Gynecologic Neoplasms Research Articles

Resultados de 1.000 cirugías ginecológicas laparoscópicas sucesivas

ObjectivesTo review the indications and outcomes of 1,000 consecutive laparoscopic surgeries. Material and methodsWe carried out an observational, retrospective study of the first 1,000 gynecological laparoscopic procedures performed in our hospital. Data on complications and conversions were recorded. ResultsBetween January 2005 and November 2011, we performed 1000 laparoscopic surgeries: 452 (45.2%) ovarian procedures, 200 (20%) hysterectomies for benign causes, 105 (10.5%) gynecological neoplasms, 88 (8.8%) tubal ligations, 75 (7.5%) diagnostic laparoscopies, 56 (5.6%) myomectomies, 19 (1.9%) sacropexies and 5 (0.5%) appendectomies. There were 22 major complications (2.2%) and 32 conversions to open surgery (3.2%). ConclusionThe laparoscopic approach to gynecological surgery is safe and effective.

Clear cell adenocarcinoma of the uterine cervix in a 24-year-old woman. Case report and review of the literature.

Carcinoma of the uterine cervix is the most common gynecologic malignant neoplasm all over the world [1, 2], but the second one in Poland after carcinoma of the endometrium [3]. In 2009 in Poland the number of its new cases was 3102, and the age-adjusted incidence rate was 10.2 per 100 000 women. In the age group 20-24 year the age-adjusted incidence rate of the cervical cancer was 0.4 per 100 000, and there were 6 new cases noted in Poland. It constituted 1.86% of the cancer incidence rate of all localizations in this age group in Poland [3]. The most common histological type of malignant cervical neoplasms is squamous cell carcinoma. Adenocarcinomas account only for approximately 15% of malignant cervical tumors [1, 2, 4, 5]. The screening based on exfoliative cytology introduced in the 1950s by Papanicolau, followed by colposcopy in appropriate patients, is an effective method for identifying squamous intraepithelial lesions [1, 2].

Second primary gynecologic neoplasms among breast cancer survivors.

1588 Background: Excess of risk of several second primary malignancies after treatment for breast cancer (BC) has been reported. This risk can be related with shared risk factors, cancer susceptibility genes or prior treatments received. Hormonal factors and hormone therapy are known to be risk factors for both BC and some gynecological malignancies. The aim of this study was to asses gynecological cancer risk as a second neoplasm among BC patients in our population. Methods: Patients diagnosed with invasive BC (CIE10: C50.0-C50.9) and registered in the Girona Cancer Registry from 1980 to 2006 were included in our study. We analyzed their incidence of second gynaecological malignancies except for contralateral BC. Standardized Incidence Ratios (SIR) and absolute excess of risk (AER) of these patients compared to general population were calculated. Results: 6.209 patients were diagnosed of invasive BC in this period, with median age at diagnosis 62 years, median follow-up 4 years. 84 of them developed a second malignancy of gynaecological origin (SIR 1,98 CI 95% 1,59-2,44; AER 104,01/100.000 person-year). We observed 4 uterine cervix (SIR 0.64 IC95% 0,20-1,54), 3 vulvar-vaginal (SIR 0,96 IC95% 0,24-2,60), 13 ovarian (SIR 1,13 IC95% 0,63-1,89) and 63 uterine corpus neoplasms (UC), as well as 1 genital female tract neoplasm unspecified. High and statistically significant SIR was observed for gynecological malignancies in general and specifically for UC(SIR 3.14 IC 95% 2,44-4,00). With this finding, histology of UC cases was reviewed. 12 out of 63 were malignant histologies, not otherwise specified. Among the remaining 51, there were 8 type II (1 clear cell and 7 serous adenocarcinoma, 15.7%), 34 type I (endometrioid adenocarcinoma, 66.7%) and 6 carcinosarcomas (11.8%). There were also 2 adenosarcomas (3.9%) and 1 mucinous adenocarcinoma (1.9%). Conclusions: Women with previous BC have an elevated risk of developing a second primary gynecological malignancy compared with general population, particularly for UC. These patients should be followed up for its early detection. We detected a slight increase in unfavourable uterine carcinoma histologies respect to the general population. Further investigation of this finding is warranted.

