Pulmonary Toxicity after a Quick Course of Combinatorial Vincristine, Bleomycin, and Cisplatin Neoadjuvant Chemotherapy in Cervical Cancer

Pulmonary toxicity is one of the most serious adverse effects associated with a quick course of vincristine, bleomycin, and cisplatin neoadjuvant chemotherapy (NAC-VBP). The aim of this study was to evaluate pulmonary toxicity related to a quick course NAC-VBP. A total of consecutive 61 patients, who underwent at most 3 cycles of NAC-VBP every 10 days in the International Federation of Gynecology and Obstetrics (FIGO) stage IB-IIB cervical cancer from 1995 to 2007, were retrospectively analyzed. Of the 61 study subjects, 7 (11.5%) were identified to have pulmonary toxicity and 2 (3.3%) died of pulmonary fibrosis progression despite aggressive treatment and the use of a multidisciplinary approach. No factor predisposing pulmonary toxicity was identified. Initial symptoms were non-specific, but bronchiolitis obliterans organizing pneumonia and interstitial pneumonitis were characteristic findings by high-resolution computed tomography of the chest. The benefit of steroid therapy was uncertain and was associated with steroid-induced diabetes mellitus requiring insulin therapy in two patients. Fatal pulmonary toxicity is a major concern of a quick course NAC-VBP. In conclusion, these patients require special monitoring for bleomycin-induced pulmonary toxicity.

Expression and mutational analysis of TGF-beta/Smads signaling in human cervical cancers / 부인종양

OBJECTIVE: To define the molecular basis of TGF-beta1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-beta1, TGF-beta1 receptors, and Smads, the regulators of the TGF-beta1 signaling pathway, in human cervical cancers. METHODS: Expression of TGF-beta1, TGF-beta1 receptors, and Smads transcripts were determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR), and sequence alteration was analyzed using RT-PCR-single-strand conformation polymorphism (SSCP) analysis. Genomic levels of TGF-beta1, TGF-beta1 receptors and Smads was also measured by quantitative genomic PCR. RESULTS: Abnormal overexpression of TGF-beta1 and abnormal reduction of type II TGF-beta1 receptor were identified in 36% (18 of 50) and 20% (10 of 50) of cervical cancer tissues, respectively. 22% (11 of 50) in Smad2 and 14% (7 of 50) in Smad4 revealed tumor specific mRNA reduction less than a half of normal means. In addition, no evidence for sequence alterations of the gene was found by RT-PCR-SSCP analysis. CONCLUSION: Our study demonstrates that disruption of TGF-beta/Smad signaling pathway exist in human cervical cancer, suggesting that abnormal expressions of the member of TGF-beta/Smad signaling pathway might contribute to the malignant progression of human cervical tumors via suppressing the tumor suppression function of TGF-beta1 1's tumor suppression function.

Clinical Characteristics of Metastatic Tumors to the Ovaries

Approximately 5-30% of the ovarian cancers are metastatic malignancies. The prevalence of metastatic ovarian tumors varies with the incidence rates and spread patterns of primary malignancies. We evaluated the prevalence, pre- and postoperative characteristics of metastatic ovarian cancer in Korean women. We reviewed the records for 821 ovarian malignancies with pathological consultation from 1996- 2006 and recorded patient demographical, radiological, histopathological, and survival data. The study included 112 cases of histologically confirmed metastatic ovarian cancer. Metastatic ovarian cancer accounted for 13.6% of all ovarian malignancy, primarily arising from the gastrointestinal tract. The preoperative detection rate with imaging was 75%, and none of the radiological or serological features were useful for differential diagnosis. In multivariate analysis for prognostic variables, the only significant factor was the primary tumor site (p=0.004). Furthermore, extensive resection increased survival for some patients. The differential diagnosis of metastatic ovarian cancer can be problematic, so multiple diagnostic approaches are necessary. The extent of cytoreductive surgery for this type of tumor must be decided on a case-by-case basis.

