Relevant bibliographies by topics / High-grade serous ovarian carcinoma

Academic literature on the topic 'High-grade serous ovarian carcinoma'

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Published: 6 September 2023

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Journal articles on the topic "High-grade serous ovarian carcinoma"

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Casey, Laura, and Naveena Singh. "Ovarian High-Grade Serous Carcinoma." Surgical Pathology Clinics 12, no. 2 (June 2019): 515–28. http://dx.doi.org/10.1016/j.path.2019.01.007.

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Pannu, Harpreet K., Weining Ma, Emily Craig Zabor, Chaya S. Moskowitz, Richard R. Barakat, and Hedvig Hricak. "Enhancement of Ovarian Malignancy on Clinical Contrast Enhanced MRI Studies." ISRN Obstetrics and Gynecology 2013 (February 13, 2013): 1–8. http://dx.doi.org/10.1155/2013/979345.

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Purpose. To assess if there is a significant difference in enhancement of high grade serous carcinoma of the ovary compared with other ovarian malignancies on clinically performed contrast enhanced MRI studies. Methods. In this institutional-review–board-approved study, two radiologists reviewed contrast enhanced MRI scans in 37 patients with ovarian cancer. Readers measured the signal intensity (SI) of ovarian mass and gluteal fat pre- and postcontrast administration. Percentage enhancement (PE) was calculated as [(post-pre)/precontrast SI] × 100. Results. Pathology revealed 19 patients with unilateral and 18 patients with bilateral malignancies for a total of 55 malignant ovaries-high grade serous carcinoma in 25/55 ovaries (45%), other epithelial carcinomas in 12 ovaries (22%), nonepithelial cancers in 8 ovaries (14%), and borderline tumors in 10 ovaries (18%). Enhancement of high grade serous carcinoma was not significantly different from other invasive ovarian malignancies (Reader 1 ; Reader 2 ). Enhancement of invasive ovarian malignancies was more than borderline tumors but did not reach statistical significance (Reader 1; Reader 2 ). Conclusion. On clinically performed contrast enhanced MRI studies, enhancement of high grade serous ovarian carcinoma is not significantly different from other ovarian malignancies.
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Kshirsagar, Malti, Wei Jiang, and Ie-Ming Shih. "DNA Damage Response is Prominent in Ovarian High-Grade Serous Carcinomas, Especially Those with Rsf-1 (HBXAP) Overexpression." Journal of Oncology 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/621685.

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DNA damage commonly occurs in cancer cells as a result of endogenous and tumor microenvironmental stress. In this study, we applied immunohistochemistry to study the expression of phosphorylated Chk2 (pChk2), a surrogate marker of the DNA damage response, in high grade and low grade of ovarian serous carcinoma. A phospho-specific antibody specific for threonine 68 of Chk2 was used for immunohistochemistry on a total of 292 ovarian carcinoma tissues including 250 high-grade and 42 low-grade serous carcinomas. Immunostaining intensity was correlated with clinicopathological features. We found that there was a significant correlation between pChk2 immunostaining intensity and percentage of pChk2 positive cells in tumors and demonstrated that high-grade serous carcinomas expressed an elevated level of pChk2 as compared to low-grade serous carcinomas. Normal ovarian, fallopian tube, ovarian cyst, and serous borderline tumors did not show detectable pChk2 immunoreactivity. There was no significant difference in pChk2 immunoreactivity between primary and recurrent high-grade serous carcinomas. In high-grade serous carcinomas, a significant correlation (P<0.0001) in expression level (both in intensity and percentage) was found between pChk2 and Rsf-1 (HBXAP), a gene involved in chromatin remodeling that is amplified in high-grade serous carcinoma. Our results suggest that the DNA damage response is common in high-grade ovarian serous carcinomas, especially those with Rsf-1 overexpression, suggesting that Rsf-1 may be associated with DNA damage response in high-grade serous carcinomas.
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Vang, Russell, Ie-Ming Shih, and Robert J. Kurman. "Ovarian Low-grade and High-grade Serous Carcinoma." Advances in Anatomic Pathology 16, no. 5 (September 2009): 267–82. http://dx.doi.org/10.1097/pap.0b013e3181b4fffa.

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Moss, Esther Louise, Tim Evans, Philippa Pearmain, Sarah Askew, Kavita Singh, Kiong K. Chan, Raji Ganesan, and Lynn Hirschowitz. "Should All Cases of High-Grade Serous Ovarian, Tubal, and Primary Peritoneal Carcinomas Be Reclassified as Tubo-Ovarian Serous Carcinoma?" International Journal of Gynecologic Cancer 25, no. 7 (September 2015): 1201–7. http://dx.doi.org/10.1097/igc.0000000000000477.

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IntroductionThe dualistic theory of ovarian carcinogenesis proposes that epithelial “ovarian” cancer is not one entity with several histological subtypes but a collection of different diseases arising from cells of different origin, some of which may not originate in the ovarian surface epithelium.MethodsAll cases referred to the Pan-Birmingham Gynaecological Cancer Centre with an ovarian, tubal, or primary peritoneal cancer between April 2006 and April 2012 were identified from the West Midlands Cancer Registry. Tumors were classified into type I (low-grade endometrioid, clear cell, mucinous, and low-grade serous) and type II (high-grade serous, high-grade endometrioid, carcinosarcoma, and undifferentiated) cancers.ResultsOvarian (83.5%), tubal (4.3%), or primary peritoneal carcinoma (12.2%) were diagnosed in a total of 583 woman. The ovarian tumors were type I in 134 cases (27.5%), type II in 325 cases (66.7%), and contained elements of both type I and type II tumors in 28 cases (5.7%). Most tubal and primary peritoneal cases, however, were type II tumors: 24 (96.0%) and 64 (90.1%), respectively. Only 16 (5.8%) of the ovarian high-grade serous carcinomas were stage I at diagnosis, whereas 240 (86.6%) were stage III+. Overall survival varied between the subtypes when matched for stage. Stage III low-grade serous and high-grade serous carcinomas had a significantly better survival compared to clear cell and mucinous cases,P= 0.0134. There was no significant difference in overall survival between the high-grade serous ovarian, tubal, or peritoneal carcinomas when matched for stage (stage III,P= 0.3758; stage IV,P= 0.4820).ConclusionsType II tumors are more common than type I and account for most tubal and peritoneal cancers. High-grade serous carcinomas, whether classified as ovarian/tubal/peritoneal, seem to behave as one disease entity with no significant difference in survival outcomes, therefore supporting the proposition of a separate classification of “tubo-ovarian serous carcinoma”.
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Voutsadakis, Ioannis A. "Low-grade serous ovarian carcinoma: an evolution toward targeted therapy." International Journal of Gynecologic Cancer 30, no. 10 (November 27, 2019): 1619–26. http://dx.doi.org/10.1136/ijgc-2019-000832.

