Hsiang-Tai Chao

Steroid cell tumors of the ovary: clinical, ultrasonic, and MRI diagnosis--a case report.

Steroid cell tumors of the ovary are rare sex-cord neoplasms which account for less than 0.1% of all ovarian tumors. They have been divided into two subtypes according to their cell of origin as follows: stromal luteoma, and Leydig cell tumors, and a third subtype with lineage unknown is a steroid cell tumor, not otherwise specified (NOS). The clinical presentation may take many forms, including pain, abdominal distention and bloating, but perhaps the most interesting and noticeable presentations are those related to the hormonal activity and virilizing properties of the tumor. No radiological features of the steroid cell tumor, NOS have been presented in the literature. This report presents the MRI and ultrasonographic findings of a patient having steroid cell tumor, NOS, of the right ovary with metastasis to the uterus.

Enhanced expression of α 2,6-sialyltransferase ST6Gal I in cervical squamous cell carcinoma

Abstract Objective Increased messenger ribonucleic acid (mRNA) expression of β-galactoside α 2,6-sialyltransferase I (ST6Gal I) is important in squamous cell carcinoma (SCC) of the cervix. In many tissues, ST6Gal I is transcriptionally regulated through the use of promoters that originate in the mRNA species that diverge in the 5′-untranslated regions. To clarify the roles of ST6Gal I mRNA species in cervical SCC, we investigated their expression, including a constitutive promoter (placental or Y + Z form), hepatic promoter (H form), and a specific lymphoblastic promoter (X form), in normal and SCC tissues of the cervix using real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR). Methods Expression of the ST6Gal I species was investigated in normal cervical tissue samples ( n = 38) and FIGO IB1 cervical SCC samples ( n = 38) by relatively quantitative real-time RT-PCR, using primers designed for amplification of a portion of the coding region common to all mRNA species or ones for amplification of the placental transcript, the hepatic transcript, or lymphoblastic transcript. Results ST6Gal I mRNA expression was significantly increased in cancerous tissues compared to that in normal tissues ( P = 0.004, Mann–Whitney U test; P t test). Expression of the Y + Z form did not appear to be affected by cancer transformation, since it was detected at comparable levels in normal and cancerous tissues ( P = 0.986), but H form expression was significantly enhanced in cancerous tissues compared to that in normal tissues ( P U test and paired t test). Surprisingly, the X form could be detected in some patients with and without cancer, but the detection rate was significantly higher in patients with cancer (86.8% vs 52.6%, respectively; P = 0.021, Fishers exact test). Although the X transcript was detected at a low level compared to the H and Y + Z transcripts, its expression was also significantly enhanced in patients with cancers compared to those without cancers ( P U test and paired t test). Conclusions An increased level of hepatic transcripts may be important in cancer transformation because the transcripts contribute to enhance ST6Gal I expression in cancerous tissues.

Rationale for using raloxifene to prevent both osteoporosis and breast cancer in postmenopausal women

Both osteoporosis with fracture and breast cancer are important health issues for postmenopausal women. It is well known that estrogen and estrogen receptors (ERs) play an important role in the pathogenesis of both diseases. In past decades, hormone therapy (HT), mainly estrogen plus progestin (EPT), has been frequently used for the purpose of preventing and treating postmenopausal osteoporosis because of its efficacy, but it also contributes to a significant increase in breast cancer. Currently, there is a dilemma regarding the use of estrogen for postmenopausal women. Fortunately, an increasing understanding of the action of estrogen has led ultimately to the design of new drugs that work by virtue of their interaction with the ER; these drugs have come to be known as selective estrogen receptor modulators (SERMs), and are not only effective in preventing osteoporosis and managing those with osteoporosis, but also in decreasing the incidence of breast cancer. Among these SERMs, raloxifene may be the most attractive agent based on the evidence from five recent large trials (Multiple Outcomes of Raloxifene Evaluation [MORE], Continuing Outcomes Relevant to Evista [CORE], Raloxifene Use for the Heart [RUTH], Study of Tamoxifen and Raloxifene [STAR], and Evista Versus Alendronate [EVA]). The former three trials showed that raloxifene not only decreases the incidence of osteoporosis-associated fractures, but also has efficacy in breast cancer prevention. The head-to-head comparison with the anti-fracture agent alendronate (EVA trial) and the chemoprevention agent tamoxifen (STAR trial) further confirmed that raloxifene is a better choice. We concluded that since there is an absence of a therapeutic effect on relieving climacteric symptoms and there is the presence of a potential risk of thromboembolism in the use of raloxifene, this drug can be prescribed for clear indications, such as the management of osteoporosis, the prevention of fracture, and decreasing the incidence of invasive breast cancer, with careful monitoring for thromboembolism. It is reasonable to use raloxifene as an appropriate medicine that targets climacteric symptom-free postmenopausal women because of its overall favorable risk-benefit safety profile using the global index proposed by the Womens Health Initiation (WHI).

