scholarly journals Regional and temporal heterogeneity of epithelial ovarian cancer tumor biopsies: implications for therapeutic strategies

Oncotarget ◽  
2016 ◽  
Vol 0 (0) ◽  
Author(s):  
Lara Paracchini ◽  
Laura Mannarino ◽  
Ilaria Craparotta ◽  
Chiara Romualdi ◽  
Robert Fruscio ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Therapeutic Strategies ◽  
Temporal Heterogeneity ◽  
Cancer Tumor ◽  
Tumor Biopsies

scholarly journals Therapeutic strategies in epithelial ovarian cancer

2012 ◽  
Vol 31 (1) ◽  
pp. 14 ◽  
Author(s):  
Ayako Kim ◽  
Yutaka Ueda ◽  
Tetsuji Naka ◽  
Takayuki Enomoto
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Therapeutic Strategies

scholarly journals Transcriptional Characterization of Stage I Epithelial Ovarian Cancer: A Multicentric Study

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1554
Author(s):  
Enrica Calura ◽  
Matteo Ciciani ◽  
Andrea Sambugaro ◽  
Lara Paracchini ◽  
Giuseppe Benvenuto ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Stage I ◽  
Molecular Heterogeneity ◽  
Low Grade ◽  
Multicentric Study ◽  
Molecular Alterations ◽  
Molecular Features ◽  
Signaling Axis ◽  
Tumor Biopsies

Stage I epithelial ovarian cancer (EOC) represents about 10% of all EOCs. It is characterized by a complex histopathological and molecular heterogeneity, and it is composed of five main histological subtypes (mucinous, endometrioid, clear cell and high, and low grade serous), which have peculiar genetic, molecular, and clinical characteristics. As it occurs less frequently than advanced-stage EOC, its molecular features have not been thoroughly investigated. In this study, using in silico approaches and gene expression data, on a multicentric cohort composed of 208 snap-frozen tumor biopsies, we explored the subtype-specific molecular alterations that regulate tumor aggressiveness in stage I EOC. We found that single genes rather than pathways are responsible for histotype specificities and that a cAMP-PKA-CREB1 signaling axis seems to play a central role in histotype differentiation. Moreover, our results indicate that immune response seems to be, at least in part, involved in histotype differences, as a higher immune-reactive behavior of serous and mucinous samples was observed with respect to other histotypes.

scholarly journals Role of Mitochondria in Interplay between NGF/TRKA, miR-145 and Possible Therapeutic Strategies for Epithelial Ovarian Cancer

Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 8
Author(s):  
Daniela B. Vera ◽  
Allison N. Fredes ◽  
Maritza P. Garrido ◽  
Carmen Romero
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Epithelial Ovarian Cancer ◽  
Therapeutic Strategies ◽  
Apoptotic Pathway ◽  
Invasion And Migration ◽  
High Affinity Receptor ◽  
And Migration ◽  
Laboratory Group

Ovarian cancer is the most lethal gynecological neoplasm, and epithelial ovarian cancer (EOC) accounts for 90% of ovarian malignancies. The 5-year survival is less than 45%, and, unlike other types of cancer, the proportion of women who die from this disease has not improved in recent decades. Nerve growth factor (NGF) and tropomyosin kinase A (TRKA), its high-affinity receptor, play a crucial role in pathogenesis through cell proliferation, angiogenesis, invasion, and migration. NGF/TRKA increase their expression during the progression of EOC by upregulation of oncogenic proteins as vascular endothelial growth factor (VEGF) and c-Myc. Otherwise, the expression of most oncoproteins is regulated by microRNAs (miRs). Our laboratory group reported that the tumoral effect of NGF/TRKA depends on the regulation of miR-145 levels in EOC. Currently, mitochondria have been proposed as new therapeutic targets to activate the apoptotic pathway in the cancer cell. The mitochondria are involved in a myriad of functions as energy production, redox control, homeostasis of Ca+2, and cell death. We demonstrated that NGF stimulation produces an augment in the Bcl-2/BAX ratio, which supports the anti-apoptotic effects of NGF in EOC cells. The review aimed to discuss the role of mitochondria in the interplay between NGF/TRKA and miR-145 and possible therapeutic strategies that may decrease mortality due to EOC.