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Low-grade serous ovarian carcinoma and its high-grade serous ovarian carcinoma counterpart differ in their precursor lesions, molecular profile, natural history, and response to therapies. As such, low-grade serous ovarian carcinoma needs to be studied separately from high-grade serous ovarian carcinoma, despite challenges stemming from its rarity. A deeper understanding of the pathogenesis of low-grade serous ovarian carcinoma and the most common molecular defects and pathways involved in the carcinogenesis of the ovarian epithelium from normal to serous borderline ovarian tumors to low-grade serous ovarian carcinoma will help develop better therapies. By adopting targeted approaches there may be an opportunity to integrate novel therapies without the need for robust numbers in clinical trials. This manuscript will discuss low-grade serous ovarian carcinoma and focus on the arising treatments being developed with an improved understanding of the pathogenesis of this disease.
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Kenda Šuster, Nataša, Snježana Frković Grazio, Irma Virant-Klun, Ivan Verdenik, and Špela Smrkolj. "Cancer Stem Cell–Related Marker NANOG Expression in Ovarian Serous Tumors: A Clinicopathological Study of 159 Cases." International Journal of Gynecologic Cancer 27, no. 9 (November 2017): 2006–13. http://dx.doi.org/10.1097/igc.0000000000001105.

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ObjectiveThe objectives of this study were to assess cancer stem cell–related marker NANOG expression in ovarian serous tumors and to evaluate its prognostic significance in relation to ovarian serous carcinoma.MethodsNANOG protein expression was immunohistochemically evaluated in the ovarian tissue microarrays of 20 patients with benign ovarian serous tumors, 30 patients with borderline ovarian serous tumors, and 109 patients with ovarian serous carcinomas, from which 106 were of high-grade and 3 of low-grade morphology Immunohistochemical reaction was scored according to signal intensity and the percentage of positive cells in tumor samples. Pursuant to our summation of signal intensity and positive cell occurrence, we divided our samples into 4 groups: NANOG-negative, NANOG–slightly positive, NANOG–moderately positive, and NANOG–strongly positive group. Complete clinical data were obtained for the ovarian serous carcinoma group, and correlation between clinical data and NANOG expression was analyzed.ResultsA specific brown nuclear, or cytoplasmic reaction, was considered a positive NANOG staining. In terms of the ovarian serous carcinoma group, 69.7% were NANOG positive, 22.9% slightly positive, 22.9% moderately positive, and 23.9% strongly positive. All NANOG-positive cases were of high-grade morphology. Benign and borderline tumors and low-grade serous carcinomas were NANOG negative. There was no significant correlation between NANOG expression and clinical parameters in terms of the ovarian serous carcinoma group.ConclusionsPositive NANOG expression is significantly associated with high-grade ovarian serous carcinoma and is absent in benign, borderline, and low-grade serous lesions. In our study, there was no correlation between NANOG expression and clinical parameters, including its use in the prognosis of ovarian serous carcinoma.
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Ricciardi, Enzo, Thaïs Baert, Beyhan Ataseven, Florian Heitz, Sonia Prader, Mareike Bommert, Stephanie Schneider, Andreas du Bois, and Philipp Harter. "Low-grade Serous Ovarian Carcinoma." Geburtshilfe und Frauenheilkunde 78, no. 10 (October 2018): 972–76. http://dx.doi.org/10.1055/a-0717-5411.

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AbstractIn the early 2000s a two-tier grading system was introduced for serous ovarian cancer. Since then, we have increasingly come to accept that low-grade serous ovarian carcinoma (LGSOC) is a separate entity with a unique mutational landscape and clinical behaviour. As less than 10% of serous carcinomas of the ovary are low-grade, they are present in only a small number of patients in clinical trials for ovarian cancer. Therefore the current treatment of LGSOC is based on smaller trials, retrospective series, and subgroup analysis of large clinical trials on ovarian cancer. Surgery plays a major role in the treatment of patients with LGSOC. In the systemic treatment of LGSOC, hormonal treatment and targeted therapies seem to play an important role.
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De Leo, Antonio, Donatella Santini, Claudio Ceccarelli, Giacomo Santandrea, Andrea Palicelli, Giorgia Acquaviva, Federico Chiarucci, et al. "What Is New on Ovarian Carcinoma: Integrated Morphologic and Molecular Analysis Following the New 2020 World Health Organization Classification of Female Genital Tumors." Diagnostics 11, no. 4 (April 14, 2021): 697. http://dx.doi.org/10.3390/diagnostics11040697.