Uncommon Primary Pelvic Retroperitoneal Masses in Adults: A Pattern-based Imaging Approach

There is a broad spectrum of primary pelvic retroperitoneal masses in adults that demonstrate characteristic epidemiologic and histopathologic features and natural histories. These masses may be classified into five distinct subgroups using a pattern-based approach that takes anatomic distribution and certain imaging characteristics into account, allowing greater accuracy in their detection and characterization and helping to optimize patient management. The five groups are cystic (serous and mucinous epithelial neoplasms, pelvic lymphangioma, tailgut cyst, ancient schwannoma), vascular or hypervascular (solitary fibrous tumor, paraganglioma, pelvic arteriovenous malformation, Klippel-Trénaunay-Weber syndrome, extraintestinal GIST [gastrointestinal stromal tumor]), fat-containing (lipoma, liposarcoma, myelolipoma, presacral teratoma), calcified (calcified lymphocele, calcified rejected transplant kidney, rare sarcomas), and myxoid (schwannoma, plexiform neurofibroma, myxoma).Cross-sectional imaging modalities help differentiate the more common gynecologic neoplasms from more unusual masses. In particular, the tissue-specific multiplanar capability of high-resolution magnetic resonance imaging permits better tumor localization and internal characterization, thereby serving as a road map for surgery.

Clonality in gynecologic neoplasms: is it time to reevaluate clonality studies in gynecologic neoplasms? Is it possible to confirm multicentricity with clonality studies?

This article reviews issues with clonality applied to gynecologic neoplasms. It is our opinion that the current interpretation of clonality studies in gynecologic neoplasms needs to be reevaluated because multicentricity, probably a common mechanism of tumor development in gynecology, cannot be confirmed with clonality.

Frequency of Serous Tubal Intraepithelial Carcinoma in Various Gynecologic Malignancies

Serous tubal intraepithelial carcinoma (STIC) has been implicated in the pathogenesis of pelvic serous carcinoma. We hypothesized that, if this is the case, the frequency of STIC should be substantially lower in endometrial serous carcinomas, in nonserous gynecologic malignancies, and in benign gynecologic neoplasms than in ovarian or peritoneal serous carcinomas. From 2007 to 2009 the fallopian tubes of 342 consecutive gynecologic cases were entirely submitted for histology using the Sectioning and Extensively Examining the FIMbriated end protocol. This study included 300 of these cases (277 TAH-BSO, 23 BSO) after exclusion. The hematoxylin and eosin-stained slides from the fallopian tubes were independently reviewed by 2 gynecologic pathologists who were blinded to all other findings; disagreements were resolved by a third pathologist. Among 46 cases of ovarian malignancies, STIC was identified in 6 (18.8%) of 32 cases of serous carcinoma, but not in any other subtype. Similarly, STIC coexisted in 4 (14.3%) of 28 cases of endometrial serous carcinoma; however, no STIC was identified in any of the 74 cases of nonserous endometrial malignancies. STIC was identified in 2 (28.6%) of 7 cases of peritoneal serous carcinoma. No STIC was identified among 15 nongynecologic malignancies, 90 cases of benign conditions, and 27 cases of other conditions including 4 cases of cervical adenocarcinoma in situ and high-grade cervical intraepithelial lesions, 8 cases of endometrial atypical complex hyperplasias, and 15 cases of ovarian borderline tumors. In conclusion, the fallopian tube may be the origin of some pelvic serous carcinomas. Other possibilities that may explain the origin of pelvic high-grade serous carcinoma are discussed. Given that STIC coexisted with 14% of endometrial serous carcinomas, a more unifying theory may be that gynecologic serous carcinomas and STIC are multifocal lesions.

