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Item Cell Origins of High-Grade Serous Ovarian Cancer(MDPI, 2018-11) Kim, Jaeyeon; Park, Eun Young; Kim, Olga; Schilder, Jeanne M.; Coffey, Donna M.; Cho, Chi-Heum; Bast, Robert C.; Biochemistry and Molecular Biology, School of MedicineHigh-grade serous ovarian cancer, also known as high-grade serous carcinoma (HGSC), is the most common and deadliest type of ovarian cancer. HGSC appears to arise from the ovary, fallopian tube, or peritoneum. As most HGSC cases present with widespread peritoneal metastases, it is often not clear where HGSC truly originates. Traditionally, the ovarian surface epithelium (OSE) was long believed to be the origin of HGSC. Since the late 1990s, the fallopian tube epithelium has emerged as a potential primary origin of HGSC. Particularly, serous tubal intraepithelial carcinoma (STIC), a noninvasive tumor lesion formed preferentially in the distal fallopian tube epithelium, was proposed as a precursor for HGSC. It was hypothesized that STIC lesions would progress, over time, to malignant and metastatic HGSC, arising from the fallopian tube or after implanting on the ovary or peritoneum. Many clinical studies and several mouse models support the fallopian tube STIC origin of HGSC. Current evidence indicates that STIC may serve as a precursor for HGSC in high-risk women carrying germline BRCA1 or 2 mutations. Yet not all STIC lesions appear to progress to clinical HGSCs, nor would all HGSCs arise from STIC lesions, even in high-risk women. Moreover, the clinical importance of STIC remains less clear in women in the general population, in which 85–90% of all HGSCs arise. Recently, increasing attention has been brought to the possibility that many potential precursor or premalignant lesions, though composed of microscopically—and genetically—cancerous cells, do not advance to malignant tumors or lethal malignancies. Hence, rigorous causal evidence would be crucial to establish that STIC is a bona fide premalignant lesion for metastatic HGSC. While not all STICs may transform into malignant tumors, these lesions are clearly associated with increased risk for HGSC. Identification of the molecular characteristics of STICs that predict their malignant potential and clinical behavior would bolster the clinical importance of STIC. Also, as STIC lesions alone cannot account for all HGSCs, other potential cellular origins of HGSC need to be investigated. The fallopian tube stroma in mice, for instance, has been shown to be capable of giving rise to metastatic HGSC, which faithfully recapitulates the clinical behavior and molecular aspect of human HGSC. Elucidating the precise cell(s) of origin of HGSC will be critical for improving the early detection and prevention of ovarian cancer, ultimately reducing ovarian cancer mortality.Item A rare case of invasive mucinous adenocarcinoma of fallopian tube fimbria with metastasis to ipsilateral ovary, uterine serosa, myometrium and pelvis: Case report and review of literature(Elsevier, 2015-06) Liang, Sharon X.; Brandler, Tamar C.; Contreras, Diana; Roy, Rajasree; Cheng, Liang; Fadare, Oluwole; Department of Pathology and Laboratory Medicine, IU School of MedicineMucinous adenocarcinoma of the fallopian tube is exceptionally rare and the detailed clinicopathologic features of these tumors have not yet been reported in English literature. Here we report a moderately differentiated mucinous adenocarcinoma arising in the tubal fimbria in a 70-year-old woman. Patient had a history of cholecystectomy for gallstones and gastric banding who presented with gastrointestinal discomfort and was found to have a large adnexal mass on imaging studies. Serum CA-125 was moderately elevated. Recent mammography, upper endoscopy and colonoscopy were completely normal. She underwent surgical staging for the adnexal mass. Frozen section and final pathology diagnosis revealed moderately differentiated adenocarcinoma arising in the left fimbria. Carcinoma had spread to the ipsilateral ovary and pelvic soft tissue at the time of her presentation. Tumor was strongly immunoreactive to CK7 and CEA, and was negative for CK20, CDX-2, PAX-8, WT-1, p16, ER, and vimentin. TP53 showed wild-type phenotype by immunohistochemistry. Molecular studies showed no mutation in codon 12 and 13 of the k-ras gene, and no mutation was detected in the BRAF and EGFR genes. In addition, the non-tumorous fimbria epithelium showed a spectrum of mucinous alterations with variable nuclear atypia: cytologically bland areas that were reminiscent of mucinous metaplasia were positive for p53 and showed minimal proliferation as assessed by Ki-67, and cytologically atypical stratified mucinous epithelium that was positive for p53 and Ki-67. The patient received 3 cycles of Folfox and was regularly followed at a 3–6 month interval. Her carcinoma recurred in abdomen at 32 months post surgery. After excluding the possibility of an extra-gynecologic tract primary through extensive clinical investigations and post-surgical follow-up, we concluded that this tumor most likely represented a mucinous adenocarcinoma of tubal origin.