Does Baby Powder Cause Cancer? A Jury Says Yes. Scientists Aren’t So Sure

Does Baby Powder Cause Cancer? A Jury Says Yes. Scientists Aren't So SureIf you’re a woman, there’s a good chance you’ve used Johnson’s Baby Powder at some point. It smells good, and it can keep you dry.

But is it dangerous?

Dr. Daniel Cramer says yes. He’s a professor of obstetrics and gynecology at Brigham and Women’s Hospital in Boston. He says talc — the mineral in talcum powder — can cause ovarian cancer.

“Overall, women may increase their risk in general by about 33 percent by using talc in their hygiene,” Cramer says.

On Monday, a California jury awarded Eva Echeverria $417 million in a case against Johnson & Johnson. Echeverria, who is suffering from terminal ovarian cancer, claimed it was caused by Johnson’s Baby Powder, which she used on her perineum for decades.

Hers wasn’t the first jury award against the company. And thousands more cases are pending.

It has opened a long-simmering question about whether talcum powder used in the genital area can cause cancer.

Cramer, who has served as a paid consultant on several ovarian cancer cases against Johnson & Johnson, published one of the first studies noting an association between talc and ovarian cancer in 1982.

“This story goes back a long, long way, back into the ’70s when people noted that ovarian cancer had many similarities to asbestos exposure,” he says. “Meanwhile another group in England found talc that was deeply embedded in ovaries and said there might be a story here.”

In fact, talc is a mineral that is sometimes mined alongside asbestos. And asbestos, a known carcinogen, was found in the past in some talc products.

After his first study on the talc-cancer association, Cramer followed up with an article in 1985 calling on companies like Johnson & Johnson to put warning labels on their talcum powder products.

Johnson & Johnson declined to be interviewed for this story. The company said in a statement that it plans to appeal the California verdict.

“We are guided by the science, which supports the safety of Johnson’s Baby Powder,” wrote company spokeswoman Carol Goodrich in a statement. “In April, the National Cancer Institute’s Physician Data Query Editorial Board wrote, ‘The weight of evidence does not support an association between perineal talc exposure and an increased risk of ovarian cancer.’ We are preparing for additional trials in the U.S., and we will continue to defend the safety of Johnson’s Baby Powder.”

Some researchers agree that the link between talc and ovarian cancer isn’t all that clear.

The International Agency for Research on Cancer, part of the World Health Organization, in 2010 called talc a possible carcinogen.

“It’s not proof positive,” says Joellen Schildkraut, a professor of public health at the University of Virginia. “These studies are suggestive. They support the idea.”

Her research shows there’s a stronger link between talc and ovarian cancer among African-American women than there is among white women. But to her, even that link isn’t proof.

“I would not call this conclusive. It’s consistent with other reports in the past. It’s suggestive of a stronger association, but it is not conclusive,” she says.

There are theories about how talcum powder could cause cancer. If women put it on their underwear or on feminine products, it could get into their reproductive system. Then, talc particles could make their way to the ovaries — research has already shown that can happen, and talc has been found in ovarian tumors. The talc could then cause irritation and inflammation that, over time, could lead to cancer.

“We can say that it is associated with an increased risk [of cancer],” says Shelley Tworoger, a cancer epidemiologist at the Moffitt Cancer Center in Tampa, Fla. “And there are biologic mechanisms by which we think that talc could actually impact ovarian cancer. But I would stop short of saying that it necessarily causes ovarian cancer.”

But she says there’s certainly enough information out there to guide women.

“Why use it?” she says. “I don’t know if I should say this or not, but … why not just be safe and not use it?”

