Leukemia inhibitory factor (LIF) is expressed in the ovary and controls follicular growth. LIF has been reported to accelerate the primordial to primary follicle transition, the growth of cultured preantral follicles, and the maturation of oocytes. Previous reports on factors that regulate follicular growth have largely employed cultured follicles. However, there are several types of follicles and somatic cells in the ovary that are likely to interact with one another to regulate follicular growth. Therefore, a novel approach is essential for understanding the function of factors that regulate follicular growth in the ovary. In this study, we evaluated the function of LIF using cultured ovarian tissue. Ovarian tissue slices were cultured in the presence or absence of recombinant LIF and neutralizing anti-LIF antibody to enable continuous monitoring of follicular growth within the context of the ovary as well as analysis of the process of follicular growth. The results revealed that LIF inhibited the growth of primary, secondary, and antral follicles. Furthermore, we verified the inhibitory function of LIF using the neutralizing antibody, which accelerated follicular growth. These results suggest that LIF is likely to coordinate follicular growth in the ovary. The culture and analysis methods employed in this study are thus effective for clarifying the tissue-level functions of factors that regulate follicular growth within the ovary.
A 70-year-old man consulted our hospital complaining of gross hematuria and bilateral hydronephrosis. Cystoscopic findings suggested non-papillary sessile tumor at the bladder neck. CT findings revealed bilateral hydronephrosis caused by the stricture of lower ureters. Tumorous structure existed between bladder and prostate. Abundant fatty tissue was observed around bladder and rectum, the shape of the bladder was distorted to inverted tear-drop and the bladder was transferred anteriorly, showing findings of pelvic lipomatosis. Urethrocystography revealed elongation of prostatic urethra and anterior displacement of the bladder. Transurethral tumor resection was performed under spinal anesthesia. Pathological diagnosis was proliferative cystitis and no malignant cells were observed. Transperineal tumor biopsy also revealed no malignant cells. The patient was followed under administration of "Saireitou" (chinese medicine) and cetirizine hydrochloride, followed by antibiotics and anti-inflammatory enzyme preparations.
Despite a high cure rate for those who are diagnosed early with melanoma, there are currently no effective treatments for those who have post surgery melanoma recurrence and metastasis. Therefore, we have directed our research focus on preventing tumor recurrence and metastasis following the surgical removal of primary tumor by targeted immunotherapy. The target selected is the cell surface chondrotin sulfate proteoglycan 4 (CSPG4), which plays an important role in signaling pathways regulating tumor cell - survival, -growth and - motility. To implement CSPG4-targeted immunotherapy of melanoma, we have utilized the CSPG4-specific fully human monoclonal antibody scFv-FcC21. The latter was generated by fusing to human IgG1 Fc (Fc) the single chain of variable regions of heavy and light chains (scFv) C21 isolated by panning a phage display human scFv library with live CSPG4+ melanoma cells. The specificity of scFv-Fc C21 was tested with a panel of CSPG4+ and CSPG4- cell lines by flow cytometry. The anti-tumor activity of scFv-Fc C21 was tested by assessing its ability to inhibit tumor cell migration and cell growth in vitro and human melanoma cell-derived lung metastasis in vivo. Moreover, scFv-Fc C21 was tested for its ability to prevent post-surgery human melanoma recurrence and metastasis in SCID mice. Flow cytometric analysis showed that scFv-Fc C21 stained specifically the cell surface of a panel of CSPG4+ human melanoma cell lines but did not stain CSPG4- melanoma cell lines. Additionally, scFv-Fc C21 inhibited significantly melanoma cell migration and growth in vitro. Importantly, scFv-Fc C21 suppressed by 87% in vivo human melanoma cell-derived established lung metastasis. Lastly, scFv-Fc C21 prevented tumor recurrence and lung metastasis following the surgical removal of primary tumor in 100 and 83% of the mice tested, respectively. In contrast, 100% mice treated with the isotype control scFv-Fc had both local tumor recurrence and lung metastasis. The mechanism(s) of action mediated by scFv-Fc C21 is likely due to its blockade role in CSPG4 signaling transduction in melanoma cells as i) scFv-FcC21 in vitro treated melanoma cells MV3 cells had a decreased level of Protein kinase C alpha (PKCα) and FAK. Moreover, scFv-Fc C21 in vitro treatment inhibited the activation of FAK, Erk1/2, PDK1 and Akt and ii) scFv-Fc C21 in vivo treated primary tumors had a marked reduction in the level of PKCα, FAK, Src and β-catenin and in the activation of FAK, Erk1/2, PDK1 and Akt signaling pathways compared to those from mice treated with the control scFv-Fc 119. Our results strongly indicate that the fully human antibody scFv-Fc C21 holds promise in targeting CSPG4 to prevent post-surgery melanoma recurrence and metastasis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4408.
Follow-up pelvic MRI incidentally revealed that a 35-year old female patient had an urachal cyst on the bladder dome. A histerectomy for cervical cancer had previously been performed. The urachal cyst was 1.1cm in diameter and transurethral en bloc resection was successfully performed. Histopathologically, the cyst was surrounded by a smooth muscle layer with the wall consisting of columnar and glandular epithelial cells. Transurethral en bloc resection is a useful procedure to excise and confirm the pathogenesis for a limited case of a small urachal cyst that extrudes into the urinary bladder.
Clinical stage distribution has been changed between 1987 and 2006. Furthermore, overall and cause specific survival rates were better in screen detected prostate cancer than non-screen detected prostate cancer, because of increases in earlier stage of prostate cancer in SC group.
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