An 86-year-old Japanese woman underwent an examining laparoscopy for removing the huge pelvic tumor. At laparoscope examination, the cystic tumor was found within the left broad ligament, while the ovaries, fallopian ...An 86-year-old Japanese woman underwent an examining laparoscopy for removing the huge pelvic tumor. At laparoscope examination, the cystic tumor was found within the left broad ligament, while the ovaries, fallopian tubes and uterus showed almost normal appearance. The tumor was removed together by total laparoscopic hysterectomy and bilateral salpingo-oophorectomies after the suction of serous content in the broad ligament. Cytological findings of the ascites suggested serous carcinoma. The resected ovaries and fallopian tubes were grossly and histologically normal. Histological examination of the solid part of broad ligament tumor, closely next to the fallopian tube, revealed a serous adenocarcinoma. Immunohistochemically, the tumor cells were strongly positive for CK7, WT-1, estrogen receptor, AE1/AE3 and EMA, and negative for CK20, D2-40 and calretinin. Also, they were negative for progesterone receptor and p53. The authors diagnosed the primary tumor as being a serous cystadenocarcinoma of the broad ligament [pTIC3NxM0, as modified and adapted to post-surgical staging of ovarian cancer (FIGO 2014)]. The patient has been receiving 6 cycles of adjuvant chemotherapies with one course with paclitaxel (PTX) and carboplatin (CBDCA) and five with PTX, CBDCA and Bevacizumab, and has no signs of recurrence and metastasis six months after the operation.展开更多
There is evidence to suggest that follicle-stimulating hormone （FSH） can facilitate the neovascularization of ovarian cancers by increasing vascular endothelial growth factor （VEGF） expression in cancer cells, alt...There is evidence to suggest that follicle-stimulating hormone （FSH） can facilitate the neovascularization of ovarian cancers by increasing vascular endothelial growth factor （VEGF） expression in cancer cells, although the underlying molecular mechanism of this process is not well known. Therefore, we investigated the effect of FSH on VEGF expression in the ovarian cancer cell lines SKOV-3 and ES-2. Treatment with FSH significantly increased VEGF expression in a dose- and time-dependent manner. In addition, FSH treatment enhanced the expression of survivin and hypoxlainducible factor-1 （HIF-1α）. Knockdown of survivin or HIF-1α suppressed VEGF expression, but only knockdown of survivin inhibited FSH-stimulated VEGF expression. Pretreatment with LY294002, a phosphoinositide 3-kinase （PI3K）/AKT inhibitor, neutralized the enhanced expression of survivin induced by FSH, but treatment with U0126, a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor, had no such effect. We further showed that ovarian serous cystadenocarcinoma samples had much higher incidence of positive AKT and phosphorylated AKT （pAKT） protein staining than did benign ovarian cystadenoma samples （p 〈 0.01）. The 5-year survival rate was only about 15% in patients with ovarian serous cystadenocarcinoma who had AKT and pAKT expression, whereas it was about 80% in those who did not have AKT or pAKT expression. Taken together, these results indicate that FSH increases the expression of VEGF by upregulating the expression of survivin, which is activated by the PI3K/AKT signaling pathway. Understanding the role of the PI3K/AKT pathway in FSH-stimulated expression of survivin and VEGF will be beneficial for evaluating the prognosis for patients with ovarian serous cystadenocarcinoma and for pursulug effective treatment against this disease.展开更多
The human WFDC2 protein, also known as human epididymal secretory protein 4 （HE4）, is a new markerof tumor progressionJ that is used for the differential diagnosis of ovarian cystadenocarcinomas. At present, the pat...The human WFDC2 protein, also known as human epididymal secretory protein 4 （HE4）, is a new markerof tumor progressionJ that is used for the differential diagnosis of ovarian cystadenocarcinomas. At present, the pathology of ovarian carcinomas is defined by the “dualistic model”2 and “heterogeneity of ovarian carcinomas”3 theories. Previously, it was considered that ovarian carcinomas originate from the ovaries themselves. The ＂dualistic model＂ assumes an external origin for ovarian carcinomas, in which it is considered that serous ovarian carcinomas originate from secondary implantation of oviduct mucosa epithelium. Epithelial ovarian carcinomas are not a single disease, but a set of ＂heterogeneous diseases＂.3展开更多