The effect of HER-2 polymorphism according to age on the risk and pathologic feature of endometrial cancer / 대한산부인과학회지

OBJECTIVE: To evaluate the relationship between single nucleotide polymorphisms (SNPs) in the HER-2 gene and age on the risk and pathologic feature of endometrial cancer. METHODS: We included 125 women with histologically confirmed endometrioid adenocarcinoma who underwent complete surgical staging. The control group consisted of 302 patients with benign gynecologic disease who underwent hysterectomy. Nine SNPs spanning the HER-2 gene were genotyped by SNP-IT assay using SNPstream(r) Genotyping System. Of 9 SNPs, 5 that were either monomorphic or had a lowallele frequency ( or =10%; these were included in the final analysis. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) after adjustment for BMI. RESULTS: The mean age for endometrial cancer patients was 53.4+/-11.5 (range, 29-81) years. Forty-seven patients (38%) were or =50 years. Cases had a significantly higher BMI than controls (P<0.001). After adjustment for BMI, there was no significant relationship between HER-2 polymorphism and the risk of endometrial cancer based on age. Furthermore, HER-2 polymorphism did not affect the pathologic features of endometrial cancer based on age. CONCLUSION: Although there is no potential association among HER-2 polymorphisms, age, and endometrial cancer risk, large studies are needed in the future to assess the role of this polymorphism in endometrial cancer and for its combined effect.

The effect of HER-2 polymorphism according to age on the risk and pathologic feature of endometrial cancer / 대한산부인과학회지

OBJECTIVE: To evaluate the relationship between single nucleotide polymorphisms (SNPs) in the HER-2 gene and age on the risk and pathologic feature of endometrial cancer. METHODS: We included 125 women with histologically confirmed endometrioid adenocarcinoma who underwent complete surgical staging. The control group consisted of 302 patients with benign gynecologic disease who underwent hysterectomy. Nine SNPs spanning the HER-2 gene were genotyped by SNP-IT assay using SNPstream(r) Genotyping System. Of 9 SNPs, 5 that were either monomorphic or had a lowallele frequency ( or =10%; these were included in the final analysis. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) after adjustment for BMI. RESULTS: The mean age for endometrial cancer patients was 53.4+/-11.5 (range, 29-81) years. Forty-seven patients (38%) were or =50 years. Cases had a significantly higher BMI than controls (P<0.001). After adjustment for BMI, there was no significant relationship between HER-2 polymorphism and the risk of endometrial cancer based on age. Furthermore, HER-2 polymorphism did not affect the pathologic features of endometrial cancer based on age. CONCLUSION: Although there is no potential association among HER-2 polymorphisms, age, and endometrial cancer risk, large studies are needed in the future to assess the role of this polymorphism in endometrial cancer and for its combined effect.

Role of 5'-CpG island hypermethylation of the FHIT gene in cervical carcinoma / 부인종양

OBJECTIVE: The abnormal expression of fragile histidine triad (FHIT) gene has been frequently reported in a variety of epithelial malignancies including cervical carcinoma. Furthermore, in a recent study it was proposed that transcriptional inactivation of FHIT, as a consequence of aberrant 5'-CpG island methylation, plays an important role in the carcinogenesis of human cervical carcinoma. The authors sought to determine whether abnormal FHIT transcription occurs in human cervical carcinoma, and if so, whether this abnormal expression is associated with aberrant 5'-CpG island methylation. In addition, the clinical significance of FHIT inactivation was investigated in Korean women with cervical cancer. METHODS: To examine for abnormal transcripts of the FHIT gene, quantitative RT-PCR, genomic DNA-PCR and nonisotopic RT-PCR-SSCP analysis were performed using the standard method. The methylation status was determined by methylation specific PCR and bisulfite DNA sequencing. RESULTS: The FHIT gene was down-regulated in 15 of 58 (25.9%) cervical carcinomas. FHIT promoter hypermethylation was detected in 15 of 15 (100%) abnormally expression in cervical carcinomas. Bisulfite DNA sequencing confirmed these findings and a significant correlation was found between CpG site hypermethylation and low FHIT expression. However, no significant correlation was found between reduced FHIT expression and clinicopathological characteristics. CONCLUSION: In this study, FHIT inactivation in cervical cancer was found to be strongly correlated with 5'-CpG island hypermethylation rather than a genetic alteration. Furthermore, no significant relation was found between a lack of FHIT expression and the prognostic factors of cervical cancer in our Korean cohort.

