pups were sacrificed. Evaluations included gestation length and those listed above. Endometriotic lesion diameter was significantly reduced in pregnant animals when compared with nonpregnant controls, but the reduction was not a full regression. Lactation returned the mean lesion diameter to pre-pregnancy dimensions. When effects of endometriosis on pregnancy were evaluated, no effects on the litter size, pup weight, or gestation length were found, but trends toward increased resorptions and malformations were evident. Thus, in the mouse model of induced endometriosis, pregnancy produced a significant reduction in endometriotic lesion diameter while fertility was largely unaffected by the surgically induced endometriosis. The mouse model of endometriosis thus appears more resistant than the rat model to effects of endometriosis on fertility.

Animals↗
PubMed2006

Cyclooxygenase-2 expression is higher in ovarian cancer tissue adjacent to endometriosis than in ovarian cancer without comorbid endometriosis.

OBJECTIVES: The purpose of this study was to examine if COX-2, CK7 and CK20 are involved in the malignant transformation of endometriosis. METHODS: We compared COX-2, CK7 and CK20 expressions between isolated endometriosis lesions and endometriosis lesions adjacent to ovarian carcinoma and between isolated ovarian carcinoma and ovarian carcinoma with implants of endometriosis. Immunoreactivity was quantified using an immunohistochemical scoring system that corresponds to an image analysis-based system. RESULTS: There was no difference in COX-2, CK7 and CK20 expressions between the isolated endometriosis lesions and the endometriosis lesions adjacent to ovarian carcinoma. Similarly, CK7 and CK20 were equally expressed between the isolated ovarian carcinoma and the ovarian carcinoma with implants of endometriosis. The COX-2 over-expression rate was greater in ovarian carcinoma that was associated with endometriosis than in isolated ovarian carcinoma (27.8% versus 5.6%, P = 0.083). In endometrioid type ovarian carcinoma, the difference in COX-2 expression was statistically significant (50% versus 0%, P = 0.023). CONCLUSIONS: COX-2 over-expression may be a result of the malignant transformation of endometriosis to endometrioid type ovarian cancer or may represent an interaction between the two cellular components. With respect to cytokeratins, neither CK7 nor CK20 appear to be involved in the malignant transformation of endometriosis.

Carcinoma, Endometrioid↗
PubMed2006

Use of proteomic analysis of endometriosis to identify different protein expression in patients with endometriosis versus normal controls.

OBJECTIVE: To use proteomic techniques, including two-dimensional electrophoresis (2-DE), Western blot, and mass spectrometry, to screen and identify proteins that were expressed differently in patients with endometriosis versus normal controls. DESIGN: First, we aimed to find a difference in the way serum and eutopic endometrial proteins were expressed in women with and without endometriosis. Second, we were interested in searching for endometriotic proteins, which were specifically recognized by sera from patients with endometriosis. SETTING: Collaborative investigation in an academic research environment. PATIENT(S): Consenting women of reproductive age taking no medications and with laparoscopically proven endometriosis. INTERVENTION(S): Surgical excision of eutopic and ectopic endometrial biopsy and phlebotomization of patients with endometriosis and controls. MAIN OUTCOME MEASURE(S): Protein expression. RESULT(S): Thirteen protein spots from serum correlated with 11 known proteins and 11 protein spots from endometrium correlated with 11 known proteins were found differently expressed between women with and without endometriosis. Some proteins may be cytoskeletons, and some may be involved in the regulation of cell cycle, signal transduction, or immunological function. Three proteins, which were identified as vimentin, beta-actin, and ATP synthase beta subunit, hybridized significantly differently between endometriosis sera and normal sera. CONCLUSION(S): The data help to establish a human endometriosis proteome database and broaden our understanding of the pathogenesis of endometriosis. Further study of the proteins identified herein will assist in the eventual development of new diagnoses and treatments for endometriosis.

Actins↗
PubMed1997

Changing trends in the diagnosis of endometriosis: a comparative study of women with pelvic endometriosis presenting with chronic pelvic pain or infertility.

OBJECTIVE: To compare demographic, epidemiologic, and medical data and to evaluate diagnostic trends in women with endometriosis and chronic pelvic pain symptoms or endometriosis and infertility. DESIGN: Retrospective analysis. SETTING: Institute for the Study and Treatment of Endometriosis. PATIENT(S): Six hundred ninety-three consecutive patients with endometriosis and chronic pelvic pain (n = 357) or endometriosis and infertility (n = 336). INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Demographic and epidemiologic parameters, diagnostic trends. RESULT(S): Women with pelvic symptoms were younger, had less formal education, more frequent family history, and higher frequency and intensity of pelvic complaints. Mean ages at first symptom and diagnosis were lower in the pain group, but stage of endometriosis at first diagnosis was more advanced. The mean "diagnostic delay" was longer in the pelvic pain than in the infertile group (6.35 versus 3.13 years), but it decreased during three consecutive 5-year intervals in both groups, and there was also a gradual decrease in the frequency of advanced endometriosis at the time of first diagnosis. CONCLUSION(S): Demographic and epidemiologic parameters in women with endometriosis differ, depending whether chronic pelvic pain or infertility are the presenting symptoms. In the pain group, diagnostic delay is longer and endometriosis at diagnostic laparoscopy more advanced, indicating progressiveness of the disease. During the last 15 years, diagnostic delay steadily decreased and the frequency of advanced endometriosis at first diagnosis declined.

Adolescent↗
PubMed2005

Effect of endometriosis on IVF/ICSI outcome: stage III/IV endometriosis worsens cumulative pregnancy and live-born rates.

BACKGROUND: Women with endometriosis often need IVF to conceive-most women need several cycles of treatment. METHODS: To evaluate the impact of moderate to severe endometriosis on cumulative IVF outcome, we carried out an observational study on 98 consecutive women who underwent IVF or ICSI treatment and had endometriosis diagnosed by laparoscopy or laparotomy and classified as minimal to mild endometriosis (American Society for Reproductive Medicine I/II) (n = 31) or moderate to severe endometriosis (American Society for Reproductive Medicine III/IV) (n = 67). The reference group consisted of 87 consecutive women with tubal infertility. The main outcome measures were cumulative pregnancy and live birth rates. RESULTS: There was a significantly lower pregnancy rate per fresh embryo transfer after pooled cycles (1-4) among women with stage III/IV endometriosis (22.6%) compared to stage I/II group (40.0%) or tubal infertility (36.6%). After 1-4 IVF/ICSI treatments, including frozen embryo transfer, 56.7% of the women with stage III/IV endometriosis were pregnant and 40.3% gave birth. The corresponding values were 67.7/55.8% when endometriosis was stage I/II and 81.6/43.7% in the controls respectively. CONCLUSION: Stage III/IV endometriosis means a worse prognosis for IVF/ICSI treatments compared to milder stages or tubal factors. Lower implantation and multiple pregnancy rates offer some support to our practice to continue two embryo transfers in this group.

Adult↗