Chemotherapy with Niraparib can extend the life of ovarian cancer patients who have already undergone 4 or more chemotherapy treatments.
American researchers give hope to ovarian cancer patients who have undergone several rounds of chemotherapy treatment and have lost all chances of lengthening their life with any other treatment. The researchers have revealed that the anti-cancer drug, Niraparib, can extend the life of these overly treated ovarian patients.
One of the leading journals in the field of cancer research, The Lancet Oncology, published this research on April 1, 2019.
This research is lead by the gynecologic oncologist Dr. Kathleen Moore. She is the director of the Stephenson Cancer Center at the University of Oklahoma Health Sciences Center.
In this study, the researchers have primarily studied the effect of anticancer drug, Niraparib, on ovarian cancer patients who have no BRCA mutation and who received multiple chemotherapy treatments.
Only 25% of the ovarian cancer patients have mutations in the BRCA gene. And a lot of research has been done on devising new treatment for curing ovarian cancer with BRCA mutation. This led to significantly limited options in curing the 75% of ovarian cancer patients. In this study, the researchers have examined the significance of Niraparib in this 75 % of ovarian cancer patients.
What is Niraparib?
Niraparib is an anticancer drug which functions as PARP inhibitor. It is commercially available as Zejula. Patients who have received or are receiving platinum-based drugs (such as cisplatin) take this medicine.
What is the Function of PARP Inhibitor in BRCA associated Cancers?
PARP inhibitor assist in treating cancer. It inhibits the function of PARP- poly ADP Ribose Polymerase enzyme. This enzyme helps in programmed cell death, repair of DNA, and other critical cellular processes.
PARP is an essential component in repairing the breaks (when a single nucleotide is missing in one of the DNA strands). If the function of PARP halts, after the replication of this unrepaired DNA, the resulting double-stranded DNA will have breaks in both strands.
Additionally, in healthy cells, BRCA proteins repair the double-stranded breaks in the DNA through a process called Homologous Recombinational Repair- HRR. In the case of mutation in the BRCA gene, this process of DNA repair cannot happen which initiate cancer.
PARP enzyme identify the breaks in the DNA and start making changes in its structure along with synthesizing another enzyme to call for help from DNA binding enzymes, thus to initiate the repair.
Here in case of ovarian cancer cells, this positive function of PARP in repairing damaged DNA of cancerous cells can enhance the intensity and metastasis of ovarian cancer.
Therefore, inhibiting the function of PARP enzyme through PARP inhibitor (Niraparib) is effective in limiting the growth of cancer cells.
Women who are suffering through ovarian cancer with BRCA mutation respond positively to chemotherapy treatments and PARP inhibitor. However, there is a lack of research in finding the effect of PARP inhibitor in ovarian cancer patients without BRCA mutation.
Ovarian cancer with BRCA mutation has great treatment options also because these patients develop a condition called as homologous recombination deficiency- HRD.
This condition is the opposite of homologous recombination repair- HRR. In this condition, if the cancer cells create breaks or damage in the DNA during division, these damages cannot be repaired.
PARP Inhibitor Improved the Survival of Ovarian Cancer Patients
The researchers studied the effect of 463 ovarian cancer patients. All of these patients received chemotherapy more than four times previously. And then they considered the response of their tumors for platinum-based therapy.
According to the lead author, Dr.Moore, on average, the participants of this study showed an increase of 20 months in their survival time before the progression of the tumor.
The researchers interpreted their findings as,
"We observed clinically relevant activity of niraparib among women with heavily pretreated ovarian cancer, especially in patients with HRD-positive platinum-sensitive disease, which includes not only patients with a BRCA mutation but also a population with BRCA wild-type disease. We identified no new safety signals. Our data support expansion of the treatment indication for poly(ADP-ribose) polymerase (PARP) inhibitors to include patients with HRD-positive ovarian cancer beyond those with BRCA mutations."