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Ovarian carcinomas represent a heterogeneous group of neoplasms consisting of separate entities with distinct risk factors, precursor lesions, pathogenesis, patterns of spread, molecular profiles, clinical course, response to chemotherapy, and outcomes. The histologic subtype and the related molecular features are essential for individualized clinical decision-making. The fifth edition of the World Health Organization classification of tumors of the female genital tract divides ovarian carcinomas into at least five main and distinct types of ovarian carcinomas: high-grade serous carcinoma, low-grade serous carcinoma, endometrioid carcinoma, clear cell carcinoma, and mucinous carcinoma. Molecular pathology has improved the knowledge of genomic landscape of ovarian carcinomas identifying peculiar alterations for every histologic subtype. It is well-known that high-grade and low-grade serous carcinomas are separate entities with entirely different morphologic and molecular characteristics. TP53 and BRCA mutations are typical of high-grade serous carcinoma, whereas BRAF and KRAS mutations frequently occur in low-grade serous carcinoma. Endometrioid and clear cell carcinomas are frequently associated with endometriosis. Endometrioid tumors are characterized by β-catenin alterations, microsatellite instability, and PTEN and POLE mutations, while ARID1A mutations occur in both endometrioid and clear cell carcinomas. Mucinous carcinomas are uncommon tumors associated with copy-number loss of CDKN2A and KRAS alterations and metastasis from other sites should always be considered in the differential diagnosis.
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Wu, Jingjing, and Jian-Jun Wei. "HMGA2 and high-grade serous ovarian carcinoma." Journal of Molecular Medicine 91, no. 10 (May 19, 2013): 1155–65. http://dx.doi.org/10.1007/s00109-013-1055-8.

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Dissertations / Theses on the topic "High-grade serous ovarian carcinoma"

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Everitt, Gemma Louise Ann. "The inflammatory infiltrate of high-grade serous carcinoma omental metastasis." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8038.

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The aim of this thesis is to investigate the role of inflammatory infiltrates and chemokines in metastasis of high-grade serous ovarian cancer, HGSC, to the omentum using human tissue biopsies and a 3- dimensional (3D) cell culture model. In ten patients with metastatic HGSC, omental tumour deposits contained a prominent leukocyte infiltrate of CD3+ T cells (9% of total cells) and CD68+ macrophages (11% of total cells). The presence of CD68+ macrophages showed a significant positive correlation with tumour cell proliferation analysed by Ki67 expression. Four ovarian cancer cell lines were co-cultured on a 3D model mimicking the microenvironment of the omentum for two weeks. The model was composed of collagen embedded human fibroblasts covered in a confluent layer of human primary mesothelial cells. The mesothelial cells in the 3D model significantly increased the growth (p = 0.002) and invasion (p = 0.0004) of the ovarian cancer cells. CXCL12 is the macrophage chemoattractant and ligand for the major chemokine receptor expressed on ovarian cancer cells. An association between CXCL12 and extracellular matrix remodelling was identified in two independent gene expression microarrays of ovarian cancer biopsies. The expression of CXCL12 in the HGSC omental metastases measured by quantitative Real Time-PCR positively correlated with decorin expression. Antibody mediated neutralisation of CXCL12 reduced growth (p = 0.012) and invasion (p = 0.029) in the 3D model. Mimicking an infiltrate of CD68+ macrophages in this multicellular 3D in vitro system also produced measurable changes in inflammatory cytokine and chemokine expression. There is currently a demand for more accurate models of HGSC and a necessity to study its metastasis that presents itself as the major clinical problem in patients. Therefore the development of this 3D model to mimic tumour-promoting inflammation in HGSC metastasis will provide researchers with an essential tool for testing novel therapeutic strategies.
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Sheets, Jordan N. "Inhibitory Functions of SUSD2 in the Progression of High-Grade Serous Ovarian Carcinoma." Thesis, University of South Dakota, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10633628.

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Sushi Domain Containing 2 (SUSD2) encodes a type I transmembrane protein containing several functional domains inherent to adhesion molecules. A clinically annotated HGSOC tissue microarray was stained with an anti-SUSD2 antibody. Patients with tumors that had weak SUSD2 staining had a shorter median survival (31.7 months) compared to patients that had tumors with strong SUSD2 staining (49.1 months; p value = 0.0083).

To investigate the role of SUSD2 in HGSOC, stable OVCAR3, OVSAHO and KURAMOCHI cell lines were established through transfection of shRNA targeted to SUSD2 transcripts (SUSD2 knock-down [KD] cell lines) or non-targeting shRNA (SUSD2 NT) cell lines. Boyden chamber and wound healing assays demonstrated that OVCAR3, OVSAHO and KURAMOCHI SUSD2 KD cells migrated at significantly higher rates than their SUSD2 NT counterpart cell lines. RT-qPCR and western immunoblot analysis indicated an inverse relationship between SUSD2 and well characterized mesenchymal genes, such as TWIST1, ZEB1 and CHD2. In addition, OVCAR3 and KURAMOCHI SUSD2 KD spheroids displayed increased mesothelial clearance ability compared to SUSD2 NT spheroids.

To explore the potential for SUSD2 to inhibit late-stage HGSOC metastasis, female athymic nude mice were injected with either OVCAR3 NT or OVCAR3 KD cells. Fewer nodules were observed in the pancreas and omentum of the OVCAR3 NT mice when compared to the OVCAR3 KD mice. Furthermore, OVCAR3 KD mice had a significantly shorter median survival compared to OVCAR3 NT mice (175 days compared to 185.5 days, respectively; p-value = 0.0047).

KURAMOCHI lysate was immunoprecipitated for SUSD2-associated immunocomplexes and subjected to liquid chromatography, tandem mass spectrometry (LC-MS/MS) analysis, yielding a list of candidate SUSD2-interacting proteins associated with RNA processing. Immunofluorescence analysis of OVCAR3, KURAMOCHI and SKBR3 cells and western immunoblot analysis of their subcellular extracts revealed SUSD2 to be present in cell nuclei, mitochondria and cytoplasm; however, SUSD2 was relatively less abundant in SKBR3 nuclei.

Our findings suggest that increased SUSD2 expression in HGSOC impedes metastasis, consistent with prolonged survival observed in HGSOC patients with high SUSD2-expressing primary tumors. The differences in subcellular distribution between HGSOC cells and breast cancer cells may explain alternate functions of SUSD2 in different cancers.

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Cole, Alexander John. "The role of p53 and histone H2B monoubiquitination in high-grade serous ovarian carcinoma." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17639.