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Retaining One Normal BRCA Gene In Breast, Ovarian Cancers Influences Patient Survival

Retaining One Normal BRCA Gene In Breast, Ovarian Cancers Influences Patient SurvivalDetermining which cancer patients are likely to be resistant to initial treatment is a major research effort of oncologists and laboratory scientists. Now, ascertaining who might fall into that category may become a little easier for physicians taking care of people with BRCA1/2 mutations. Researchers in the Perelman School of Medicine at the University of Pennsylvania found a relationship between the genetics of tumors with germline BRCA1/2 mutations and whether the tumor retains the normal copy of the BRCA1/2 gene, and risk for primary resistance to a common chemotherapy that works by destroying cancer cells’ DNA. The team published their study this week in Nature Communications.

Researchers estimate that 5 percent of breast cancers and 20 percent of ovarian cancers are attributable to germline mutations in BRCA1 and BRCA2, the focus of the current study. Overall, 252,710 people will be diagnosed with breast cancer this year and 40,610 will die of the disease, according to the National Cancer Institute. For ovarian cancer, NCI projects 22,440 new cases and 14,080 deaths.

There are many reasons patients may be resistant to treatment—the immune system, the complex landscape of a tumor, or a patient’s own genes can all play a role. Without explicitly looking for it, the Penn team found another mechanism of resistance to a standard treatment for patients with BRCA-associated cancers. “Our primary question was not aimed at evaluating resistance to therapy, but we did end up there,” said senior author Katherine Nathanson, MD, deputy director of the Abramson Cancer Center, and director of Genetics at the Basser Center for BRCA.

Her group evaluated the genetic profiles of 160 breast and ovarian cancers associated with germline mutations in BRCA1 and BRCA2, in the largest study of these tumors to date. They were interested in determining what types of secondary, additional changes occur in primary BRCA1/2 germline mutation-associated cancers that might act in concert with mutant BRCA1 and BRCA2 to drive the cancers.

The team evaluated how frequently the non-mutated version of the gene lost its function in concert with the original BRCA1/2 germline mutation-associated cancers. In oncology terms, this double-hit status is called “loss of heterozygosity,” or LOH, to signify that both versions (one inherited from mother, one from father) of the normal BRCA gene have been hobbled.

Historically, it had been thought that all tumors associated with germline BRCA1/2 mutations lose the second version of the gene, or LOH. The investigators were surprised to find that was not the case in a surprisingly large percentage of patients. In addition, they found that other genetic and clinical features of patients whose tumors did not undergo LOH (LOH-negative) were significantly different from those that did undergo LOH (LOH-positive).

Notably, they evaluated the overall survival of patients with ovarian tumors with and without loss of heterozygosity. LOH-negative status was associated with worse overall survival in ovarian cancer patients treated with platinum chemotherapy, with a median of 39 months, compared to 71 months in the LOH-positive group who received the same treatment.

The researchers believe the patients with LOH-negative tumors (those with one working copy of BRCA1 or BRCA2 and the other copy carrying the germline mutation) had tumor cells that could still repair the chemotherapy-induced DNA damage in order to survive. In contrast, the investigators surmise that the LOH-positive group (with both gene copies disabled) responded better to the same therapy because their tumor cells died more readily.

“Identifying the LOH status of BRCA1/2 carriers may be useful to predict who might be at risk for primary resistance to DNA-damaging agents such as platinum, which has important implications for treatment of patients with these mutations,” said the study’s first author Kara N. Maxwell, MD, PhD, an instructor of Hematology/Oncology. “We only need to determine the LOH at a specific gene’s location, which is more cost effective than sequencing a patient’s whole genome, for example, and compatible with standard testing.”

By looking at a person’s individual genetics and type of cancer, the Penn team hopes to be able to better tailor care soon after an initial diagnosis to improve survival. Nathanson surmises that knowing a person’s LOH status could guide treatment decisions. She suggests that certain drugs already in today’s cancer treatment arsenal will likely work for patients who are at risk for resistance due to their LOH genetics; however, it’s a matter of choosing the right one.

