Ovarian cancer has been dubbed "the silent killer" because of its overall 5-year survival rate of 47%: By the time a woman receives the diagnosis, the prognosis is unfavorable. Some argue that ovarian cancer could more appropriately be labeled the “whispering disease.” Because no specific test diagnoses it, there must be improvements in education regarding the signs and symptoms. The human body is an incredibly well-oiled machine that is reactive, based on a cause-and-effect principle. When something is wrong, the body creates a response that should raise an alert.

Consider the general signs and symptoms of ovarian cancer, which include bloating, abdominal pain, trouble eating or feeling full quickly, and increased urinary frequency. These nonspecific complications can be caused by countless factors, making it nearly impossible to correlate these symptoms to an ovarian cancer diagnosis.

Awareness is just the beginning of an enormous need to do more surrounding this disease. In the past couple of years, new treatment options for ovarian cancer have emerged, but the biggest gap involves the lack of a specific diagnostic tool that can detect the disease prior to the advanced stage.

Unfortunately, after a 2-year battle, my mom was one of the roughly 14,000 women who fell victim to ovarian cancer in 2017. Her illness was, for obvious reasons, one of the worst experiences of my life but it was also one of the best. It afforded me the opportunity to spend more time and grow closer to my mother during this devastating time. I remember sitting in multiple infusion suites with my mom and observing the other women. The experiences I witnessed were powerful. These women were not only selfless but truly resilient warriors. They inspired me to become more involved in the national fight against ovarian cancer and help be their voice.

To all the women who have won their battles and to those who have fallen victim, thank you for your strength and inspiration.


This form of cancer originates from 1 of the 3 ovarian cell types (their subtypes will not be covered here):

EPITHELIAL CELLS account for approximately 90% of all ovarian cancer diagnoses. Epithelial cell tumors arise from the cells that cover the outer surface of the ovaries. This is the most common form of ovarian cancer.

GERM CELLS account for 3% of ovarian cancer diagnoses. Germ cell tumors originate from the cells that are responsible for creating the eggs.

STROMAL CELLS account for 2% of ovarian cancer diagnoses. Stromal cell tumors start from the cells responsible for releasing female hormones and structurally holding the ovaries together.

It is important to note that not all tumors found on or near the ovaries are considered cancerous. The doctor will likely take a sample of a section of the tumor and send it to a pathology department to determine its origin and whether or not the tumor is cancerous.


Currently, the only ways to detect ovarian cancer involve consulting a physician regarding symptoms and using a blood test known as cancer antigen (CA) 125, which measures the amount of the protein CA 125 in the blood. However, it is deficient as a screening marker because high levels of CA 125 often result from other common conditions, such as endometriosis or pelvic inflammatory disease. In some ovarian cancer cases, a high CA 125 level may not be seen. Therefore, this cannot be used as a reliable, foolproof marker for screening and diagnosing ovarian cancer.


Newer treatments for ovarian cancer, poly (ADP-ribose) polymerase (PARP) inhibitors, have garnered significant attention over the past few years. The PARP enzyme plays a critical part in cell development by repairing the DNA when it becomes damaged and, in turn, promoting cell and tumor growth; these new medications work by inhibiting PARP’s ability to fuel tumor growth. PARP inhibitors are considered targeted therapy, which implies that the medication is designed to attack a specific kind of cell, as opposed to traditional, less specific chemotherapy agents.

This targeted approach gives PARP inhibitors a more favorable list of adverse effects (AEs) compared with traditional chemotherapy agents. Because chemotherapy medications kill both healthy and cancerous cells, AEs are more likely to occur.

Currently, the FDA has approved 3 PARP inhibitors, all available in the marketplace: olaparib (Lynparza), rucaparib (Rubraca), and niraparib (Zejula).

OLAPARIB initially was approved by the FDA on December 17, 2014, and became the first PARP inhibitor to gain approval. Lynparza is an oral medication that can be used to treat advanced ovarian cancer associated with defected BRCA genes. On August 17, 2017, the FDA approved olaparib for patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who had a complete or partial response to platinum-based chemotherapy. Olaparib is available only via the limited distribution model through Biologics oncology pharmacy. 

RUCAPARIB was approved on December 19, 2016. The oral treatment is indicated as a monotherapy for advanced ovarian cancer in women with deleterious BRCA-mutated tumors, including both germline and somatic BRCA mutations. On April 6, 2018, rucaparib was granted a new indication for maintenance treatment of women with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who had a complete or partial response to platinum-based chemotherapy. Rucaparib is available via the limited distribution model through CVS Specialty, Avella Specialty Pharmacy, Biologics, and US Bioservices, as well as in-office dispensing pharmacies. Therefore, a pharmacy in a physician practice has eligibility to contact their wholesaler directly for product access.

NIRAPARIB was approved by the FDA on March 27, 2017. This oral medication is indicated for the maintenance treatment of women with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who had a complete or partial response to platinum-based chemotherapy. Unlike rucaparib and olaparib, niraparib does not require patient selection with a biomarker test, meaning is does not require the patient to have BRCA-mutated status. Niraparib’s product access is similar to rucaparib in that it is available via a limited distribution model with just a few specialty pharmacies.