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SUNDAY, June 4, 2017 (HealthDay News) -- A twice-daily pill could help some advanced breast cancer patients avoid or delay follow-up sessions of chemotherapy, a new clinical trial reports.

The drug olaparib (Lynparza) reduced the chances of cancer progression by about 42 percent in women with breast cancer linked to BRCA1 and BRCA2 gene mutations, according to the study.

Olaparib delayed cancer progression by about three months. The drug also caused tumors to shrink in three out of five patients who received the medication, the researchers reported.

"Clearly the drug was more effective than traditional chemotherapy," said Dr. Len Lichtenfeld, deputy chief medical officer for the American Cancer Society.

"This is a group where a response is more difficult to obtain -- a young group with a more aggressive form of cancer -- and nonetheless we saw a close to 60 percent objective response rate," he said.

The study was funded by AstraZeneca, the maker of Lynparza.

Olaparib works by cutting off the avenues that malignant cancer cells use to stay alive, said lead researcher Dr. Mark Robson. He's a medical oncologist and clinic director of Clinical Genetics Service at Memorial Sloan Kettering Cancer Center in New York City.

The drug inhibits PARP, an enzyme that helps cells repair damaged DNA, Robson said.

Normal cells denied access to PARP will turn to the BRCA genes for help, since they also support the repair of damaged DNA, Robson said.

But that "backup capability" is not available to breast cancer cells in women with BRCA gene mutations, Robson said.

"When you inhibit PARP, the cell can't rescue itself," Robson said. "In theory, you should have a very targeted approach, one specifically directed at the cancers in people who have this particular inherited predisposition."

Olaparib already has been approved by the U.S. Food and Drug Administration for use in women with BRCA-related ovarian cancer. Robson and his colleagues figured that it also should be helpful in treating women with breast cancer linked to this genetic mutation.

The study included 302 patients who had breast cancer that had spread to other areas of their body (metastatic breast cancer). All of the women had an inherited BRCA mutation.

They were randomly assigned to either take olaparib twice a day or receive standard chemotherapy. All of the patients had received as many as two prior rounds of chemotherapy for their breast cancer. Women who had hormone receptor-positive cancer also had been given hormone therapy.

After 14 months of treatment, on average, people taking olaparib had a 42 percent lower risk of having their cancer progress compared with those who received another round of chemotherapy, Robson said.

The average time of cancer progression was about seven months with olaparib compared with 4.2 months with chemotherapy.

Tumors also shrank in about 60 percent of patients given olaparib. That compared with a 29 percent reduction for those on chemotherapy, the researchers said.

Severe side effects also were less common with olaparib. The drug's side effects bothered 37 percent of patients compared with half of those on chemo. The drug's most common side effects were nausea and anemia.

"There were fewer patients who discontinued treatment because of toxicity compared to those who received chemotherapy," Robson said. "Generally it was pretty well tolerated."

Only about 3 percent of breast cancers occur in people with BRCA1 and BRCA2 mutations, the researchers said in background notes.

Despite this, the results are "quite exciting," said Dr. Julie Fasano, an assistant professor of hematology and medical oncology at the Icahn School of Medicine at Mount Sinai in New York City.

Olaparib could wind up being used early in the treatment of metastatic breast cancer as an alternative to chemotherapy, and future studies might find that the drug is effective against other forms of breast cancer, Fasano said.

"It may be a practice-changing study, in terms of being able to postpone IV chemotherapy and its associated side effects" like hair loss and low white blood cell counts, Fasano said.

Lichtenfeld noted that olaparib also places less burden on patients.

"It may be easier for women to take two pills a day rather than go in for regular chemotherapy," Lichtenfeld said. "Clearly, this is a treatment that will garner considerable interest.

The findings were scheduled to be presented Sunday at the American Society of Clinical Oncology's annual meeting, in Chicago. The study was also published June 4 in the New England Journal of Medicine.

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Drug Helps Fight Breast Tumors Tied to 'Cancer Genes' - Sioux City Journal

By Laurie McginleyThe Washington Post

The oncologist was blunt: Stefanie Joho's colon cancer was raging out of control and there was nothing more she could do. Flanked by her parents and sister, the 23-year-old felt something wet on her shoulder. She looked up to see her father weeping.

"I felt dead inside, utterly demoralized, ready to be done," Joho remembers.

But her younger sister couldn't accept that. When the family got back to Joho's apartment in New York's Flatiron district, Jess opened her laptop and began searching frantically for clinical trials, using medical words she'd heard but not fully understood. An hour later, she came into her sister's room and showed her what she'd found.

"I'm not letting you give up," she told Stefanie. "This is not the end."

That search led to a contact at Johns Hopkins University, and a few days later, Joho got a call from a cancer geneticist co-leading a study there.

"Get down here as fast as you can!" Luis Diaz said. "We are having tremendous success with patients like you."

What followed is an illuminating tale of how one woman's intersection with experimental research helped open a new frontier in cancer treatment with approval of a drug that, for the first time, targets a genetic feature in a tumor rather than the disease's location in the body.