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Ovarian cancer is the eleventh most frequently diagnosed cancer in women and the fifth most common cause of cancer-related deaths. Epithelial ovarian cancer accounts for ~90% of cases. Serous epithelial ovarian cancer (SEOC) is the most common and aggressive histological subtype. Clinically, SEOC can be divided into type I and II tumours. Type II tumours (high grade serous ovarian carcinoma (HGSOC)), are generally diagnosed at later stages, grow aggressively and possess a mutation in the TP53 gene, which codes for the tumour suppressor protein p53. Mortality rates of HGSOC have remained largely unchanged for decades due to a lack of sensitive biomarkers and poor response to primary treatment. Finding new strategies to treat patients and identify early disease is critical to improving patient outcomes. Post-translational histone modifications describe the chemical and protein alteration of histone tail residues which are capable of altering gene expression. Monoubiquitination of lysine 120 on histone H2B (H2Bub1) disrupts chromatin strands and has important physiological functions including transcription, DNA repair, differentiation and crosstalk. Recent research has demonstrated that H2Bub1 is lost in cancer suggesting it may play an important role in malignancy. Interestingly, several studies have reported a link between the tumour suppressor p53 and H2Bub1, including a direct interaction of p53 with the H2Bub1 E3 ligase RNF20, and H2Bub1 enrichment at the p53 target gene CDKN1A. Consequently, this link may prove important in HGSOC where TP53 mutations occur almost ubiquitously and result in the loss of wildtype p53 function. 2 At the commencement of this work no study had comprehensively investigated the relationship between TP53 mutation status and p53 immunohistochemistry (IHC) using massively parallel sequencing (MPS) in HGSOC. The aim of this work was to determine the accuracy of p53 IHC to determine TP53 mutation status. We used MPS and IHC to characterise HGSOCs for TP53 mutation and p53 expression. Mutations in TP53 were identified in 94% (68/72) of HGSOCs, 62% of which were missense. Missense mutations demonstrated high p53 staining by IHC, as did 35% (9/26) of non-missense mutations. Low p53 staining was seen by IHC in 62% of HGSOC associated with non-missense mutations. Most wildtype TP53 tumours (75%, 6/8) displayed intermediate p53 expression levels. The overall sensitivity of detecting a TP53 mutation based on classification as ‘Low’, ‘Intermediate’ or ‘High’ for p53 IHC was 99%, with a specificity of 75%. We suggest p53 IHC can be used as a surrogate marker of TP53 mutation in HGSOC; however, this will result in misclassification of a small proportion of TP53 wildtype and mutant tumours. H2B monoubiquitination can be catalysed by five E3 ligases, and removed by up to eleven deubiquitinases. Loss of H2Bub1 has been reported in a range of malignancies, where it associates with higher tumour stage/grade, metastasis and poor patient survival. The aim of this section of work was to investigate H2Bub1 levels in HGSOC and correlate them with p53 mutation status/IHC, the deubiquitinase USP7 and the polycomb repressive complex subunit enhancer of zeste homolog 2 (EZH2), which is capable of negatively regulating H2Bub1 levels by competing for the same substrate. H2Bub1 was lost in 68% of HGSOC samples, but did not correlate with overall patient survival. P53 intermediate IHC and wildtype TP53 status correlated with higher H2Bub1 IHC staining, while USP7 expression was inversely correlated with H2Bub1 IHC. EZH2 expression did not correlate with H2Bub1 IHC or with patient overall survival. In vitro experiments using wildtype and mutant p53 3 constructs transfected into p53 functionally null (herein referred to as null) cell lines appeared to contradict the p53 and H2Bub1 IHC data, warranting further investigation. Along with other studies, our data suggested a link between p53 and H2Bub1. Consequently, this work aimed to investigate the effects of p53 on H2Bubl levels. We treated p53 wildtype cell lines with cisplatin, which activated p53 and resulted in global loss of H2Bub1 levels. In contrast, treatment of p53 null cell lines did not significantly alter H2Bub1 levels. Transfection of wildtype p53 into the same null cell lines resulted in a significant decrease in H2Bub1 levels compared to the vector only control. Downregulation of the main H2Bub1 E3 ligase, RNF20, and treatment with cisplatin showed a decrease of p53 levels in RNF20 sRNA treated cells compared to control siRNA. Chromatin immunoprecipitation coupled with next generation sequencing (ChIP-seq) of a p53 wildtype cell line treated with cisplatin, demonstrated H2Bub1 enrichment at p53 target genes. RNA-seq demonstrated an increased expression of these H2Bub1 enriched p53 target genes. Downregulation of RNF20 using siRNA, sensitised MCF7 and A2780 cells to cisplatin treatment. Together, this work suggested a functional link between H2Bub1 and p53. Chemoresistance is a hallmark of HGSOC and has been linked to the presence of cancer stem cells (CSCs). Ovarian CSCs make up a small subpopulation of cells within the primary tumour mass and express the markers CD133 and ALDH. Recent reports have suggested H2Bub1 plays an important role in stem cell differentiation and maintenance. The aim of this section was to investigate the role of H2Bub1 in ovarian CSCs. H2Bub1 was shown to be depleted in CD133+ cells and spheroids enriched for ALDH, consistent with a more stem-like phenotype. Decreasing H2Bub1 levels through RNF20 downregulation resulted in a profound effect on the CSC populations, where ALDH+ populations increased and the CD133+ 4 populations decreased. Spheroid culture of the RNF20 downregulated cells resulted in larger and more numerous spheroids than the shRNA control suggesting RNF20 and hence H2Bub1, can influence spheroid formation. Together, this data suggests H2Bub1 may play an important role in CSC differentiation.
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Cheng, Jung-Chien. "Role of E-cadherin in the serous borderline ovarian tumor and low-grade serous ovarian carcinoma cell invasion." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43651.