Advances in research on Xiaochaihu decoction in treatment of tumors

Xiaochaihu decoction as a classic prescription of Traditional Chinese Medicine has been used widely in clinic.In recent years,the applications of Xiaochaihu decoction in treatment of tumors have attracted more and more attention.In this paper,the clinical research on effectiveness of Xiaochaihu decoction in integrative treatment of traditional and western medicine for liver cancer,gynecologic neoplasms,esophageal squamous cell carcinoma and cancerous fever was summarized.The researches on immunoloregulation and direct inhibition of tumor cells of Xiaochaihu decoction were also reviewed.

Nodular Histiocytic Aggregates in the Greater Omentum of Patients With Ovarian Cancer

Nodular histiocytic aggregate (NHA) of the omentum is a rare benign proliferative process composed predominantly of histiocytes with scattered mesothelial cells. NHA is a differential diagnosis for neoplasms or metastatic tumors in cancer patients. To further clarify this clinical pitfall issue, the authors investigated surgical samples of the greater omentum from 96 patients with gastrointestinal malignancies and 53 patients with gynecologic neoplasms. Visible NHA of greater omentum was identified in 3 patients with ovarian neoplasms (borderline mucinous cystadenoma, low-grade papillary serous cystadenocarcinoma, and juvenile granulosa-cell tumor) but in none of the patients with gastrointestinal malignancies. Similar lesion was also identified on the cell blocks from peritoneal washings in 1 of the 3 patients. Grossly, the lesions formed small yellow-red nodules on the greater omentum, and the NHA lesion was also found diffusely on the surface of the appendix and fallopian tubes in 2 of the 3 patients. Histological study showed that typical NHA changes over an inflammatory background, which may indicate that NHA is a consequence of a chronic inflammatory process of omentum. The predominant infiltration of T lymphocytes in the NHA lesions indicates that the aggregation of histiocytes may be related to the activation of T-cell immunity. This report has first demonstrated visible NHA in the greater omentum of patients with ovarian malignancies, and awareness of this entity should be brought to clinicians to avoid misdiagnosis.

Metronomic doxifluridine chemotherapy combined with the anti-angiogenic agent TNP-470 inhibits the growth of human uterine carcinosarcoma xenografts

Uterine carcinosarcoma is a highly aggressive gynecological neoplasm that responds poorly to conventional chemotherapy and radiotherapy. Metronomic chemotherapy is accepted as a new approach for cancer treatment, and its underlying mechanism seems to involve the suppression of angiogenesis. However, the efficacy of metronomic and anti-angiogenic therapies against uterine carcinosarcoma is unknown. The anti-angiogenic effect of doxifluridine was assessed in vitro using human umbilical vein endothelial cells (HUVEC) co-cultured with FU-MMT-1 human uterine carcinosarcoma cells. The antitumor and anti-angiogenic effects of metronomic doxifluridine (delivered via oral gavage) in combination with TNP-470 were evaluated in vivo. Tumor vascularity was assessed by contrast-enhanced color Doppler ultrasound, laser Doppler and microvessel density staining. Doxifluridine suppressed tube formation of HUVEC and vascular endothelial growth factor production by FU-MMT-1 cells. Metronomic doxifluridine alone significantly suppressed tumor growth compared with the untreated (control) group, while metronomic doxifluridine in combination with TNP-470 significantly inhibited tumor growth compared with each treatment alone. A significant reduction of intratumoral vascularity was observed in FU-MMT-1 xenografts following treatment with metronomic doxifluridine in combination with TNP-470, as compared with each treatment alone. Intestinal bleeding was only observed when the maximum tolerated dose of doxifluridine was administered in combination with TNP-470. Metronomic doxifluridine chemotherapy in combination with TNP-470 might be effective for uterine carcinosarcoma without marked toxicity, possibly acting via its potent anti-angiogenic effects. Clinical studies are needed to evaluate the safety and efficacy of this treatment in humans.

