Tumor evolution and chemoresistance in ovarian cancer

Abstract

Development of novel strategies to overcome chemoresistance is central goal in ovarian cancer research. Natural history of the cancer development and progression is being reconstructed by genomic datasets to understand the evolutionary pattern and direction. Recent studies suggest that intra-tumor heterogeneity (ITH) is the main cause of treatment failure by chemoresistance in many types of cancers including ovarian cancer. ITH increases the fitness of tumor to adapt to incompatible microenvironment. Understanding ITH in relation to the evolutionary pattern may result in the development of the innovative approach based on individual variability in the genetic, environment, and life style. Thus, we can reach the new big stage conquering the cancer. In this review, we will discuss the recent advances in understanding ovarian cancer biology through the use of next generation sequencing (NGS) and highlight areas of recent progress to improve precision medicine in ovarian cancer.

Factors in Oncogenesis: Viral Infections in Ovarian Cancer

“…If the HPV and/or herpesviruses are drivers of OC pathogenesis, the natural question appears: what therapeutic strategies could be used to manage OC patients? So far, vaccination with DCs pulsed with modified or unchanged tumor-associated antigens (TAAs) has been tested in plenty of immunotherapy trials devoted to advanced OC; however, this has had hardly satisfactory results [169,170]. Another approach to the treatment of patients with OC is based on the vaccination with both long and short peptides (e.g., p53, Her-2/Neu, and NY-ESO-1 or survivin, WT1, and Ca125, respectively) or, alternatively, with carbohydrate epitopes (e.g., GM2, Globo-H, Levis y, sialyl-Tn, and Thompson Friedreich antigen) conjugated to the carrier protein KLH [171].…”

Genetic heterogeneity and evolutionary history of high-grade ovarian carcinoma and matched distant metastases

“…11,12 Like tumour evolution, many competing models of metastasis exist, some of which include the linear progression model, where metastases arise from late-occurring advanced clonal subpopulations; parallel progression, suggesting early metastatic seeding and the independent acquisition of primary tumour mutations, with widespread disease at an early time point, and metastasis crossseeding, where clones from distinct metastatic sites, not present in the primary tumour, can disseminate to a new metastatic site. 13,14 As various models of tumour evolution and metastatic progression in cancer can have diverse clinical implications for the clinical diagnosis, prognosis and treatment of the patient, 15,16 such as the need for systemic adjuvant therapy in patients displaying parallel metastatic progression to counteract early systemic spread of tumour cells, understanding these models is of great clinical significance. 17 Given the low survival and high recurrence rate, there is a potential need to report and understand the metastatic evolution of HGSOC.…”

Claudin 10 acts as a novel biomarker for the prognosis of patients with ovarian cancer

“…OC is considered a mixture of these representative histological types with different molecular etiologies, tumor progression features and disease prognoses. This hinders the efficacy of current treatments for OC, such as platinum-based combination chemotherapy, surgery and neoadjuvant chemotherapy (3,4). Unfortunately, the majority of patients with OC (>70%) are diagnosed at an advanced or metastatic stage (III or IV) and their 5-year overall survival rate is ~40%, while the 5-year overall survival rate of patients with stage I OC is ~90% (5,6).…”