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E-cadherin is a membrane glycoprotein located at cell adherens junctions. A switch from E-cadherin to N-cadherin expression has been considered a hallmark of the epithelial-mesenchymal transition (EMT), which is primarily due to the up-regulation of the transcription factors Snail, Slug, Twist and ZEB1. Epithelial ovarian cancer cells with low E-cadherin expression are more invasive, and the absence of E-cadherin expression in ovarian cancer is associated with poor prognosis and survival. Serous borderline ovarian tumors (SBOT) are slow-growing, non-invasive ovarian epithelial neoplasms. SBOT are considered distinct entities that give rise to invasive low-grade serous carcinomas (LGSC), which have a relatively poor prognosis and are unrelated to high-grade serous carcinomas (HGSC). The mechanisms underlying the progression of non-invasive SBOT to invasive LGSC are not understood. We have established short-term cultures of SBOT cells from tumor biopsies and have shown that inactivation of p53, Rb and/or PP2A by the SV40 large T (LT) and small T (ST) antigens allows SBOT cells to acquire characteristics associated with neoplastic progression, including increased cell motility, invasion and EMT. However, the overexpression of N-cadherin does not induce cell invasion in SBOT cells. In this study, using loss- and gain-of-function approaches, we show that p53 acts as a tumor suppressor in the regulation of SBOT and LGSC cell invasion by regulating E-cadherin expression through PI3K/Akt-mediated transcriptional and epigenetic machineries. In high-grade ovarian cancer cultures, it has been shown that epidermal growth factor (EGF) and transforming growth factor-beta (TGF-β) induce cell invasion by activating the EMT. However, the effects of EGF and TGF-β on SBOT and LGSC cell invasion remain unknown. We show that EGF induces SBOT cell invasion by activating the EMT. In addition, our results suggest that there are EMT-independent mechanisms that mediate EGF-induced LGSC cell invasion. Interestingly, we show a dual function for TGF-β in which it induces invasion in SBOT cells by activating the EMT and promotes apoptosis in LGSC cells. Overall, this study demonstrates that the loss of E-cadherin expression in SBOT may play an important role in the transition to invasive LGSC.
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Virtanen, Siru Sirkku Pauliina. "Phenotypic and functional characterisation of cancer stem cells in human high-grade serous ovarian carcinoma." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648879.

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Murakami, Ryusuke. "Establishment of a novel histopathological classification of high-grade serous ovarian carcinoma correlated with prognostically distinct gene expression subtypes." Kyoto University, 2016. http://hdl.handle.net/2433/215449.

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Dawson, Amy. "Targeted therapy in low-grade serous ovarian carcinoma : characterization of MEK inhibitor response in novel patient-derived cell lines." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59456.

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Low-grade serous ovarian carcinoma, or LGSOC, predominantly occurs in pre- menopausal women at lower frequency than the more common high-grade serous ovarian carcinoma. It tends to harbour few, but distinct, mutations, with a significant proportion of RAS oncogene mutations. Aberrations of the RAS-MAPK signaling pathway in LGSOC have led to the initiation of several clinical trials of MEK inhibitors in this disease. Due to the relative rarity of LGSOC, few representative model systems are available. Accordingly, there has been a lack of preclinical investigational drug testing in this disease. In this study, 11 histotype-specific cell lines have been derived and molecularly characterized in order to further elucidate the molecular biology of the disease, and serve as an important platform to test novel therapeutics in LGSOC. The most common missense mutations by HotSpot mutational profiling analysis were oncogenic KRAS/NRAS mutations, and varying levels of copy number aberration were seen. All cell lines were uniquely identifiable by short-tandem repeat analysis, with the exception of two patient-paired cell lines. The phenotypic and molecular responses to the 4 MEK inhibitors (MEKi) trametinib, selumetinib, refametinib, and binimetinib have been characterized in selected LGSOC cell lines through IC50 analysis, proliferation, viability, and apoptosis assays, and on-target drug effects by Western blot. Of the 4 MEKi, trametinib exhibited the best anti-proliferative effects and inhibition of MEK kinase activity. Biological and on-target data from two of the cell lines reveals an exquisite sensitivity to MEK inhibition. Reverse-phase protein array and quantitative mass spectrometry global proteomic analysis on control and MEKi-treated LGSOC cell lines was performed in order to examine basal proteomic differences between MEKi-sensitive and resistant LGSOC cell lines and gather data for examining proteomic changes upon MEKi treatment. Three significantly differentially expressed protein candidates (PKCα, EGFR, and Smac/DIABLO were identified between sensitive and resistant cell lines under control and MEKi treatment conditions by both proteomic platforms. Results from therapeutic testing in these pathologically reviewed, histotype- specific LGSOC models allow for a comparison of the overall efficacies of the 4 MEKi, characterization of drug sensitivity in novel cell lines, and identification of potential functional markers of MEKi response.
Medicine, Faculty of
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Howe, Eleanor Arden. "MicroRNA expression and activity in high-grade serous ovarian cancer." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:9d17590c-550b-4ae9-ac8d-15387cf70e5f.