Laparoscopic adrenalectomy for isolated adrenal metastasis from cervical squamous cell carcinoma and endometrial adenocarcinoma

Metastatic spread of gynecologic neoplasms to the adrenal gland is a rare condition. There is no consensus on the role of adrenalectomy for metastatic gynecologic neoplasms, given its extremely low incidence. We present two patients who underwent laparoscopic adrenalectomy for an isolated adrenal metastasis, one originating from squamous cell carcinoma of the cervix, and the other from endometrial adenocarcinoma.

Efficient inhibition of ovarian cancer by short hairpin RNA targeting claudin-3

Ovarian cancer is one of the most lethal gynecologic neoplasms. Even though various new chemotherapeutics have been developed for the treatment of ovarian cancer, drug resistance and undesired serious side effects remain unavoidable obstacles for chemotherapeutic approaches. New strategies to overcome the therapeutic dilemma are needed. Claudin-3 (CLDN3) is a recently discovered gene generally overexpressed in human ovarian cancers but not in normal ovarian tissue. Its high expression has been identified to associate with the invasion, proliferation and survival of cancer cells, making it a promising target for gene therapy of ovarian cancer. However, in gene therapy, traditional gene carriers such as virus or cationic liposomes suffer from distressing shortcomings of potential carcinogenicity, obvious cytotoxicity and immunogenicity. Nanoparticles (NPs) based on PLGA are a novel gene delivery system with good biodegradability, excellent biocompatibility and low toxcity for in vivo gene delivery compared with traditional gene carriers. We constructed a plasmid expressing shRNA targeted CLDN3 (pshCLDN3) encapsulated with PLGA-NPs, and administered it by i.p. injection to nude mice bearing intraperitoneal SKOV3 ovarian cancer, to investigate the antitumor potential of knocking down CLDN3. After 12 times of administration, the tumors of each group were compared. The underlying antitumor mechanisms were revealed by immunostaining of CD31, Ki-67 and TUNEL assay, to exhibit possible alterations in microvessel density, cell proliferation and cell apoptosis. Our study demonstrated that i.p. administration of pshCLDN3 effectively suppressed the expression of CLDN3 and, thus, inhibited the growth of ovarian tumors, significantly reducing tumor weight by 67.4% compared with blank controls (p<0.05). Immunostaining of CD31, Ki-67 and TUNEL assay demonstrated decreased angiogenesis (p<0.05), reduced proliferation (p<0.05) and increased apoptosis (p<0.05) in the pshCLDN3 treated group compared with controls. No obvious toxicity of PLGA-NPs was observed either in vitro or in vivo. Our results indicated that knockdown of CLDN3 by pshCLDN3 encapsulated in PLGA NPs may provide a promising approach for the treatment of ovarian cancer.

Abstract 1532: Small-molecule Stat3 inhibitor sensitizes Cisplatin-resistant ovarian cancer cells to Cisplatin-induced apoptosis

Abstract Ovarian Cancer causes the highest number of gynecologic neoplasm related deaths in the United States. The disease and its progression to drug resistance remain poorly understood. While the aberrant activation of the Signal Transducer and Activator of Transcription (Stat) 3 protein is prevalent in ovarian cancer and is detected in chemotherapy resistance, its exact role in the development and maintenance of the drug resistance phenotype remains poorly understood. We sought to investigate the molecular mechanisms by which constitutive Stat3 activity may support Cisplatin resistance in ovarian cancer. Compared to the sensitive A2780S ovarian cancer line, which does not harbor aberrant Stat3 activity, the SKOV3 line harboring constitutively-active Stat3 was partially sensitive to Cisplatin and showed evidence of moderate apoptosis in response to Cisplatin treatment. Compared to the sensitive A2780S cells, the partly-resistant, SKOV3 cells over-express c-Myc, Survivin, and Bcl-xL, and the XIAP anti-apoptotic factor, as well as VEGF pro-angiogenic factor and the matrix metalloproteinases, MMP-2 and MMP-9. The inhibition of constitutively-active Stat3 in SKOV3 cells by the small-molecule inhibitor, S3I-201 suppressed the expression of the anti-apoptotic and the pro-angiogenic factors, and induced moderate degree of apoptosis. Significantly, treatment with S3I-201 enhanced the sensitivity of SKOV3 cells to Cisplatin. Furthermore, the combined treatment of SKOV3 cells with Cisplatin and S3I-201 strongly inhibited colony formation and cell migration in vitro. Our study together identifies potential mechanisms by which aberrant Stat3 activity might support Cisplatin resistance in ovarian cancer, raising the potential that the combination therapy with Stat3 inhibitors would be effective therapeutic and chemo-sensitizing modalities for ovarian cancer and the recurrent disease. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1532. doi:10.1158/1538-7445.AM2011-1532