Expression of MTA1 and nm23-H1 protein in ovarian carcinomas in relation to lymph node metastasis / 부인종양

OBJECTIVE: Cancer metastasis is a complex process involving a sequential series of multi-step genetic events, which produces an imbalance between stimulatory and inhibitory genes for metastasis. Presently, we examined the expression of metastatic tumor antigen 1 (MTA1) and nonmetastatic protein 23 homologue H1 (nm23-H1) proteins in metastasized epithelial ovarian cancer cells. METHODS: Fifty-one primary epithelial ovarian tumors and corresponding lymph nodes (LNs) were examined immunohistochemically for expression of MTA1 and nm23-H1. Expression of these proteins was statistically evaluated. RESULTS: The frequency of MTA1 expression was 30.3% (10/33) in stage III/IV LNs but was absent (0/18) in stage I/II LNs (p=0.01). MTA1 expression was observed in 50% (6/12) of metastasizing LNs but in only 10.3% (4/39) of non-metastasizing LNs (p=0.01). In contrast with MTA1, nm23-H1 expression was evident in 16 of 18 (88.9%) stage I/II ovarian cancer tissue samples but only in 20 of 33 (60.6%) stage III/IV tissues (p=0.05), and nm23-H1 production was also observed in 75.6% (34/45) of ovarian cancer tissue with residual tumors under 2 cm in diameter, but in 2/6 (33.3%) of cancer tissue with residual tumors exceeding 2 cm in diameter (p=0.03). CONCLUSION: The degree of expression and imbalance of MTA1 and nm23H1 are correlated with ovarian cancer LN metastasis.

Functional analysis of CDC7 protein which is interacted with HPV E6 / 대한산부인과학회지

OBJECTIVE: Human papillomaviruses are associated with the majority of cervical cancers. There is a wide effort focused on searching for the target of the involvement of p53-independent HPV-16E6 interacting proteins. We identified Cdc7 (cell division cycle 7-related protein kinases) as a binding partner of E6 and investigated its biological function in cervical cancer cells. METHODS: The baits, E6, fused to the LexA-BD subunit using pBTM116 vector were used to screen an oligoneucleotide primed human HeLa cDNA library cloned in pGAD10 vector. Yeast two-hybrid screens were performed. Immunoprecipitation assay was performed to determine whether E6-Cdc7 interaction occurred. Cells treated with siRNA were analysed by flow cytometry. RESULTS: We have delinated the interactions of E6 with five proteins, namely the IRF-3 (interferon regulatory factor-3), PRKCL?1 (protein kinase C-like 1), PIST (PDZ/coiled-coil domain binding gene), BARD1 (BRCA1 assocated ring domain 1), and Cdc7. The in vitro result of the interaction between E6 and Cdc7 was confirmed by immunoprecipitation experiments. Down-regulation of Cdc7 by small interfering RNA in HeLa cell lines causes an abortive S phase, leading to cell death. CONCLUSION: We have identified the new protein of interaction with HPV E6, Cdc7 kinase. It has been implicated in S phase signaling of cell cycle and the inhibition of Cdc7 induced cell death. But, further investigation is needed to know the biologic function of Cdc7 kinase in cervical carcinogenesis.

