scholarly journals Low-grade Serous Ovarian Carcinoma

2018 ◽  
Vol 78 (10) ◽  
pp. 972-976 ◽  
Author(s):  
Enzo Ricciardi ◽  
Thaïs Baert ◽  
Beyhan Ataseven ◽  
Florian Heitz ◽  
Sonia Prader ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Clinical Trials ◽  
Ovarian Carcinoma ◽  
Systemic Treatment ◽  
Hormonal Treatment ◽  
Current Treatment ◽  
Low Grade ◽  
Separate Entity ◽  
Serous Ovarian Carcinoma ◽  
Number Of Patients

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.

Low-grade serous ovarian carcinoma: an evolution toward targeted therapy

2019 ◽  
Vol 30 (10) ◽  
pp. 1619-1626 ◽  
Author(s):  
Ioannis A Voutsadakis
Keyword(s):  
Clinical Trials ◽  
Targeted Therapy ◽  
Ovarian Carcinoma ◽  
Molecular Profile ◽  
Low Grade ◽  
High Grade ◽  
Novel Therapies ◽  
Precursor Lesions ◽  
Molecular Defects ◽  
Serous Ovarian Carcinoma

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.

Circulating tumor DNA analysis to reveal genomic profiles for epithelial ovarian cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 5543-5543
Author(s):  
Yang Xiang ◽  
Shan Zhu ◽  
Weiran Wang ◽  
Dongyan Cao ◽  
Xi-Run Wan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Epithelial Ovarian Cancer ◽  
Circulating Tumor Dna ◽  
Stage Iii ◽  
Signal Pathways ◽  
Low Grade ◽  
Serous Ovarian Carcinoma ◽  
Ctdna Analysis ◽  
Tumor Dna

5543 Background: Circulating tumor DNA (ctDNA) analysis in epithelial ovarian cancer (EOC) was previously reported, however with limited samples or limited genes. Here, we reported an analysis of ctDNA in EOC cohort using targeted sequencing with a 1021-gene panel. Methods: Patients with EOC were enrolled, and treatment-naïve tumor tissues and blood samples were collected. We utilized a 1021-gene NGS panel in matched tissue DNA and ctDNA to identify somatic mutations with white blood cell DNA as a germline control. Results: Mutations were identified in all of the 65 tissues and in 53 (81.5%) ctDNA. The median ctDNA mutation allelic frequency was 2.5%, ranging from 0.1% to 36.2%. A median of 66.7% (12.5%-100.0%) of tissue derived mutations were observed in ctDNA. Besides, there were 91 ctDNA private mutations, including TP53 gene mutations. The most frequently mutated genes were TP53 (55.4%), PIK3CA (13.8%) and ARID1A (12.3%) in ctDNA analysis, which were consistent with tissue analysis (60.0%, 26.2% and 20.0% of tissues with TP53, PIK3CA and ARID1A mutations, respectively). Mutations of TP53 (37/42) in high-grade serous ovarian carcinoma (HGSOC), PIK3CA (10/11) and ARID1A (8/11) in ovarian clear cell carcinoma, BRAF (4/5) in low-grade serous ovarian carcinoma and PIK3CA (3/5), ARID1A (2/5) and PTEN (2/5) in endometrioid carcinoma were observed as the most commonly genetic aberrations in ctDNA in different sub-types of EOC, which located in different signal pathways and suggested different pathogenesis. In total, 90.5% (38/42) of HGSOC were ctDNA positive, comparing with 65.2% (15/23) of other EOC subtypes (p = 0.012). In addition, 56.5% (13/23) of stage I~II EOC were ctDNA positive, comparing with 94.7% (36/38) of stage III (p = 0.002). No association between ctDNA positivity and other clinic characteristics was observed, including pathological differentiation, CA125, lesion density (solid vs. cystic-solid and cystic). Multivariable analysis suggested FIGO stage III (p = 0.008) as an independent predictor of ctDNA detection. Conclusions: In summary, genomic characterization of EOC may offer insights into tumorigenesis and identify potential therapeutic targets in this disease.