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miRNAs are critical modulators in the development and progression of cancer. Emerging evidence suggests that they are drivers of ovarian cancer. A better understanding of the molecular underpinnings of the development, progression and chemoresistance of the disease is critical for the development of new, more effective therapies. Here we explore the expression patterns of miRNAs as they relate to gene expression, as they differ across molecular subtypes of the disease. We examine the correlation structure of miRNA expression with mRNA expression in two distinct genomic datasets and report on patterns in correlation structure in several subsets of the data. We find that the datasets show consistency in their correlation structure, and in the specific miRNA-mRNA pairs that are either highly positively or negatively correlated. The data include a larger number of strong positive and strong negative correlations than would be expected by chance, indicating that biological relationships between the types of data are detectable in these datasets. We further find an enrichment for positively-correlated miRNA-mRNA pairs in which the miRNA is encoded in close proximity to the mRNA. The correlation of miRNA and mRNA is apparently unaffected by miRNA and mRNA expression level; similarly the two molecular subtypes do not contain differences in their correlation. We find that the recently described poorer prognosis, or angiogenic, subtype has a generally lower miRNA activity than the second, non-angiogenic, subtype. The subtypes are characterized by a consistent pattern of differential miRNA expression. We also report on a switch-like relationship between the expression levels of certain miRNAs and the genes that are anticorrelated with them. We propose these miRNAs drive many of the differences in the subtypes both directly, by RISC-mediated repression of target messages and indirectly, by repressing transcription factors that regulate expression in the cell. We build models of patient survival and time-to-relapse based on these miRNA expression data and inferred miRNA activity scores, using several types of univariate and variable selection models. We find essentially no survival-predictive information provided by the RE score data. While the direct miRNA expression measurements may contain some predictive power, we find that a larger dataset and the segretation of that dataset into distinct molecular phenotypes is likely to be necessary to produce a useful model of survival in ovarian cancer.
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Todeschini, P. "NON-CODING RNAS IN HIGH-GRADE SEROUS EPITHELIAL OVARIAN CANCER." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/488108.

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Abstract Introduction: High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecologic malignancy, mainly because the disease is frequently diagnosed at an advanced stage and is characterized by the early onset of chemoresistant recurrences. The lack of reliable diagnostic and prognostic markers, together with the lack of effective therapies, are the major obstacles to the clinical management of patients with HGSOC. A new class of non-coding RNAs (ncRNAs), such as microRNA (miRNAs) and long non-coding RNAs (LncRNAs), with a function of gene expression regulation, have been discovered to play an important role in human cancers. Increasing evidences suggest that ncRNAs are involved in cancer progression and development of chemoresistance, and support their role as potential diagnostic, predictive and prognostic biomarkers. The hypoxic condition within the tumor microenvironment, improving the tumor neovascularization, represents an essential event contributing to the development of a more aggressive HGSOC phenotype. Recently, a group of miRNAs, termed hypoxia regulated-miRNAs (HRMs), have been identified as key elements in response to hypoxia, regulating important mechanisms involved in tumor progression. The complexity of hypoxia molecular mechanisms has not been fully elucidated yet in HGSOC, therefore there is an urgent need to discover novel biomarkers clinically useful to select patients with hypoxic tumor, that may benefit of tailored treatments. Aims of the study: My PhD project aims at elucidating transcriptional and post-transcriptional signatures characterizing HGSOC, both at the serum and tissue levels. In detail, the research effort includes: i) the investigation of circulating miRNAs as novel potential biomarkers for HGSOC detection; ii) the analysis of mRNA, miRNA and lncRNA expression profiles of HGSOC and normal tissues; iii) the evaluation of hypoxia-regulated miRNA expression in HGSOC and normal tissues. Methods: Sera from 168 HGSOC stage III-IV patients and 65 healthy donors were gathered together from two independent collections and stratified into a training set, for miRNA marker identification, and a validation set, for data validation. Nine synthetic viral/C.Elegans spike-in oligos were added to serum samples before RNA extraction, to allow accurate normalization. miRNA expression profiles were obtained using Agilent Microarray Technologies®. An innovative statistical approach for microarray data normalization, based on the contribute of spike-in oligos and the most invariant miRNAs, was developed to identify, in the training set, differentially expressed miRNAs. Signature validation in both the training and validation sets was performed by Real Time quantitative PCR (RT-qPCR) and confirmed by droplet digital PCR (ddPCR). A total of 99 tumor biopsies were collected from HGSOC stage III-IV patients, partially matched with the serum sample cohort (n=76). Thirty normal tissues were obtained from normal ovary (HOSE) and luminal fallopian tube surface epithelia, both representing the normal counterpart for HGSOC, whose histogenesis is still a matter of debate. Gene and miRNA expression profiles were obtained using Agilent Microarray Technologies®. miRNA expression levels were correlated with patient outcomes, as overall survival (OS) and progression-free survival (PFS). Additionally, a subgroup of 14 chemo-resistant and 14 chemo-sensitive HGSOC patients, together with 10 normal tissues were deep sequenced for the discovery of novel HGSOC specific coding and non-coding transcripts. Results: A panel of 97 miRNAs emerged significantly differentially expressed (92 up-regulated and five down-regulated) between sera of HGSOC patients and healthy donors by microarray analysis. Among them, the following miRNAs, i.e., miR-1246, miR-595, miR-574-5p, miR-483-3p, miR-4290, miR-2278, miR-32, miR-4281, and miR-3148, exhibiting both the highest average expression and log fold change measured in patients compared to healthy donors, were selected for further validation. miR-1246, miR-595 and miR-2278 were confirmed as significantly over-expressed in serum of HGSOC patients compared to controls by RT-qPCR (all p-values<0.03), in both the training and validation sets. Receiver Operating Characteristic (ROC) curve analysis revealed miR-1246 as the best diagnostic biomarker, with a sensitivity of 87%, a specificity of 77% and an accuracy of 84%. The absolute quantification of circulating miR-1246 by ddPCR confirmed its potential as diagnostic biomarker in HGSOC. Microarray analysis of tissue miRNA profiling revealed a total of 265 miRNAs significantly dysregulated (123 up-regulated and 142 down-regulated) in HGSOC compared to normal tissues. A group of nine miRNAs (i.e., miR-199b-5p, miR-423-5p miR-455-3p, miR-22-3p, miR-199a-3p, miR-15b-5p, miR-140-5p, miR-1246, and miR-320c) were associated with platinum response and prognosis. In particular, among tumor samples, miR-1246 up-regulation was consistently associated with platinum-resistance, poor OS and poor PFS (p-values<0.05). Kaplan-Meier survival curves, according to miR-1246 expression levels obtained by RT-qPCR, showed that OS and PFS decreased in patients with high miR-1246 expression compared to those with low miR-1246 expression (p-value<0.001, HR=2.57; p-value=0.024, HR=1.68; respectively). In addition, multivariate analysis revealed miR-1246 over-expression as an independent prognostic factor for poor OS and PFS (p-value=0.002, HR=2.31; p-value<0.05, HR=1.59; respectively). Interestingly, compared to normal tissues, both with microarray and RT-qPCR techniques, miR-1246 showed a down-regulation compared to HOSEs (p-value<0.0001), but we did not detect a significantly differential expression compared to fallopian tubes. This result mirrors the global miRNA expression trend revealed by principal component analysis (PCA) on microarray data. Subsequently, we focused our analysis on a group of 16 miRNAs belonging to the group of hypoxia-regulated miRNAs (HRMs) emerged from literature as relevant in other solid tumors. Among them, we confirmed miR-210 and miR-27a-3p/23a-3p/24-3p cluster as significantly up-regulated in HGSOC vs normal tissues by RT-qPCR (all p-values≤0.002). More interestingly, we validated the significant over-expression of miR-23a-3p in the group of patients resistant to platinum-based chemotherapy compared to platinum-sensitive patients (p-value=0.03). In addition, in univariate survival analysis miR-23a-3p over-expression showed a significant correlation with decreased progression-free survival (p-value=0.009, HR=1.8), but not with overall survival variable. Importantly, miR-23a-3p over-expression has emerged as an independent prognostic marker for shortened progression-free survival in multivariate Cox regression analysis (p-value=0.01, HR=1.78). Finally, the preliminary analysis of the transcriptome sequencing allowed us to identify 1371 transcripts differentially expressed between platinum-resistant and platinum-sensitive samples. Among them, 125 transcripts showed a complete match of intron chain with known transcripts, 686 were potentially novel isoforms or showed a generic overlap with known transcripts. The remaining 560 sequences, if validated, could be novel intergenic transcripts or transcripts with an exonic overlap with reference ones. Conclusions: This study demonstrates, for the first time, miR-1246 as a potential diagnostic serum biomarker in HGSOC, as assessed by three independent technologies (microarray, RT-qPCR and ddPCR) and validated in two independent cohorts of patients. Moreover, high-throughput analysis reveals most of the gene and miRNA dysregulated in HGSOC biopsies compared to the normal counterpart. In particular, our findings indicate, for the first time, that miR-1246 over-expression correlates with a platinum-resistant HGSOC phenotype and may constitute a novel prognostic factor for HGSOC patients. Furthermore, our results regarding HRMs suggest an important role of miRNAs in response to hypoxic conditions within HGSOC. Particularly, the miR-23a-3p over-expression in the group of platinum-resistance patients may contribute to explain the importance of hypoxia in HGSOC mechanism of drug resistance and could represent an independent prognostic marker for HGSOC patients. Lastly, preliminary data emerged from transcriptome analyses, suggesting a prominent non-coding role in HGSOC platinum resistance, will be integrated with gene and miRNA expression profiles previously obtained, with the aim to identify tumor circuits associated with response to treatment and prognosis, as well as to better elucidate the molecular mechanisms characterizing HGSOC progression and adaptation to hypoxic tumor microenvironment.
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Moore, Elizabeth. "Improving earlier non-invasive diagnosis of high-grade serous ovarian cancer." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/285405.