Epithelial ovarian cancer tumor microenvironment is a favorable biomarker resource

2011 ◽  
Vol 120 ◽  
pp. S48-S49
Author(s):  
E. Hoskins ◽  
B. Hood ◽  
M. Sun ◽  
T. Krivak ◽  
T. Conrads ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Microenvironment ◽  
Epithelial Ovarian Cancer ◽  
Cancer Tumor

A blood gene expression signature for epithelial ovarian cancer

2021 ◽  
Author(s):  
Oliwier Morin ◽  
Brandon Weston ◽  
James D. Klingensmith ◽  
Mairead Paul
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Screening Method ◽  
Specific Antigen ◽  
Gene Expression Signature ◽  
Screening Tools ◽  
Human Prostate Cancer ◽  
Diagnostic Screening ◽  
Blood Gene Expression ◽  
Cancer Tumor

In the industrialized world, epithelial ovarian cancer is the most fatal kind of gynecologic cancer1. A significant element in the mortality rate linked with epithelial ovarian cancer is late diagnosis2, which is caused by a lack of appropriate diagnostic and screening tools, such as the mammography in breast cancer. 3 and the prostate specific antigen (PSA) blood test, both of which are used to diagnose human prostate cancer. 4.5 Radiologic screening might be prohibitively expensive6. We explored previously published microarray data7 in order to identify genes expressed in the blood that may be used to differentiate individuals with epithelial ovarian cancer from those who were not. We found a core collection of 31 genes, ten of which satisfactorily differentiated control individuals from those with epithelial ovarian cancer on their own. Seven out of ten of these genes were also differently expressed in epithelial ovarian cancer tumor tissue8,9. These data may be used to construct a blood-based, quantitative PCR diagnostic screening method for the population-wide identification of epithelial ovarian cancer.

scholarly journals Utilizing Patient-Derived Epithelial Ovarian Cancer Tumor Organoids to Predict Carboplatin Resistance

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1021
Author(s):  
Justin W. Gorski ◽  
Zhuwei Zhang ◽  
J. Robert McCorkle ◽  
Jodi M. DeJohn ◽  
Chi Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cell Receptor ◽  
Debulking Surgery ◽  
Chemotherapy Sensitivity ◽  
Interval Debulking Surgery ◽  
Cancer Tumor ◽  
B Cell Receptor Signaling ◽  
Serous Epithelial Ovarian Cancer ◽  
Tumor Organoids

The development of patient-derived tumor organoids (TOs) from an epithelial ovarian cancer tumor obtained at the time of primary or interval debulking surgery has the potential to play an important role in precision medicine. Here, we utilized TOs to test front-line chemotherapy sensitivity and to investigate genomic drivers of carboplatin resistance. We developed six high-grade, serous epithelial ovarian cancer tumor organoid lines from tissue obtained during debulking surgery (two neoadjuvant-carboplatin-exposed and four chemo-naïve). Each organoid line was screened for sensitivity to carboplatin at four different doses (100, 10, 1, and 0.1 µM). Cell viability curves and resultant EC50 values were determined. One organoid line, UK1254, was predicted to be resistant to carboplatin based on its EC50 value (50.2 µM) being above clinically achievable Cmax. UK1254 had a significantly shorter PFS than the rest of the subjects (p = 0.0253) and was treated as a platinum-resistant recurrence. Subsequent gene expression analysis revealed extensively interconnected, differentially expressed pathways related to NF-kB, cellular differentiation (PRDM6 activation), and the linkage of B-cell receptor signaling to the PI3K–Akt signaling pathway (PI3KAP1 activation). This study demonstrates that patient-derived tumor organoids can be developed from patients at the time of primary or interval debulking surgery and may be used to predict clinical platinum sensitivity status or to investigate drivers of carboplatin resistance.

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