Laparoscopic surgery for heterotopic pregnancies: a case report and a brief review

A heterotopic pregnancy is in effect a multiple pregnancy with one or more intrauterine pregnancies coexisting with an ectopic pregnancy and is rarely spontaneous. With the increasing popularity of ovulation induction performed during assisted reproductive techniques, it will not be surprising to observe that this phenomenon has increased significantly. However, diagnosis is often delayed because of its rarity and difficulty. We report a case of a woman with a viable intrauterine pregnancy who had a complication of ovarian hyper-stimulation syndrome secondary to ovulation induction following in vitro fertilization and embryo transfer, but who, during hospitalization, presented with clinically progressive abdominal pain. An unruptured ectopic pregnancy of the right fallopian tube was diagnosed accidentally by laparoscopy and laparoscopic salpingectomy was immediately performed. Post-operative follow-up revealed that the intrauterine pregnancy continued normally. She delivered a normal female baby at 38 weeks of gestation. The promising neonatal outcome might suggest that laparoscopy might be safely performed to aid differential diagnosis in an uncertain condition during pregnancy: therefore, laparoscopic surgery might be an appropriate method to manage some carefully selected patients with HP. A brief review of the published literature on the role of laparoscopy in the diagnosis and management of heterotopic pregnancy is given.

Rapid detection of trisomy 21 by homologous gene quantitative PCR (HGQ-PCR)

Abstract Down’s syndrome results from the production of three copies of chromosome 21 within a cell. We have devised a method termed the homologous gene quantitative polymerase chain reaction (HGQ-PCR), which uses one pair of primers and which can directly identify the additional copy of chromosome 21 by simultaneously amplifying two highly homologous genes of the human liver-type phosphofructokinase located on chromosome 21 (PFKL-CH21) and the human muscle-type phosphofructokinase located on chromosome 1 (PFKM-CH1) for self-detecting determination. On analysis of 34 cases of Down’s syndrome, including two cases of unbalanced translocation 46, XY, der (14; 21) (q10; q10), + 21, and 100 normal individuals, the relative ratio of the PFKM-CH1/PFKL-CH21 product was 1.33 ± 0.323 (mean ± SD) and 0.40 ± 0.16 (mean ± SD) for disomy DNA and trisomy DNA, respectively. The difference between these two groups was highly significant (P < 0.001). These results indicate that this quantitative method is practical and may be used for the prenatal diagnosis of Down’s syndrome caused by trisomy 21.

The Role of Selective Estrogen Receptor Modulators on Breast Cancer: From Tamoxifen to Raloxifene

The link between hormones and breast cancer growth and development has been recognized for more than a century. Estrogen stimulates the proliferation of breast epithelial cells, and both endogenous and exogenous estrogens have been implicated in the pathogenesis of breast cancer. Classically, estrogen action at target sites around the body is mediated through related but distinct estrogen receptors (ERs), designated ERalpha and ERbeta, to alter gene expression. This accumulating understanding of the mechanism of action of estrogen led ultimately to the design of antiestrogenic agents that work by virtue of their interaction with the ER; these drugs have come to be known as selective estrogen receptor modulators (SERMs). Tamoxifen, a SERM, emerged as the first antiestrogenic agent that is clinically applicable to breast cancer. Tamoxifen became the gold standard and established the principles of tumor targeting and identified the appropriate treatment strategy to aid survivorship in breast cancer patients, with enhancement of disease-free survival and a 50% decrease in recurrences observed in ER-positive patients 15 years after diagnosis. However, because of the many adverse events in the use of tamoxifen, some of which have contributed to significant morbidity and mortality, drug modification which has resulted in fewer incidences of adverse events without compromising the therapeutic effect for breast cancer prevention may face an easier road to acceptance. Raloxifene may be a better alternative, since evidence from large clinical trials showed that raloxifene not only decreases the incidence of osteoporosis and related fractures, but also offers benefits for breast cancer prevention. The results from the Study of Tamoxifen and Raloxifene (STAR) trial showed the superiority of raloxifene over tamoxifen, not only for the equal efficacy in the prevention of invasive breast cancer but also for the fewer serious adverse events. Taken together, without other competition so far, raloxifene is recommended for postmenopausal women with osteoporosis who also need breast cancer prevention.