A case of clear cell adenocarcinoma of the uterine cervix in a 6-year-old girl / 대한산부인과학회지

The clear cell adenocarcinoma of uterine cervix is very rare tumor, and only 4-9% of entire adenocarcinoma appears to be diagnosed as clear cell adenocarcinoma. Its risk factor and pathogenesis are not exactly known, but intrauterine exposure to DES (diethyl stilbestrol) and associated non-steroidal estrogen during pregnancy before 18weeks is one known risk factor, and also hormonal change or genetic cause are suggested as the risk factors. The peak age of its occurrence has bimodal pattern, which are groups before 24 years-old and after 45 years-old, and clear cell adenocarcinoma arising in latter group is not associated with intrauterine DES exposure. It is also reported that 25% of young women who has clear cell adenocarcinoma had no history of hormonal exposure. The treatment and prognosis is similar to other kinds of uterine cervical adenocarcinoma. With a short literature review, we are reporting a case of 6-year-old girl who visited our clinic because of vaginal mass naturally fallen off with a minor bleeding which was finally diagnosed as clear cell adenocarcinoma, and had no maternal history of DES exposure during pregnancy.

Preoperative MR imaging for differentiation of immature from mature ovarian teratomas / 대한산부인과학회지

OBJECTIVE: The purpose of this study was to differentiate immature from mature ovarian teratomas, using magnetic resonance (MR) imaging and to evaluate the MR imaging appearance of immature teratomas. METHODS: The patients with pathologic diagnosis of ovarian teratomas between January 1995 and December 2005 were restrospectively reviewed for clinicopathologic characteristics. RESULTS: Of the 787 patients studied, 773 (98.2%) patients were mature cystic teratomas and 14 (1.8%) patients were immature teratomas. Ten patients with immature teratoma (71.4%) were diagnosed preoperatively and 4 patients (28.6%) were diagnosed postoperatively. Preoperative MRI was performed in 4of 14 patients surgically proved immature teratomas. At MR imaging, the immature teratomas characteristically have a large, irregular solid component containing coarse calcifications and numerous variable-sized cysts. Small punctuate foci of fat help diagnosing these tumors. CONCLUSION: Preoperative MR imaging are relatively specific in the detection of immature teratomas. This suggests that preoperative MR imaging is helpful in differentiating immature from mature ovarian teratomas.

Genomic gain and loss of cervical cancer using BAC Chip / 대한산부인과학회지

OBJECTIVE: Cervical cancer has long been linked to the sexually transmitted human papillomavirus (HPV), and the oncoproteins E6 and E7 disrupt the functions of tumour suppressor genes, resulting in genetic alteration. It was shown that loss of heterozygosity at 6p is a common genetic alteration in cervical cancer. However, the molecular genetics of cancer have only recently been understood, and for the development of cervical cancer additional genetic alterations in host cell genes are required. The present study has identified the differential changes of the cervical cancer-associated genetic alterations by a genome-wide array based comparative genomic hybridization (array-CGH). METHODS: We analyzed 15 cases of cervical cancer from St. Mary's hospital of The paraffin-fixed tissue samples were microdissected under microscope and DNA was extracted by the procedures of proteinase K digestion and chloroform extraction. Array-based CGH and genomic PCR were carried out with statistical analyses such as hierarchical clustering and Gene Ontology. The BAC array used in this study consisted of 1,440 human BACs, the space among the clones were approximately 2.08 megabase (Macrogen, Seoul, Korea). RESULTS: All of 15 cases of cervical cancer showed specific gains and losses. The analysis limit of average gains and losses was 53%. A significant positive correlation was found between 1p36.32, 3p14.2, 3q27.1, 7p21.1, 8q24.3 and 11q13.1 changes through the cervical carcinogenesis. The high-level of gain regions, BAC clones encoded GSDMDC1, RECQL4, TP73, ABCF3, ALG3, HDAC9, ESRRA and RPS6KA4 genes. Frequently gained BAC clones encoded genes were PRSS8, FUS, COL18A1, PCOLN3, MAFG and ASPSCR1. The genes encoded by frequently lost BAC clones were PTPRG, GRM7, ZDHHC3, EXOSC7, LRP1B and NR3C2. Also, hierarchical clustering of the expression data readily distinguished genomic alterations in cervical cancer. A subset of cellular processes from each gene was clustered by Gene Ontology database. CONCLUSION: Using Array-CGH, genomic alterations related to cervical cancer were identified to determine whether induction of chromosomal imbalances occurs prior to carcinogenesis. The high resolution of array-CGH combined with human genome database would give a chance to find out possible target genes present in the gained or lost clones.

