Platinum-resistant ovarian cancer remains one of the most difficult settings in gynecologic oncology. In the US, about 21,010 women are expected to receive a new diagnosis of ovarian cancer in 2026, and about 12,450 women are expected to die from the disease.
While many patients initially respond to platinum-based chemotherapy, advanced ovarian cancer frequently recurs, and many patients with recurrent disease eventually develop resistance to platinum-based treatment.
Platinum-resistant ovarian cancer is commonly defined as disease progression within six months of the last dose of platinum-based chemotherapy. Once disease reaches this point, treatment options are limited, response rates to standard single-agent chemotherapy have often been reported in the low double digits and benefits are usually short-lived. Patients may also have accumulated significant toxicities from earlier lines of systemic therapy, making tolerability a central concern alongside efficacy.
CureLab Oncology, a biotech company developing anti-cancer biologics, is exploring a DNA-based therapeutic strategy designed to influence the tumor microenvironment, support anti-tumor immune activity and enhance the effects of chemotherapy. Its lead clinical candidate, elenagen, is an investigational p62/SQSTM1-encoding plasmid DNA therapy designed to reshape the tumor microenvironment.
In a randomized Phase II study in platinum-resistant ovarian cancer, the investigational DNA-based immunotherapy was evaluated in combination with gemcitabine. The study, recently published in the International Journal of Gynecological Cancer and presented at the 27th Congress of the European Society of Gynaecological Oncology (ESGO 2026), reported median overall survival of 13 months with gemcitabine alone compared with 25 months with the addition of elenagen. The combination was also associated with a 59% relative reduction in the risk of death. Safety profiles were reported to be similar between arms, with no new toxicity signals.
To discuss the clinical and scientific implications of these findings, Xtalks spoke with Gabriel Levin, MD, a Gynecologic Oncologist at the McGill University Health Centre and Director of Oncology at CureLab Oncology, and Alexander Shneider, PhD, CEO of CureLab Oncology and inventor of the investigational DNA-based immunotherapy.
The Clinical Challenges of Platinum-Resistant Ovarian Cancer
For Dr. Levin, platinum resistance marks a difficult turning point in ovarian cancer care because it signals that the tumor has learned to escape one of the most effective treatment backbones available.
“Platinum-resistant ovarian cancer is an old definition of how the tumor is responsive to our usual backbone, which is platinum-based chemotherapy,” Dr. Levin explained. “It means that disease progressed within six months from the last dose of platinum-based chemotherapy.”
Once ovarian cancer becomes platinum-resistant, treatment options become substantially more constrained. According to Dr. Levin, response rates to later-line chemotherapy are often modest, generally in the low 15% range or less, and the benefit is usually short-lived.
“It’s difficult to treat those patients because once we define the cancer as platinum-resistant ovarian cancer, it means that the cancer has learned how to escape our most effective backbone therapy,” he said.
Patients have often already received multiple courses of systemic therapy by this point, and cumulative toxicities such as bone marrow suppression, alopecia and neuropathy can affect treatment tolerance and quality of life.
Dr. Levin noted that a large proportion of advanced ovarian cancers are not curable and recur after first-line therapy. Eventually, many patients reach a platinum-resistant stage, where treatment options are limited and care may move toward palliation.
“The unmet needs are more effective treatments and more tolerable treatments,” he said. “We need options that really improve overall survival, control the patient’s symptoms and are accessible and improve quality of life because it’s not only about prolonging lives, it’s also about living lives which are respectful and have some quality.”
He also emphasized the need for therapies that can be used broadly, rather than only in biomarker-selected populations. While precision oncology has created important advances, not all patients have actionable biomarkers, and platinum-resistant ovarian cancer remains an area where broadly applicable strategies are needed.
What the Phase II Data Showed
The Phase II findings presented by Dr. Levin at ESGO 2026 evaluated CureLab Oncology’s investigational DNA-based immunotherapy in combination with gemcitabine for platinum-resistant ovarian cancer. The study compared gemcitabine alone with gemcitabine plus the investigational therapy.
The reported overall survival signal was notable: median overall survival was 13 months in the control arm compared with 25 months in the combination arm.
“The finding of the overall survival from the Phase II trial is overwhelming,” Dr. Levin said. “It’s unheard of, reaching an overall survival of 25 months in the setting of platinum-resistant ovarian cancer.”
For Dr. Levin, the result is important not only because of the magnitude of the survival difference, but also because it may suggest effects beyond short-term tumor control.
“Moving the needle from 13 months, which was the control arm, to 25 months is a huge signal and potentially meaningful change in how we can manage platinum-resistant ovarian cancer and not only delay progression, but also prolong the life of this patient,” he said.
He added that the effect may point to longer-term changes in the tumor microenvironment that could influence responses to later lines of therapy. However, he was clear that the findings require confirmation.
“It was only a Phase II trial, and it needs to be further verified in a Phase III randomized controlled trial,” Dr. Levin said.
No New Toxicity Signals Reported
In oncology, improvements in efficacy are often accompanied by added toxicity. This is especially important in platinum-resistant ovarian cancer, where patients may have already experienced substantial treatment-related adverse effects.
In the Phase II trial, safety profiles were reported to be similar between arms, with no new toxicity signals associated with adding CureLab Oncology’s investigational DNA-based immunotherapy to the chemotherapy backbone.
“We noticed that in our Phase II trial that patients had no additive toxicity from treatment with elenagen, which is highly unusual,” Dr. Levin said.
This is clinically relevant because patients with platinum-resistant ovarian cancer often need therapies that can extend survival without further compromising quality of life. If confirmed in larger studies, the lack of new toxicity signals could help inform future treatment protocols and combination strategies.
How the DNA-Based Immunotherapy Is Designed to Work
CureLab Oncology’s investigational therapy is a plasmid-based therapy encoding p62/SQSTM1. Dr. Shneider described the plasmid as a molecular envelope: a circular DNA structure that can carry a selected genetic sequence.
“Imagine you went to Staples and bought an envelope, a standard envelope. Then you can put into this envelope any sort of a letter,” Dr. Shneider said. “Now instead of an envelope which you buy at Staples, imagine a circular DNA, let’s call it a plasmid. So it’s the same envelope but on a molecular level.”
The selected gene was p62/SQSTM1. Dr. Shneider said the original hypothesis was immunological: because cancer cells overexpress p62, a plasmid encoding the gene could help train the immune system to recognize and eliminate cells producing too much of the protein.
“My original idea was to put in there a gene called p62, and the original hypothesis was to use this gene for purely immunological reasons,” he explained. “It would train our immunity to identify and eliminate those cells which have too much of this gene, too much of this protein.”
The choice of p62 was deliberate. According to Dr. Shneider, cancer cells are biochemically dependent on overproducing p62, meaning they cannot easily stop expressing it to escape immune recognition.
“My entire previous life in vaccinology taught me that you need to select such a target that the cancer cells would not be able to omit, would not be able to stop producing,” he said. “p62 is a protein which cancer cells cannot stop overproducing because they’re biochemically addicted to it.”
However, he said subsequent work showed the immune-targeting hypothesis was only one part of a more complex mechanism.