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What Is Immunotherapy? The Basics on These Cancer Treatments

What Is Immunotherapy? The Basics on These Cancer TreatmentsSome of the most promising advances in cancer research in recent years involve treatments known as immunotherapy. These advances are spurring billions of dollars in investment by drug companies, and are leading to hundreds of clinical trials. Here are answers to some basic questions about this complex and rapidly evolving field.

What is immunotherapy?

Immunotherapy refers to any treatment that uses the immune system to fight diseases, including cancer. Unlike chemotherapy, which kills cancer cells, immunotherapy acts on the cells of the immune system, to help them attack the cancer.

What are the types of immunotherapy?

Drugs called checkpoint inhibitors are the most widely used form of immunotherapy for cancer. They block a mechanism that cancer cells use to shut down the immune system. This frees killer T-cells — a critically important part of the immune system — to attack the tumor. Four checkpoint inhibitors have been approved by the Food and Drug Administration and are on the market. They are given intravenously.

Another form of immunotherapy, called cell therapy, involves removing immune cells from the patient, altering them genetically to help them fight cancer, then multiplying them in the laboratory and dripping them, like a transfusion, back into the patient. This type of treatment is manufactured individually for each patient, and is still experimental.

Bispecific antibodies are an alternative to cell therapy, one that does not require individualizing treatment for each patient. These antibodies are proteins that can attach to both a cancer cell and a T-cell, that way bringing them close together so the T-cell can attack the cancer. One such drug, called Blincyto, has been approved to treat a rare type of leukemia.

Vaccines, another form of immunotherapy, have had considerably less success than the others. Unlike childhood vaccines, which are aimed at preventing diseases like measles and mumps, cancer vaccines are aimed at treating the disease once the person has it. The idea is to prompt the immune system to attack the cancer by presenting it with some piece of the cancer.

The only vaccine approved specifically to treat cancer in the United States is Provenge, for prostate cancer. Another vaccine, BCG, which was developed to prevent tuberculosis, has long been used to treat bladder cancer. As a weakened TB bacterium, BCG appears to provoke a general immune system reaction that then works against the cancer. Researchers hope that other vaccines may yet be made to work by combining them with checkpoint inhibitors.

Which types of cancer are treated with immunotherapy?

Checkpoint inhibitors have been approved to treat advanced melanoma, Hodgkin’s lymphoma and cancers of the lung, kidney, bladder and head and neck. The drugs are being tested in many other types of cancer.

So far, cell therapy has been used mostly for blood cancers like leukemia and lymphoma.

Which cancer drugs are checkpoint inhibitors?

The four on the market are: Yervoy (ipilimumab) and Opdivo (nivolumab), made by Bristol-Myers Squibb; Keytruda (pembrolizumab), by Merck; and Tecentriq (atezolizumab), by Genentech.

How well does immunotherapy work?

Though immunotherapy has been stunningly successful in some cases, it still works in only a minority of patients. Generally, 20 percent to 40 percent of patients are helped by checkpoint inhibitors — although the rate can be higher among those with melanoma. Some patients with advanced disease have had remissions that have lasted for years. In some cases, combining two checkpoint inhibitors increases the effectiveness. But for some people the drugs do not work at all, or they help just temporarily.

Cell therapy can produce complete remissions in 25 percent to 90 percent of patients with lymphoma or leukemia, depending on the type of cancer. In some cases the remissions can last for years, but in others relapses occur within a year.

What are the side effects?

Checkpoint inhibitors can cause severe problems that are, essentially, autoimmune illnesses, in which the immune system attacks healthy tissue as well as cancer. One result is inflammation. In the lungs it can cause breathing trouble; in the intestine it can cause diarrhea. Joint and muscle pain, and rheumatoid arthritis can also occur, and the immune system can also attack vital glands like the thyroid and pituitary. In rare cases, the immune system can attack the heart, especially when patients take two checkpoint inhibitors at the same time. These reactions are dangerous, but can often be controlled with steroid medicines like prednisone and other immune-suppressing drugs.