Clinical analysis of synchronous primary neoplasms of the female reproductive tract / 대한산부인과학회지

OBJECTIVE: A histopathologic review of synchronous primary neoplasms of the female reproductive tract was presented and the possible correlation among discrete tumor subsets, natural history, and survival was evaluated. METHODS: Between 2000 and 2005, 20 patients with synchronous primary cancers of the gynecologic malignancy were identified. Clinical and pathologic informations were obtained from medical records. Kaplan-Meier survival analysis was performed. RESULTS: The patients with Synchronous primary malignancies constituted 0.63% of all genital malignancies. The most frequently observed synchronous neoplasms were those of the ovary with the endometrium (40%). The mean age of patient with synchronous ovarian and endometrial cancer was 45.2 years. 8 patients underwent the hysterectomy with bilateral salpingo-oophorectomy and adjuvant therapy. The mean survival is 57 months (SE 10.0, 95% Confidence interval 37-77). CONCLUSION: Synchronous ovarian and endometrial cancers were detected in relatively early age and the prognosis was favorable.

The mechanism of cell death in etoposide treated cervical cancer cells: apoptotic and non-apoptotic programmed cell death / 부인종양

OBJECTIVE: Etoposide is a potent and widely used antineoplastic agent. It is able to induce apoptosis in most cell types. However, very little is known about its mechanism of action. In this study, we demonstrate the cytotoxic signal that induced by etoposide and investigate how etoposide exerts antitumor activity in HPV-16 (+) CaSki cervical carcinoma cells. METHODS: Antiproliferation activity was measured in CaSki cell lines by using MTT assays, DNA fragmentation assay. Cell cycle distribution was analyzed using flow cytometry. Expression of proteins involved in the apoptotic pathway was analyzed by Western blotting (WB). Electron microscopic (EM) and biochemical studies (Western blotting, RT-PCR) revealed that non-apoptotic death was associated with autophagosomes/-autolysosomes. These parameters have also been measured in cells treated with 3-methyladenine (an autophagy inhibitor), zVAD-fmk (a pan-caspase inhibitor) and both. RESULTS: The etoposide induced apoptosis. In cell cycle analysis, etoposide-treated CaSki cells were few induced hypodiploid DNA content, suggesting that apoptotic cell death. EM study revealed that autophagic appearance in the presence of etoposide exhibited by autophagosomes/autolysosomes. It was confirmed by LysoTracker probe and WB against Beclin 1, APG 5, APG 12 and p53. When autophagy was blocked by 3-MA, not only the protein expression of Beclin 1, but also the antitumor effect of etoposide was suppressed. On the other hand, the addition of zVAD-fmk could induce a few etoposide-induced autophagy. And etoposide-treated CaSki cells were rescued by combination of 3-MA and zVAD-fmk. CONCLUSION: Our results suggest that etoposide not only initiated apoptosis but ultimately caused cell death through autophagy. In this study, we demonstrate novel features for the action of etoposide in HPV-16 (+) CaSki cervical carcinoma cells. Autophagic cell death induction by some anticancer agents underlines the potential utility of its induction as a new cancer treatment modality.