Risk of Anal Cancer in a Cohort With Human Papillomavirus–Related Gynecologic Neoplasm

To assess the development of anal cancer in women diagnosed with a human papillomavirus-related cervical, vulvar, or vaginal neoplasm. Using data from National Cancer Institute's Surveillance, Epidemiology and End Results program from 1973 through 2007, 189,206 cases with either in situ or invasive cervical, vulvar, or vaginal neoplasm were followed for 138,553,519 person-years for the development of subsequent primary anal cancer. Standardized incidence ratios were calculated from the observed number of subsequent anal cancers compared with those expected based on age-, race-, and calendar year-specific rates in the nonaffected population. Anal cancer developed in 255 women with a history of in situ or invasive gynecologic neoplasm, aggregate standardized incidence ratio of 13.6 (95% confidence interval [CI] 11.9-15.3), indicating a 13-fold increase in anal cancer compared with expected. The standardized incidence ratio for anal cancer incidence among women with in situ vulvar cancer was 22.2 (95% CI 16.7-28.4) and was 17.4 (95% CI 11.5-24.4) for those with invasive vulvar cancer. The standardized incidence ratio for anal cancer incidence in women with in situ cervical cancer was 16.4 (95% CI 13.7-19.2) and was 6.2 (95% CI 4.1-8.7) for women with invasive cervical cancer. The standardized incidence ratio for anal cancer incidence among women with in situ vaginal cancer was 7.6 (95% CI 2.4-15.6) and was 1.8 (95% CI 0.2-5.3) for invasive vaginal cancer. Women with human papillomavirus-related gynecologic neoplasm are at higher risk for developing anal cancer compared with the general population. This high-risk population may benefit from close observation and screening for anal cancer.

Ovarian Hilus Cell Heterotopia

The eutopic location of ovarian hilus cells in the hilar stroma of the ovary and in the adjacent mesovarium is widely recognized. Hilus cell heterotopia, that is, the presence of normal hilus cells in an abnormal site, is rare and there are only a few case reports and 1 earlier systematic study of this phenomenon in the literature. Hilus cell heterotopia has been reported in the fimbrial stroma of the fallopian tube, paratubal and parafimbrial cyst walls and usually takes the form of discrete, circumscribed nodules or clusters of hilus cells. We report a series of 6 cases of hilus cell heterotopia, all of which were identified in association with other underlying pelvic pathology and in patients over 40 years of age. We have shown that hilus cell heterotopia is not limited to the fallopian tube but can also involve the subcapsular ovarian cortex and may have an infiltrative (rather than a nested) growth pattern that can resemble metastatic carcinoma, potentially mimicking a metastatic lobular carcinoma of the breast. This is particularly relevant in patients in whom staging procedures are carried out for gynecologic pelvic neoplasms, and for those few patients who also have a history of concurrent carcinoma, particularly of the breast.