Cell therapy can also lead to severe and potentially fatal reactions resulting from the overstimulation of the immune system. The reactions can usually be controlled, but patients may need to be treated in an intensive care unit.

What does immunotherapy cost? Does insurance cover it?

Checkpoint inhibitors can cost $150,000 a year. Many insurers will pay if the drug has been approved for the type of cancer the patient has. But sometimes there are high co-payments. Patients in clinical trials may get the drugs free.

Manufacturers have not said yet how much they will charge for cell therapies, assuming they win approval and reach the market. But experts expect the price to be as high as a few hundred thousand dollars.

Where can I get immunotherapy?

Any oncologist can prescribe the checkpoint inhibitors that are on the market. Patients with cancers for which the drugs have not been approved may find insurers reluctant to pay, but may be able to get the drugs for free by volunteering for clinical trials.

Cell therapies are available only through clinical trials now. Most of the study sites are major medical centers.

How can I find out about clinical trials in immunotherapy?

Information is available on the Cancer Research Institute website, or by calling 1-855-216-0127 (Monday through Friday, 8:30 a.m. to 6 p.m. E.T.). Another source is

To read this full article on The New York Times, please click here.

FDA Approves Olaparib Tablets for Maintenance Treatment in Ovarian Cancer

FDA Approves Olaparib Tablets for Maintenance Treatment in Ovarian CancerOn August 17, 2017, the U.S. Food and Drug Administration (FDA) granted regular approval to olaparib tablets (Lynparza) for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer, who are in a complete or partial response to platinum-based chemotherapy.

With the addition of the new indication, a tablet formulation of olaparib is introduced. The FDA approved olaparib capsules in 2014 for the treatment of patients with deleterious or suspected deleterious germline BRCA-mutated advanced ovarian cancer who have been treated with three or more prior lines of chemotherapy. Today, the FDA also approved olaparib tablets for this indication. Olaparib tablets and capsules are not interchangeable. Olaparib capsules are being phased out of the U.S. market, and will be available only through the Lynparza Specialty Pharmacy Network.

SOLO-2 and Study 19

The approval in the maintenance setting was based on two randomized, placebo-controlled, double-blind, multicenter trials in patients with recurrent ovarian cancers who were in response to platinum-based therapy.

SOLO-2 randomized 295 patients with recurrent germline BRCA-mutated ovarian, fallopian tube, or primary peritoneal cancer (2:1) to receive olaparib tablets 300 mg orally twice daily or placebo. SOLO-2 demonstrated a statistically significant improvement in investigator-assessed progression-free survival in patients randomized to olaparib compared with those who received placebo, with a hazard ratio (HR) of 0.30 (95% confidence interval [CI] = 0.22–0.41; P < .0001). The estimated median progression-free survival was 19.1 and 5.5 months in the olaparib and placebo arms, respectively.

Study 19 randomized 265 patients regardless of BRCA status (1:1) to receive olaparib capsules 400 mg orally twice daily or placebo. Study 19 demonstrated a statistically significant improvement in investigator-assessed progression-free survival in patients treated with olaparib vs placebo with a HR of 0.35 (95% CI = 0.25–0.49; P < .0001). The estimated median progression-free survival was 8.4 months and 4.8 months in the olaparib and placebo arms, respectively.

The most common adverse reactions (≥ 20%) in clinical trials were anemia; nausea; fatigue (including asthenia); vomiting; nasopharyngitis; diarrhea; arthralgia/myalgia; dysgeusia; headache; dyspepsia; decreased appetite; constipation; and stomatitis. The most common laboratory abnormalities (≥ 25%) were decrease in hemoglobin; increase in mean corpuscular volume; decrease in lymphocytes; decrease in leukocytes; decrease in absolute neutrophil count; increase in serum creatinine; and decrease in platelets.

The recommended olaparib tablet dose for both the maintenance therapy and later line treatment setting is 300 mg (two 150 mg tablets) taken orally twice daily with or without food.