Induction of p38 Mitogen-Activated Protein Kinase-Mediated Apoptosis Is Involved in Outgrowth of Trophoblast Cells on Endometrial Epithelial Cells in a Model of Human Trophoblast-Endometrial Interactions

Abstract During embryo implantation in species with hemochorial placentation, such as the mouse and human, trophoblast cells of the attached blastocyst penetrate the luminal epithelium of the endometrium before invasion into the endometrial stroma. Signs of apoptosis were demonstrated in luminal endometrial epithelial cells (EEC) adjacent to the trophoblast cells; however, the signaling mechanisms leading to apoptosis in EEC remain unclear. Because mitogen-activated protein kinases (MAPK) were shown to mediate apoptosis in several model systems and found to be activated in the uterus during decidualization, the possible involvement of MAPK during trophoblast-EEC interactions was studied. By coculturing BeWo human trophoblast spheroids with RL95-2 human EEC monolayers to mimic the blastocyst-endometrial interaction, we found that most spheroids rapidly attached to EEC monolayers and then progressively expanded, with marked dislodgment of EEC adjacent to the spreading trophoblast cells. Immunoblotting analysis showed that both p38 MAPK and extracellular signal-regulated kinase (ERK) were activated in EEC after coculture. However, only SB203580 (a p38 MAPK inhibitor), but not PD98059 (an ERK inhibitor), inhibited trophoblast outgrowth on EEC monolayers through the suppression of p38 MAPK activation in EEC. Furthermore, trophoblast expansion caused prominent EEC apoptosis at the spheroid-EEC interface, as detected by annexin V labeling and valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (which binds activated caspases) staining, and SB203580 significantly decreased the percentage of apoptotic cells. Our results, based on a model of human trophoblast-EEC interactions, establish that trophoblast cells cause activation of p38 MAPK in EEC and, consequently, induce apoptosis and displacement of EEC, a process that may facilitate implantation.

Use of a long-acting gonadotropin-releasing hormone agonist for treatment of steroid cell tumors of the ovary

OBJECTIVEnTo report a complete serologic response in a 50-year-old women who received long-acting gonadotropin-releasing hormone agonist (GnRH-A) therapy for steroid cell tumor of the ovary, not otherwise specified.nnnDESIGNnCase report.nnnSETTINGnUniversity hospital-based reproductive biology unit.nnnPATIENT(S)nA 50-year-old female patient exhibited persistent elevation of T (>2.0 ng/mL) after surgery for steroid cell tumor of the ovary, not otherwise specified, stage IIA for 3 months. This elevation suggested the presence of some residual active tumor.nnnINTERVENTION(S)nAll tumor evaluations, including those for tumor markers, a thorough physical examination, imaging studies, and evaluations of nuclear medicine studies were negative except for elevated serum T levels. The patient was treated with GnRH-a between the fourth month and sixth month postoperatively.nnnMAIN OUTCOME MEASURE(S)nSerum levels of T and tumor survey.nnnRESULT(S)nThe serum T levels returned to normal limits after administration of the first dose of GnRH-a. Follow-up of tumor survey was negative. The patient was alive and free of disease 26 months after treatment with GnRH-a.nnnCONCLUSION(S)nGnRH-a may be an alternative choice as adjuvant therapy for managing a persistent or recurrent hormone-producing steroid cell tumor of the ovary.

Excision of mature teratoma using culdotomy, with and without laparoscopy: a prospective randomised trial

Objective To compare the results of removing mature teratoma with laparoscopy or without laparoscopy.

USE OF A GONADOTROPIN-RELEASING HORMONE AGONIST TO MANAGE PERIMENOPAUSAL WOMEN WITH SYMPTOMATIC UTERINE MYOMAS

OBJECTIVEnTo determine the acceptability and effectiveness of a gonadotropin-releasing hormone (GnRH) agonist for the treatment of perimenopausal women with symptomatic uterine myomas.nnnMATERIALS AND METHODSnThe participants included 43 women with symptomatic myomas who wished to retain their uteri. All the women were older than 45 years old, agreed to use the GnRH agonist for menopause induction, and were without any underlying malignancy. They were treated with six courses of GnRH agonist between 2004 and 2005. The definition of re-intervention included: (1) surgical intervention, such as hysterectomy, myomectomy or laparoscopic uterine vessel occlusion, or (2) modification of GnRH agonist use. Modification of GnRH agonist use included either failure to complete a 6-month GnRH agonist treatment course, or re-use of GnRH agonist with/without interruption of continuity. Failure was defined as women who underwent surgical intervention or failed to complete the 6-month GnRH agonist treatment. Evaluations were performed every 6 months, for up to 2 years.nnnRESULTSnRe-intervention rates were 14.0% (n = 6), 23.3% (n = 10) and 32.6% (n = 14), and failure rates were 7.0% (n = 3), 11.6% (n = 5) and 16.3% (n = 7), at the end of the 6-, 12- and 24-month follow-up periods, respectively. Three patients failed to complete the 6-month GnRH agonist treatment, and four received surgical interventions.nnnCONCLUSIONnMore than 80% of women in this study benefited from the use of GnRH agonist to produce menopause, suggesting that this can be an alternative choice for managing perimenopausal women with symptomatic uterine myomas.