Gastrointestinal stromal tumors presenting as gynecological masses: usefulness of multidetector computed tomography

Large extraluminal gastrointestinal tumors (GISTs) may present as pelvic masses and thus mimic gynecological neoplasms in female patients. On clinical examination and pelvic ultrasound, these tumors resemble pedunculated fibroids or ovarian tumors. Multidetector computed tomography (CT), with its ability to perform isotropic multiplanar reconstruction, is useful in differentiating GISTs from true gynecological masses by demonstrating the pedicle sign connecting a pelvic GIST to its organ of origin. This allows a preoperative diagnosis to be made, which may be helpful in guiding therapeutic options and management. We present two cases of GISTs presenting as pelvic masses in which ultrasound findings suggested a gynecological cause, but multidetector CT with multiplanar reconstruction was able to determine their true organ of origin.

Mice-lacking LMP2, immuno-proteasome subunit, as an animal model of spontaneous uterine leiomyosarcoma

Uterine tumors are the most common type of gynecologic neoplasm. Uterine leiomyosarcoma (LMS) is rare, accounting for 2% to 5% of tumors of the uterine body. Uterine LMS develops more often in the muscle tissue layer of the uterine body than in the uterine cervix. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine LMS is not substantially correlated with hormonal conditions, and the risk factors are not yet known. Radiographic evaluation combined with PET/CT can be useless in the diagnosis and surveillance of uterine LMS. Importantly, a diagnostic biomarker, which distinguishes malignant LMS and benign tumor leiomyoma (LMA) is yet to be established. Accordingly, it is necessary to analyze risk factors associated with uterine LMS in order to establish a method of treatment. LMP2-deficient mice spontaneously develop uterine LMS, with a disease prevalence of ∼40% by 14 months of age. It is therefore of interest whether human uterine LMS shows a loss of LMP2 expression. We found LMP2 expression is absent in human LMS, but present in human LMA. Therefore, defective LMP2 expression may be one of the risk factors for LMS. LMP2 is potentially a diagnostic biomarker for uterine LMS, and gene therapy with LMP2-encording DNA may be a new therapeutic approach.

Leiomioma vulvar atípico

Uterine leiomyomas are the most common gynecologic neoplasms. However, these tumors occasionally occur in unusual locations such as the genitourinary tract (vulva, ovaries, urethra, and urinary bladder). We report the case of a 59-year-old woman with an atypical leiomyoma of the vulva.

Molecular Genetic Markers in Female Reproductive Cancers

Cancer is a complex genetic disease as a result of accumulated genomic alterations which serve as the driving force in initiating tumor development and propelling tumor progression. Recent advances in molecular genomic technology and the success of human genome project have empowered investigators with new tools in analyzing cancer genome and transcriptome in great details and have expedited the discovery of new cancer-associated genes. Decoding the genetic history present in tumor DNA, as well as identification and characterization of molecular changes involving cancer-associated genes and the pathways they controlled, has not only shed new light on the molecular etiology of cancer, but also has promises for the development of new diagnostic markers and novel therapeutics. In this special issue, the papers focus on recent findings of markers identified in female reproductive cancers including breast, ovarian, endometrial, and trophoblast tumors. The selected papers are not an exhaustive representation of the area of biomarkers in female reproductive cancers. Nonetheless, they represent the rich and many-faceted knowledge that we have the pleasure of sharing that with readers. We would like to thank the authors for their excellent contributions to this special issue and the reviewers' insightful input to ensure the quality of this special issue. Of particularly interest are the two timely review articles by A. M. Karst et al. and A. L. Gross et al. focusing on the possible precursor lesions in the development of female reproductive cancer. The tubal origin of “ovarian” cancer has recently been in the research spot-light because of the identification of potential precursor lesions of ovarian cancer, termed “serous tubal intraepithelial carcinoma” in the fallopian tubes. Both articles critically review the published studies and provide unique perspectives of the impact and significance of this new hypothesis in the field of cancer research. Review articles focusing on biomarkers including genetic (K. M. Hirshfield et al.), microRNA (H. M. Heneghan et al.), and cytokine (F. Barbieri et al.) summarize recent advances in biomarker discovery and the translational application. Those articles will serve as the source for the investigators who wish to pursue in evaluating new potential markers in the female reproductive cancer research. They also present the new challenges in biomarker discovery, validation, and verification. In addition to the five review articles, there are several exciting original research articles describing discovery and validation of biomarkers in female reproductive cancers. Those papers include the studies of fatty acid synthase (S. M. Ueda et al.), miR200c (D. R. Cochrane et al.), gene expression (S. Konstantinovsky et al.), and cytogenetic markers (F. Micci et al.). The findings from those studies could serve as biological foundation for future exploration of how those markers contribute to disease progression. The biomarkers identified in these studies could also serve as a road map for development of novel diagnosis tools and new targeted therapies. This issue also reports a synergistic effect of Pten loss and oncogenic Kras mutation on the endometrial cancer development (I. H. Kim et al.) and the result provides new insight into the pathogenesis of endometrial carcinoma. Finally, K. L. Yap et al. applied molecular genetic markers to demonstrate a lack of a Y-chromosomal complement in the majority of gestational trophoblastic neoplasms, suggesting that most trophoblastic tumors are derived from previous molar gestations. Because the molecular characters in gestational trophoblastic disease are understudied, this short report should provide new insight into the pathogenesis of this rare but highly interesting gynecological neoplasm. In conclusion, this special issue is by no means an attempt to be comprehensive in covering the field of female reproductive cancer, but it provides excellent reviews and research articles that may be useful for readers in this field. We hope that this special issue will inspire investigators in launching new research endeavor in this field and are grateful for the opportunity to manage this special issue. Tian-Li Wang Ben Davidson Phillip J. Buckhaults Chiun-Sheng Huang Gudi Poul