FDA granted this application Fast Track status.

To read this article from The ASCO Post, please click here.

Can a Blood Test Detect a Range of Cancers Earlier?

Can a Blood Test Detect a Range of Cancers Earlier?A new genetic blood test might pave the way for detecting early stage cancers that often prove fatal when caught too late, a new study suggests.

The test scans blood for DNA fragments released by cancerous tumors, explained lead researcher Dr. Victor Velculescu.

By reviewing these DNA fragments for mutations found in 58 “cancer-driver” genes, the blood test detects many early stage cancers without rendering false positives for healthy people, said Velculescu, co-director of cancer biology at the Johns Hopkins Kimmel Cancer Center, in Baltimore.

The test detected stage 1 or 2 colon, breast, lung or ovarian cancers between 59 percent and 71 percent of the time when assessing 200 patients previously diagnosed with cancer, researchers found.

“If we are able to detect cancer earlier, our chances of saving lives would be much higher,” Velculescu said. “The survival difference between late-stage and early stage disease in these cancers accounts for over a million lives worldwide each year.”

The test also proved capable of screening out cancer-free people.

Dr. Len Lichtenfeld, deputy chief medical officer for the American Cancer Society, called this “important research” that “moves us one step further down the path to developing a blood test that might find cancer earlier.”

“We still need to improve the sensitivity, but this is a step forward. It is a proof of concept,” Lichtenfeld said. “It is not a test that’s going to be available in a clinical laboratory anytime soon.”

To develop a genetic blood test for cancer, researchers must find ways to spot DNA mutations linked to cancer while ignoring natural and harmless mutations that regularly occur in humans, Velculescu explained.

Velculescu and his team developed a genetic scan that essentially “takes a fragment here and a fragment there and uses it to create a picture of what the tumor DNA looks like,” Lichtenfeld said. “That’s what makes it so elegant.”

The research team assembled a panel of 58 cancer-linked genes, and used their scan to look for tumor DNA fragments in the blood of 200 people known to have cancer.

Overall, researchers detected about 62 percent of stage 1 and 2 cancers.

The test specifically spotted early stage colon cancer 71 percent of the time, breast and lung cancer 59 percent of the time, and ovarian cancer 68 percent of the time.

The ability to catch early stage ovarian cancer is particularly needed, Lichtenfeld said. Fewer than one in five ovarian cancers are caught early, when the five-year survival rate is greater than 90 percent. Most are detected after they’ve spread, and by then the odds of five-year survival are 40 percent or less, he said.

“Finding any marker in a stage 1 ovarian cancer patient is very important, because this is a tumor that usually presents at a much later stage,” Lichtenfeld said.

The researchers also directly tested cancerous tissue removed from half of the 200 cancer patients. They found that 82 percent of the tumors contained mutations that correlated with DNA fragments found in the person’s blood.

To check the blood test’s ability to weed out healthy people, the researchers also analyzed blood from 44 volunteers without cancer. No false positives occurred.

That equates to less than one false positive for more than 3.5 million letters of DNA sequenced, since each separate test requires assessment of 80,000 DNA base pairs associated with the 58-gene screening panel, Velculescu said.

Despite these promising results, researchers need to validate the blood test in larger studies, Velculescu said.

More work also needs to be done to improve the detection rate, Lichtenfeld added. “These tests were not able to detect 100 percent of the cancers,” he said.

Finally, cancer doctors must discuss what will be done when technology evolves to the point that such tests regularly find tumors that aren’t life-threatening, Lichtenfeld said. In some cases, treatment to remove the cancer could be worse than leaving it alone.

“What’s going to be so important is to be able to distinguish cancers that will hurt people versus cancers that may not have long-term impact on survival,” Lichtenfeld said.

The report appears in the Aug. 16 issue of the journal Science Translational Medicine.