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The majority of women with ovarian cancer (OC) have advanced disease at diagnosis and 5-year survival rates of less than 25%. Women with stage I disease have significantly better 5-year survival rates of over 90%. Recent large studies using CA 125 and transvaginal ultrasound have failed to improve mortality in a screened population. There is therefore a pressing need for new diagnostic biomarkers in OC. The primary aim of my project, as a first step in developing a diagnostic circulating tumour DNA (ctDNA) biomarker for high grade serous ovarian cancer (HGSOC), was to investigate low-cost high-throughput next generation sequencing assays in plasma samples collected from women with newly diagnosed OC. The secondary aim was to apply these methods to other non-invasive samples including cervical liquid based cytology samples that might contribute to earlier diagnosis or screening for women with OC. ctDNA was detected in 30-49% of women with newly diagnosed OC from the UKOPS (n=54) and CTCR-OV04 (n=156) cohorts using targeted sequencing. Using the trimmed median absolute deviation (t-MAD) score, a quantitative measure of genome wide copy number aberration generated from shallow whole genome sequencing (sWGS) data, ctDNA was detected in 39-41% of the women with newly diagnosed disease. To improve sensitivity of ctDNA detection I developed an optimised method for targeted sequencing that has the potential to lower the limit of detection of ctDNA in HGSOC by 100 fold. I have also shown that the size profile of HGSOC ctDNA fragments is different to that of wildtype DNA fragments and shown that selecting for DNA fragments between 90-150 bp can increase rates of ctDNA detection in HGSOC. ctDNA detection increased to 53-67% of women with newly diagnosed OC using the size selected t-MAD score. I have evaluated the utility of cervical sampling for earlier diagnosis of OC by testing and optimising DNA extraction, library preparation and sequencing methods. I have detected tumour DNA in routine cervical cytology samples collected from women subsequently diagnosed with cervical and endometrial cancers. In summary I have developed methods for ctDNA detection in women with newly diagnosed HGSOC that can be applied and refined in larger prospective studies of women undergoing follow-up for treated HGSOC, women with symptoms suggestive of OC and women at high risk of OC.
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Books on the topic "High-grade serous ovarian carcinoma"

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The Tumor Microenvironment of High Grade Serous Ovarian Cancer. MDPI, 2019. http://dx.doi.org/10.3390/books978-3-03897-555-7.

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Book chapters on the topic "High-grade serous ovarian carcinoma"

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Kyo, Satoru. "Investigating the Molecular Carcinogenesis of Ovarian High-Grade Serous Carcinoma." In Current Human Cell Research and Applications, 41–56. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6013-6_4.

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Gershenson, David M. "The Continuum of Serous Ovarian Tumors of Low Malignant Potential and Low-Grade Serous Carcinoma of the Ovary." In Rare and Uncommon Gynecological Cancers, 105–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13492-0_9.