Differential protein expression of etoposide-treated CaSki cervical carcinoma cells / 부인종양

OBJECTIVE: This study was designed to examine the pharmaco-dynamic pattern of proteomic expression in cervical carcinoma cells (CaSki cell line; HPV-16 positive) after in vitro treatment by the etoposide. METHODS: We analyzed proteomic profiling in cervical carcinoma cells after etoposide treatment using two-dimensional gel electrophoresis (2-DE) with MALDI-TOF-MS used for protein identification. Then, we tested the several experimental methods for verification and functional identification, including MTT assay, PI staining, DNA fragmentation assay, FDA, FACS and Western blot analysis. RESULTS: Etoposide inhibited the CaSki cervical cancer cell growth in a dose-dependent manner and the optimal concentration of etoposide is 2micrometer(IC50) in the CaSki cervical cancer cells. The etoposide induced apoptosis, as determined by DNA fragmentation assay, FACS, and Western blot. The etoposide increased the protein expression of Fas (Apo-1/CD95), p53, pRb and caspase-3, but decreased the level of Bcl-2 and caspase-3 precursor and subsequently triggered the mitochondrial apoptotic pathway (release of cytochrome c and activation of caspase-9). To this end, we analyzed CaSki cancer cells using 2-DE. Eight proteins (XAP-5, HXC-36, serine/threonine protein phosphatase 2B catalytic subunit, G2/mitotic-specific cyclin B1, T-box transcription factor TBX20, diacylglycerol kinase, amiloride-sensitive amine oxidase, HEF-like protein, ras-related protein Rab-20) were down-regulated and nine proteins (RNA 3'-terminal phosphate cyclase-like protein, late endosomal/lysosomal Mp1 interacting protein, glia maturation factor, replication protein A 14 kDa subunit, mago sashi protein homolog, 14 kDa phosphohistidine phosphatase, protein C14 or f48, cyclin-dependent kinase 4 inhibitior A, retinoic acid-binding protein II) were up-regulated in etoposide-treated CaSki cells when compared with non-treated cells. CONCLUSION: Our results clearly indicate that etoposide induced cell death by apoptosis. These findings may provide insights into the mechanisms underlying the apparent anti-tumoral effects of etoposide.

A Case of Endometrial Cancer with Hereditary Non-Polyposis Colorectal Cancer (HNPCC) / 대한산부인과학회지

Endometrial cancer is the most common malignant disorder that can be associated with hereditary non-polyposis colorectal cancer (HNPCC), which is known as Lynch II syndrome. HNPCC is a polyposis of the colon which is inherited in an autosomal dominant pattern and can cause cancer in other organs, especially in the endometrium. The overall risk of a women with HNPCC to develop endometrial cancer is 40-60%, much higher than the 3% of the general population of women. The average age of developing endometrial cancer of a women with HNPCC is 45 years of age and is often found before development of colon cancer. We have recently experienced a case of de novo type of hereditary non-polyposis colorectal cancer associated with endometrial cancer, hence we are reporting this case with a brief review of literatures.

Two Cases of Primary Malignant Mixed Mullerian Tumor of the ovary / 대한산부인과학회지

Malignant mixed mullerian tumor of the ovary are very aggressive tumors that were usually diagnosed at an older age. They are usually at an advanced stage at the time of diagnosis, and survival after diagnosis varies by stage of disease and histological type. Despite aggressive treatment that includes surgery and chemotherapy, women with these tumors have a significantly increased risk of death giving them a very poor prognosis. The poor prognosis associated with this rare disease represents a need to new therapeutic regimens to improve patients' survival. We experienced two cases of primary malignant mixed mullerian tumor of the ovary.

Two Cases of Primary Malignant Mixed Mullerian Tumor of the ovary / 대한산부인과학회지

Malignant mixed mullerian tumor of the ovary are very aggressive tumors that were usually diagnosed at an older age. They are usually at an advanced stage at the time of diagnosis, and survival after diagnosis varies by stage of disease and histological type. Despite aggressive treatment that includes surgery and chemotherapy, women with these tumors have a significantly increased risk of death giving them a very poor prognosis. The poor prognosis associated with this rare disease represents a need to new therapeutic regimens to improve patients' survival. We experienced two cases of primary malignant mixed mullerian tumor of the ovary.