文摘An 86-year-old Japanese woman underwent an examining laparoscopy for removing the huge pelvic tumor. At laparoscope examination, the cystic tumor was found within the left broad ligament, while the ovaries, fallopian tubes and uterus showed almost normal appearance. The tumor was removed together by total laparoscopic hysterectomy and bilateral salpingo-oophorectomies after the suction of serous content in the broad ligament. Cytological findings of the ascites suggested serous carcinoma. The resected ovaries and fallopian tubes were grossly and histologically normal. Histological examination of the solid part of broad ligament tumor, closely next to the fallopian tube, revealed a serous adenocarcinoma. Immunohistochemically, the tumor cells were strongly positive for CK7, WT-1, estrogen receptor, AE1/AE3 and EMA, and negative for CK20, D2-40 and calretinin. Also, they were negative for progesterone receptor and p53. The authors diagnosed the primary tumor as being a serous cystadenocarcinoma of the broad ligament [pTIC3NxM0, as modified and adapted to post-surgical staging of ovarian cancer (FIGO 2014)]. The patient has been receiving 6 cycles of adjuvant chemotherapies with one course with paclitaxel (PTX) and carboplatin (CBDCA) and five with PTX, CBDCA and Bevacizumab, and has no signs of recurrence and metastasis six months after the operation.
文摘There is evidence to suggest that follicle-stimulating hormone （FSH） can facilitate the neovascularization of ovarian cancers by increasing vascular endothelial growth factor （VEGF） expression in cancer cells, although the underlying molecular mechanism of this process is not well known. Therefore, we investigated the effect of FSH on VEGF expression in the ovarian cancer cell lines SKOV-3 and ES-2. Treatment with FSH significantly increased VEGF expression in a dose- and time-dependent manner. In addition, FSH treatment enhanced the expression of survivin and hypoxlainducible factor-1 （HIF-1α）. Knockdown of survivin or HIF-1α suppressed VEGF expression, but only knockdown of survivin inhibited FSH-stimulated VEGF expression. Pretreatment with LY294002, a phosphoinositide 3-kinase （PI3K）/AKT inhibitor, neutralized the enhanced expression of survivin induced by FSH, but treatment with U0126, a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor, had no such effect. We further showed that ovarian serous cystadenocarcinoma samples had much higher incidence of positive AKT and phosphorylated AKT （pAKT） protein staining than did benign ovarian cystadenoma samples （p 〈 0.01）. The 5-year survival rate was only about 15% in patients with ovarian serous cystadenocarcinoma who had AKT and pAKT expression, whereas it was about 80% in those who did not have AKT or pAKT expression. Taken together, these results indicate that FSH increases the expression of VEGF by upregulating the expression of survivin, which is activated by the PI3K/AKT signaling pathway. Understanding the role of the PI3K/AKT pathway in FSH-stimulated expression of survivin and VEGF will be beneficial for evaluating the prognosis for patients with ovarian serous cystadenocarcinoma and for pursulug effective treatment against this disease.
文摘The human WFDC2 protein, also known as human epididymal secretory protein 4 （HE4）, is a new markerof tumor progressionJ that is used for the differential diagnosis of ovarian cystadenocarcinomas. At present, the pathology of ovarian carcinomas is defined by the “dualistic model”2 and “heterogeneity of ovarian carcinomas”3 theories. Previously, it was considered that ovarian carcinomas originate from the ovaries themselves. The ＂dualistic model＂ assumes an external origin for ovarian carcinomas, in which it is considered that serous ovarian carcinomas originate from secondary implantation of oviduct mucosa epithelium. Epithelial ovarian carcinomas are not a single disease, but a set of ＂heterogeneous diseases＂.3