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Shaw, Patricia A., Blaise Clarke, and Sophia H. L. George. "Precursors of High-Grade Serous Carcinoma." In Precancerous Lesions of the Gynecologic Tract, 3–22. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22509-8_1.

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Gershenson, David M. "Serous Tumors of Low Malignant Potential and Low-Grade Serous Carcinomas of the Ovary or Peritoneum." In Ovarian Cancers, 183–200. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32110-3_13.

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Zeleznik, Oana A., Gerhard G. Thallinger, John Platig, and Aedín C. Culhane. "Topological Pathway Enrichment Analysis of Gene Expression in High Grade Serous Ovarian Cancer Reveals Tumor-Stoma Cross-Talk." In Trends in Mathematics, 59–63. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55639-0_10.

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Pasquini, Luca, Roberta Riccioni, and Eleonora Petrucci. "Assessment of Tumor Heterogeneity in High-Grade Serous Ovarian Cancer: Mass Cytometry to Understand the Complex Tumor Biology." In Methods in Molecular Biology, 105–18. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2513-2_9.

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Kessler, Mirjana. "Role of Infections and Tissue Inflammation in the Pathology of the Fallopian Tube and High-Grade Serous Ovarian Cancer." In Physiology in Health and Disease, 271–312. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67951-4_9.

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Asaturova, Aleksandra, Anna Tregubova, and Alina Magnaeva. "Molecular Subtypes of High-Grade Serous Ovarian Carcinoma." In Interdisciplinary Cancer Research. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/16833_2022_102.

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Santin, Alessandro D. "3 Role of Immunohistochemical Expression of HER2/neu in High-Grade Ovarian Serous Papillary Cancer." In Molecular Genetics, Gastrointestinal Carcinoma, and Ovarian Carcinoma, 333–38. Elsevier, 2005. http://dx.doi.org/10.1016/s1874-5784(05)80089-3.

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Islam, Farhadul. "Enzymes: Tumour Associated Biomarker." In Current Cancer Biomarkers, 180–94. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815079364123010012.

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Enzymes catalyse biochemical reactions and tightly regulate biophysical and metabolic pathways to maintain cellular homeostasis. However, the unregulated activity of these enzymes results in metabolic disorders and genetic diseases, including cancer. In cancer, significant alteration of enzyme levels and/or activity can be detected during malignant transformation, thus, it can be used as a potential biomarker in clinical applications. For example, serum levels of lactate dehydrogenase (LDH), neuron-specific enolase (NSE) and thymidine kinase 1(TK1), alkaline phosphatases (ALPs), tumour M2-PK, hexokinase (HK), etc., significantly increased in patients with various cancers, such as metastatic breast cancer, intracranial germ cell tumours, ovarian serous carcinomas, oesophagus, cervical, gastrointestinal, prostate, renal cell carcinoma, head and neck and lung cancers. Also, they are associated with various clinicopathological factors, such as stage, grade, lymph node metastasis, distant metastasis, etc. In addition, overexpression of carbonic anhydrase XII (CAXII), matrix metalloproteinases (MMPs) and aldehyde dehydrogenase 1 (ALDH1), in cancer tissues, is associated with the presence of several cancers and correlated with the progression of the diseases. Therefore, screening of these enzymes at the point-of-care settings could facilitate better management of patients with cancer. This chapter summarizes the roles of cancer associated-enzymes, especially emphasizing their clinical significance in patients with various cancers.
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Conference papers on the topic "High-grade serous ovarian carcinoma"

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Mansouri, H., I. Zemni, O. Jaidane, MA Ayedi, J. Ben Hassouna, M. Hechiche, R. Chargui, and K. Ben Rahal. "287 Comparative study of ovarian low-grade and high-grade serous ovarain carcinoma." In IGCS 2020 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-igcs.247.

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Liu, Zhaojian, and JianJun Wei. "Abstract 133:MiR-182overexpression and ovarian high grade serous carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-133.

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Chandrasekaran, Akshaya, Mariam Ahmed, Wade Wang, Paula T. Hammond, and Kevin M. Elias. "Abstract 6241: PAX8-directed nanotherapeutics for high-grade serous ovarian carcinoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6241.

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Van der Ploeg, P., W. Verhaegh, J. De Hullu, A. Van der Stolpe, and J. Piek. "PO-138 Hedgehog signalling pathway activity in high-grade serous ovarian carcinoma." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.662.

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Verhaak, Roel G. W., Kyle Chang, Hoon Kim, Scott L. Carter, Nikolaus Schultz, Fengmei Zhao, Hui Shen, et al. "Abstract 4922: Patterns of tumor evolution in high grade serous ovarian carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4922.

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Liu, Jinsong. "Abstract B49: Giant cancer stem cells of high-grade ovarian serous carcinoma ." In Abstracts: AACR Special Conference: Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; October 17-20, 2015; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.ovca15-b49.

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Kuhn, Elisabetta, Robert J. Kurman, Robert A. Soslow, Guangming Han, Tian-Li Wang, and Ie-Ming Shih. "Abstract 221:TP53mutations in serous tubal intraepithelial carcinoma, the putative precursor lesion of ovarian high-grade serous carcinoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-221.

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Saglam, O., S. Vyas, B. Reid, J. Permuth, and T. Sellers. "326 Clinical outcomes associated with EZH2 expression in high-grade ovarian serous carcinoma." In IGCS Annual 2019 Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-igcs.326.

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Bapat, Sharmila A., and Sagar Varankar. "Abstract 1042: Cellular plasticity and migratory modalities in high-grade serous ovarian carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1042.

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Bapat, Sharmila A., and Sagar Varankar. "Abstract 1042: Cellular plasticity and migratory modalities in high-grade serous ovarian carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1042.

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Reports on the topic "High-grade serous ovarian carcinoma"

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Nolan, Garry P. Organizing the Cellular and Molecular Heterogeneity in High-Grade Serous Ovarian Cancer by Mass Cytometry. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599601.

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