scholarly journals Synchronous B-Cell Acute Lymphoblastic Leukemia and Serous Ovarian Carcinoma: A Case Report

2021 ◽  
pp. 1621-1626
Author(s):  
Michael Superdock ◽  
Justin Komisarof ◽  
Hani Katerji ◽  
Eric Huselton
Keyword(s):  
Ovarian Cancer ◽  
Acute Lymphoblastic Leukemia ◽  
Ovarian Carcinoma ◽  
B Cell ◽  
Lymphoblastic Leukemia ◽  
Low Grade ◽  
Unique Case ◽  
Inotuzumab Ozogamicin ◽  
Serous Ovarian Carcinoma ◽  
Cell Acute Lymphoblastic Leukemia

Adult patients with B-cell acute lymphoblastic leukemia (ALL) have higher rates of antecedent and subsequent malignancies. However, synchronous identification of ALL and ovarian cancer is exceedingly rare. We report the unique case of a 65-year-old woman with synchronous B-cell ALL and low-grade serous ovarian carcinoma diagnosed after surgical intervention for a small bowel obstruction. Treatment with inotuzumab ozogamicin followed by adnexal mass resection and postoperative letrozole was successful in achieving complete remission for both her leukemia and ovarian cancer.

MOLECULAR AND GENETIC SUBTYPES OF OVARIAN CANCER: PROSPECTS FOR FURTHER STUDIES

2019 ◽  
Vol 65 (1) ◽  
pp. 56-62
Author(s):  
Alisa Villert ◽  
Larisa Kolomiets ◽  
Natalya Yunusova ◽  
Yevgeniya Fesik
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Molecular Subtypes ◽  
Survival Rates ◽  
Consensus Algorithm ◽  
Histopathological Diagnosis ◽  
Low Grade ◽  
High Grade ◽  
Ovarian Carcinomas ◽  
Genetic Subtypes

High-grade ovarian carcinoma is a histopathological diagnosis, however, at the molecular level, ovarian cancer represents a heterogeneous group of diseases. Studies aimed at identifying molecular genetic subtypes of ovarian cancer are conducted in order to find the answer to the question: can different molecular subgroups influence the choice of treatment? One of the achievements in this trend is the recognition of the dualistic model that categorizes various types of ovarian cancer into two groups designated high-grade (HG) and low-grade (LG) tumors. However, the tumor genome sequencing data suggest the existence of 6 ovarian carcinoma subtypes, including two LG and four HG subtypes. Subtype C1 exhibits a high stromal response and the lowest survival. Subtypes C2 and C4 demonstrate higher number of intratumoral CD3 + cells, lower stromal gene expression and better survival than sybtype C1. Subtype C5 (mesenchymal) is characterized by mesenchymal cells, over-expression of N-cadherin and P-cadherin, low expression of differentiation markers, and lower survival rates than C2 and C4. The use of a consensus algorithm to determine the subtype allows identification of only a minority of ovarian carcinomas (approximately 25%) therefore, the practical importance of this classification requires additional research. There is evidence that it makes sense to randomize tumors into groups with altered expression of angiogenic genes and groups with overexpression of the immune response genes, as in the angiogenic group there is a comparative superiority in terms of survival. The administration of bevacizumab in the angiogenic group improves survival, while the administration of bevacizumab in the immune group even worsens the outcome. Molecular subtypes with worse survival rates (proliferative and mesenchymal) also benefit most from bevacizumab treatment. This review focuses on some of the advances in understanding molecular, cellular, and genetic changes in ovarian carcinomas with the results achieved so far regarding the formulation of molecular subtypes of ovarian cancer, however further studies are needed.

scholarly journals Trends of low-grade serous ovarian carcinoma in the United States

2018 ◽  
Vol 29 (1) ◽  
Author(s):  
Koji Matsuo ◽  
Hiroko Machida ◽  
Brendan H. Grubbs ◽  
Anil K. Sood ◽  
David M. Gershenson
Keyword(s):  
United States ◽  
Ovarian Carcinoma ◽  
The United States ◽  
Low Grade ◽  
Serous Ovarian Carcinoma

scholarly journals Molecular Mechanisms Regulating Organ-Specific Metastases in Epithelial Ovarian Carcinoma