Pathogenesis of Ovarian Cancer: Clues from Selected Overexpressed Genes

Ovarian cancer is the most malignant gynecologic neoplasm. Although new chemotherapeutic agents have improved patients' 5-year survival rate, the overall mortality of ovarian cancer has remained largely unchanged in the past several decades. The main reason for the lack of success in effectively treating ovarian cancer is our limited understanding of its etiology and the very few molecular diagnostic markers and therapeutic targets known so far. Identification and characterization of ovarian cancer-associated genes are fundamental for unveiling the pathogenesis of its initiation and progression, especially the development of recurrent diseases. As there are a vast number of genes for which molecular genetic changes and aberrant gene expression have been reported in ovarian cancer, this review will only focus on summarizing those exemplified genes that have been demonstrated to have biological functions in promoting ovarian cancer development and potential clinical significance. The genes to be discussed include nuclear proteins (Notch3, HBXAP [Rsf-1], NAC1 and NFkappaB), cytoplasmic proteins (fatty acid synthase and apolipoprotein E) and cell surface/secretory proteins (mucin-4, mesothelin, claudin, HLA-G, kallikrein and folate receptor and osteopontin). Since the study of ovarian cancer-associated genes is complicated by several factors unique to ovarian cancer, we will also present our views on the limitations and challenges of current ovarian cancer research.

Vaginal Schwannoma in a case with uterine myoma

Only 1% of gynecological neoplasms are vaginal, and mesenchymal tumors constitute only 2% of vaginal neoplasms. The most common form is leiomyomas. Schwannomas arise from the peripheral nerve sheath. We report a case of vaginal schwannoma associated with uterine myoma. A 52-year-old woman presented with lower abdominal pain and menorrhagia for a duration of 6 months. At sonographic examination, the patient was found to have uterine myomas and a solid mass measuring 5x4.5 cm beneath the vaginal wall. At laparotomy, the uterus with myoma was removed using our standard operation procedures. Surgical excision of the mass from vaginal aspect was also undertaken, and the histology demonstrated schwannoma. The tumor cells were vimentin (+), desmin (-), smooth muscle alpha-actin (-), HMB-45 (-), MART-1 (-) and S-100 (+). There is no evidence of recurrence during 6 months follow-up. The differential diagnosis of a mass in the vagina includes also schwannomas. Immunocytochemical labeling of the tumor cells is essential. Simple resection of the mass is the preferred method of treatment.