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Scientists Develop Blood Test That Spots Tumor-Derived DNA In People With Early-Stage Cancers

In a bid to detect cancers early and in a noninvasive way, scientists at the Johns Hopkins Kimmel Cancer Center report they have developed a test that spots tiny amounts of cancer-specific DNA in blood and have used it to accurately identify more than half of 138 people with relatively early-stage colorectal, breast, lung and ovarian cancers. The test, the scientists say, is novel in that it can distinguish between DNA shed from tumors and other altered DNA that can be mistaken for cancer biomarkers.

A report on the research, performed on blood and tumor tissue samples froScientists Develop Blood Test That Spots Tumor-Derived DNA In People With Early-Stage Cancersm 200 people with all stages of cancer in the U.S., Denmark and the Netherlands, appears in the Aug. 16 issue of Science Translational Medicine.

“This study shows that identifying cancer early using DNA changes in the blood is feasible and that our high accuracy sequencing method is a promising approach to achieve this goal,” says Victor Velculescu, M.D., Ph.D., professor of oncology at the Johns Hopkins Kimmel Cancer Center.

Blood tests for cancer are a growing part of clinical oncology, but they remain in the early stages of development. To find small bits of cancer-derived DNA in the blood of cancer patients, scientists have frequently relied on DNA alterations found in patients’ biopsied tumor samples as guideposts for the genetic mistakes they should be looking for among the masses of DNA circulating in those patients’ blood samples.

To develop a cancer screening test that could be used to screen seemingly healthy people, scientists had to find novel ways to spot DNA alterations that could be lurking in a person’s blood but had not been previously identified.

“The challenge was to develop a blood test that could predict the probable presence of cancer without knowing the genetic mutations present in a person’s tumor,” says Velculescu.

The goal, adds Jillian Phallen, a graduate student at the Johns Hopkins Kimmel Cancer Center who was involved in the research, was to develop a screening test that is highly specific for cancer and accurate enough to detect the cancer when present, while reducing the risk of “false positive” results that often lead to unnecessary overtesting and overtreatments.

The task is notably complicated, says Phallen, by the need to sort between true cancer-derived mutations and genetic alterations that occur in blood cells and as part of normal, inherited variations in DNA.

As blood cells divide, for example, Velculescu says there is a chance these cells will acquire mistakes or mutations. In a small fraction of people, these changes will spur a blood cell to multiply faster than its neighboring cells, potentially leading to pre-leukemic conditions. However, most of the time, the blood-derived mutations are not cancer-initiating.

His team also ruled out so-called “germline” mutations. While germline mutations are indeed alterations in DNA, they occur as a result of normal variations between individuals, and are not usually linked to particular cancers.

To develop the new test, Velculescu, Phallen and their colleagues obtained blood samples from 200 patients with breast, lung, ovarian and colorectal cancer. The scientists’ blood test screened the patients’ blood samples for mutations within 58 genes widely linked to various cancers.

Overall, the scientists were able to detect 86 of 138 (62 percent) stage I and II cancers. More specifically, among 42 people with colorectal cancer, the test correctly predicted cancer in half of the eight patients with stage I disease, eight of nine (89 percent) with stage II disease, nine of 10 (90 percent) with stage III and 14 of 15 (93 percent) with stage IV disease. Of 71 people with lung cancer, the scientists’ test identified cancer among 13 of 29 (45 percent) with stage I disease, 23 of 32 (72 percent) with stage II disease, three of four (75 percent) with stage III disease and five of six (83 percent) with stage IV cancer. For 42 patients with ovarian cancer, 16 of 24 (67 percent) with stage I disease were correctly identified, as well as three of four (75 percent) with stage II disease, six of eight (75 percent) with stage III cancer and five of six (83 percent) with stage IV disease. Among 45 breast cancer patients, the test spotted cancer-derived mutations in two of three (67 percent) patients with stage I disease, 17 of 29 (59 percent) with stage II disease and six of 13 (46 percent) with stage III cancers.