Cancers ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 444 ◽  
Author(s):  
Maria Barbolina
Keyword(s):  
Ovarian Cancer ◽  
Clinical Trials ◽  
Ovarian Carcinoma ◽  
Molecular Mechanisms ◽  
Epithelial Ovarian Carcinoma ◽  
Gynecologic Malignancy ◽  
Peritoneal Adhesion ◽  
Metastatic Cascade ◽  
Predominant Type ◽  
Organ Specific

Epithelial ovarian carcinoma is the most predominant type of ovarian carcinoma, the deadliest gynecologic malignancy. It is typically diagnosed late when the cancer has already metastasized. Transcoelomic metastasis is the most predominant mechanism of dissemination from epithelial ovarian carcinoma, although both hematogenously and lymphogenously spread metastases also occur. In this review, we describe molecular mechanisms known to regulate organ-specific metastasis from epithelial ovarian carcinoma. We begin by discussing the sites colonized by metastatic ovarian carcinoma and rank them in the order of prevalence. Next, we review the mechanisms regulating the transcoelomic metastasis. Within this chapter, we specifically focus on the mechanisms that were demonstrated to regulate peritoneal adhesion—one of the first steps in the transcoelomic metastatic cascade. Furthermore, we describe mechanisms of the transcoelomic metastasis known to regulate colonization of specific sites within the peritoneal cavity, including the omentum. Mechanisms underlying hematogenous and lymphogenous metastatic spread are less comprehensively studied in ovarian cancer, and we summarize mechanisms that were identified to date. Lastly, we discuss the outcomes of the clinical trials that attempted to target some of the mechanisms described in this review.

GATA3 and stemness of high-grade serous ovarian carcinoma: novel hope for the deadliest type of ovarian cancer

Human Cell ◽  
2020 ◽  
Vol 33 (3) ◽  
pp. 904-906 ◽  
Author(s):  
Amr Ahmed El-Arabey ◽  
Mohnad Abdalla ◽  
Adel Rashad Abd-Allah
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
High Grade ◽  
Serous Ovarian Carcinoma

scholarly journals Mechanisms of Chromosomal Instability in High-grade Serous Ovarian Carcinoma

2019 ◽  
Author(s):  
N. Tamura ◽  
N. Shaikh ◽  
D. Muliaditan ◽  
J. McGuinness ◽  
D. Moralli ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Single Molecule ◽  
Chromosomal Instability ◽  
Poor Prognosis ◽  
Spindle Assembly Checkpoint ◽  
Western World ◽  
Cancer Type ◽  
High Grade ◽  
Serous Ovarian Carcinoma

AbstractChromosomal instability (CIN), the continual gain and loss of chromosomes or parts of chromosomes, occurs in the majority of cancers and confers poor prognosis. Mechanisms driving CIN remain unknown in most cancer types due to a scarcity of functional studies. High-grade serous ovarian carcinoma (HGSC), the most common subtype of ovarian cancer, is the major cause of death due to gynaecological malignancy in the Western world with chemotherapy resistance developing in almost all patients. HGSC exhibits high rates of chromosome aberrations and knowledge of causative mechanisms is likely to represent an important step towards combating the poor prognosis of this disease. However, very little is known about the nature of chromosomal instability exhibited by this cancer type in particular due to a historical lack of appropriate cell line models. Here we perform the first in-depth functional characterisation of mechanisms driving CIN in HGSC by analysing eight cell lines that accurately recapitulate HGSC genetics as defined by recent studies. We show, using a range of established functional CIN assays combined with live cell imaging and single molecule DNA fibre analysis, that multiple mechanisms co-exist to drive CIN in HGSC. These include supernumerary centrosomes, elevated microtubule dynamics and DNA replication stress. By contrast, the spindle assembly checkpoint was intact. These findings are relevant for developing therapeutic approaches to manipulating CIN in ovarian cancer, and suggests that such approaches may need to be multimodal to combat multiple co-existing CIN drivers.

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