Abnormal Fragile Histidine Triad (FHIT) Expression in Cervical Carcinomas / 대한산부인과학회잡지

OBJECTIVE: The fragile histidine triad (FHIT) gene is located at chromosome 3p14.2 and encompasses the common fragile site, FRA3B, which may contribute to chromosome breakage and rearrangement of cancer cells. In this study, we examined whether transcriptional alterations of FHIT gene play a role in the development of human cervical carcinomas and the possibility that hypermethylation of CpG islands serves for FHIT inactivation. We then analyzed FHIT expression status with clinical parameters to determine whether it has any prognostic significance. METHODS: The study group included 50 squamous carcinomas, 4 adenocarcinomas, 4 adenosquamous carcinomas, 7 noncancerous tissue and the clinical stage is composed of 4 Ia, 37 Ib and 17 II. Tissue specimens were snap-frozen in liquid N2 and stored at -70degrees C until used. To examine for abnormal transcripts of the FHIT gene, quantitative RT-PCR, genomic DNA-PCR and nonisotopic RT-PCR-SSCP analysis were performed using the standard method. The methylation status was determined by methylation specific PCR. RESULTS: The FHIT gene was down-regulated in 15 of 58 (25.9%) cervical carcinomas. FHIT promoter hypermethylation was detected in 15 of 15 (100%) abnormally expression in cervical carcinomas. CONCLUSION: In this study, gene mutation is not a main mechanism for FHIT inactivation, but the aberrant promoter hypermethylation may be correlated with decreased expression of the FHIT gene. The significance of decreased expression of FHIT does not appear to be an independent prognostic factor in cervical cancers, although a still larger sample of patients will be required to asses this issue definitively.

Primary Squamous Cell Carcinoma Confined to the Endometrium of Submucosal Myoma / 대한산부인과학회잡지

Primary squamous cell carcinoma of the endometrium is extremely rare malignancy. In 1928 Fluhmann proposed three criteria to establish the diagnosis: (1) no coexisting endometrial adenocarcinoma, (2) no connection between the endometrial tumor and the squamous epithelium of the cervix, and (3) no squamous cell carcinoma of the cervix present. Historically, this malignancy has been associated with short survival (<24 months) despite complete surgical extirpation, with or without pre- or postoperative external beam irradiation. In this report, a case of endometrial squamous cell carcinoma is presented with a review of related current knowledge.

Vaginal Birth after Cesarean Delivery: Predictable Factors for Success / 대한주산의학회잡지

OBJECTIVE: The purpose of this report is to determine the predictable factors for successful vaginal birth after cesarean (VBAC). METHODS: In this study, 382 women who attempted VBAC at Kyung-Hee university hospital were included. The medical records of them were reviewed retrospectively. Informations was collected about demographics, medical history, obstetric history, neonatal birth weight, complications, treatment, and outcome of the index pregnancy. RESULTS: The overall success rate was 76.5% (292 cases). Among variables, neonatal birth weight (odds ratio, 0.2; 95% confidence interval, 0.1-0.4), Bishop score at admission (odds ratio, 1.8; 95% confidence interval, 1.5-2.1 ; p<0.05), and history of vaginal delivery (odds ratio, 3.6 ; 95% confidence interval, 1.1-11.6 ; p<0.05) were significant. The Bishop score showed most significant relationship with successful VBAC. The Bishop score 5 at admission had a sensitivity of 47.4% and a specificity of 87.6% in the prediction of successful VBAC. Malpresentation as indications of previous cesarean delivery showed more tendency to succeed than others. CONCLUSION: Several factors such as birth weight, Bishop score at admission, and history of vaginal delivery may be used to predict the success of VBAC.