They found none of the cancer-derived mutations among blood samples of 44 healthy individuals.

Despite these initial promising results for early detection, the blood test needs to be validated in studies of much larger numbers of people, say the scientists.

Velculescu and his team also performed independent genomic sequencing on available tumors removed from 100 of the 200 patients with cancer and found that 82 (82 percent) had mutations in their tumors that correlated with the genetic alterations found in the blood.

The Johns Hopkins-developed blood test uses a type of genomic sequencing the researchers call “targeted error correction sequencing.” The sequencing method is based on deep sequencing, which reads each chemical code in DNA 30,000 times. “We’re trying to find the needle in the haystack, so when we do find a DNA alteration, we want to make sure it is what we think it is,” says Velculescu.

Such deep sequencing, covering more than 80,000 base pairs of DNA, has the potential to be very costly, but Velculescu says sequencing technology is becoming cheaper, and his research team may eventually be able to reduce the number of DNA locations they screen while preserving the test’s accuracy.

He says the populations that could benefit most from such a DNA-based blood test include those at high risk for cancer including smokers — for whom standard computed tomography scans for identifying lung cancer often lead to false positives — and women with hereditary mutations for breast and ovarian cancer within BRCA1 and BRCA2 genes.

To read this entire article on EurekAlert!, please click here.

Olaparib Extends PFS in Relapsed Ovarian Cancer, With Good QOL

Olaparib Extends PFS in Relapsed Ovarian Cancer, With Good QOLOlaparib tablet maintenance therapy provided a significant improvement in progression-free survival (PFS) over placebo in patients with relapsed, platinum-sensitive ovarian cancer with a BRCA1/2 mutation, according to a new phase III trial. Toxicity was generally manageable with the therapy.

Though advanced ovarian cancer patients often respond well to first-line chemotherapy, subsequent lines of therapy after recurrence have less and less beneficial effect. “A substantial unmet need exists for well tolerated therapies that can improve long-term disease control in patients with recurrent ovarian cancer,” wrote study authors led by Eric Pujade-Lauraine, MD, PhD, of Université Paris Descartes in France.

The PARP inhibitor olaparib has shown promise in phase II all-comer studies of relapsed ovarian cancer. The new study aimed to confirm this in a phase III setting of relapsed ovarian cancer with BRCA1 or BRCA2 mutations. It included 295 patients, randomized to either olaparib (196 patients) or placebo (99 patients); all had received at least two lines of previous chemotherapy. The study was published online ahead of print in Lancet Oncology.

After a median follow-up of approximately 22 months, the investigator-assessed PFS was 19.1 months with olaparib and 5.5 months with placebo, for a hazard ratio (HR) of 0.30 (95% CI, 0.22–0.41; P < .0001). The 12-month PFS rate was 65% with the study drug, and 21% with placebo. At 24 months, these rates were 43% and 15%, respectively.

The median time to first subsequent therapy was 27.9 months with olaparib and 7.1 months with placebo. The median time to progression was not reached in the olaparib group, while it was 18.4 months in the placebo group. Overall survival data was not yet mature, but as of this analysis there was no difference between the groups, with an HR of 0.80 (95% CI, 0.50–1.31; P = .43).

Measures of quality of life, based on the FACT-O assessment, were no different between olaparib and placebo.

The overall incidence of grade 3–5 adverse events (AEs) in the study was low. The most common grade 3 or worse AE with olaparib was anemia (18% grade 3, 1% grade 4, vs 2% and 0% with placebo). Serious AEs were seen in 18% of olaparib and 8% of placebo patients.

“The improvement in PFS seen using the olaparib tablet formulation in this disease setting is compelling because patients were able to maintain a good quality of life while experiencing a delay in disease progression and, therefore, a delay until the symptoms associated with subsequent chemotherapy treatments,” the authors wrote.

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