The breakthrough, now made official by the Food and Drug Administration, immediately could benefit some patients with certain kinds of advanced cancer that aren't responding to chemotherapy. Each should be tested for that genetic signature, scientists stress.

"These are people facing death sentences," said Hopkins geneticist Bert Vogelstein. "This treatment might keep some of them in remission for a long time."

A pivotal small trial

In August 2014, Joho stumbled into Hopkins for her first infusion of the immunotherapy drug Keytruda. She was in agony from a malignant mass in her midsection, and even with the copious amounts of OxyContin she was swallowing, she needed a new fentanyl patch on her arm every 48 hours. Yet within just days, the excruciating back pain had eased. Then an unfamiliar sensation hunger returned. She burst into tears when she realized what it was.

As months went by, her tumor shrank and ultimately disappeared. She stopped treatment this past August, free from all signs of disease.

The small trial in Baltimore was pivotal, and not only for the young marketing professional. It showed that immunotherapy could attack colon and other cancers thought to be unstoppable. The key was their tumors' genetic defect, known as mismatch repair (MMR) deficiency akin to a missing spell-check on their DNA. As the DNA copies itself, the abnormality prevents any errors from being fixed. In the cancer cells, that means huge numbers of mutations that are good targets for immunotherapy.

The treatment approach isn't a panacea, however. The glitch under scrutiny which can arise spontaneously or be inherited is found in just 4 percent of cancers overall. But bore in on a few specific types, and the scenario changes dramatically. The problem occurs in up to 20 percent of colon cancers and about 40 percent of endometrial malignancies cancer in the lining of the uterus.

In the United States, researchers estimate that initially about 15,000 people with this defect may be helped by this immunotherapy. That number is likely to rise sharply as doctors begin using it earlier on eligible patients.

Joho was among the first.

Even before Joho got sick, cancer had cast a long shadow on her family. Her mother has Lynch syndrome, a hereditary disorder that sharply raises the risk of certain cancers, and since 2003, Priscilla Joho has suffered colon cancer, uterine cancer and squamous cell carcinoma of the skin.

Stefanie's older sister, Vanessa, had already tested positive for Lynch syndrome, and Stefanie planned to get tested when she turned 25. But at 22, several months after she graduated from New York University, she began feeling unusually tired. She blamed the fatigue on her demanding job. Her primary-care physician, aware of her mother's medical history, ordered a colonoscopy.

When Joho woke up from the procedure, the gastroenterologist looked "like a ghost," she said. A subsequent CT scan revealed a very large tumor in her colon. She'd definitely inherited Lynch syndrome.

She underwent surgery in January 2013 at Philadelphia's Fox Chase Cancer Center, where her mother had been treated. The news was good: The cancer didn't appear to have spread, so she could skip chemotherapy and follow up with scans every three months.

By August of that year, though, Joho started having relentless back pain. Tests detected the invasive tumor in her abdomen. Another operation, and now she started chemo. Once again, in spring 2014, the cancer roared back. Her doctors in New York, where she now was living, switched to a more aggressive chemo regimen.

"This thing is going to kill me," Joho remembered thinking. "It was eating me alive."

Genetics meets immunology

Joho began planning to move to her parents' home in suburban Philadelphia: "I thought, 'I'm dying, and I'd like to breathe fresh air and be around the green and the trees.' "

Her younger sister wasn't ready for her to give up. Jess searched for clinical trials, typing in "immunotherapy" and other terms she'd heard the doctors use. Up popped a trial at Hopkins, where doctors were testing a drug called pembrolizumab.

"Pembro" is part of a class of new medications called checkpoint inhibitors that disable the brakes that keep the immune system from attacking tumors. In September 2014, the treatment was approved by the FDA for advanced melanoma and marketed as Keytruda. The medication made headlines in 2015 when it helped treat former President Jimmy Carter for melanoma that had spread to his brain and liver. It later was cleared for several other malignancies.

Yet researchers still don't know why immunotherapy, once hailed as a game changer, works in only a minority of patients. Figuring that out is important for clinical as well as financial reasons. Keytruda, for example, costs about $150,000 a year.

By the time Joho arrived at Hopkins, the trial had been underway for a year. While an earlier study had shown a similar immunotherapy drug to be effective for a significant proportion of patients with advanced melanoma or lung or kidney cancer, checkpoint inhibitors weren't making headway with colon cancer. A single patient out of 20 had responded in a couple of trials.

Why did some tumors shrink while others didn't? What was different about the single colon cancer patient who benefited? Drew Pardoll, director of the Bloomberg-Kimmel Institute for Cancer Immunotherapy at Hopkins, and top researcher Suzanne Topalian took the unusual step of consulting with the cancer geneticists who worked one floor up.

"This was the first date in what became the marriage of cancer genetics and cancer immunology," Pardoll said.

In a brainstorming session, the geneticists were quick to offer their theories. They suggested that the melanoma and lung cancer patients had done best because those cancers have lots of mutations, a consequence of exposure to sunlight and cigarette smoke. The mutations produce proteins recognized by the immune system as foreign and ripe for attack, and the drug boosts the system's response.

And that one colon-cancer patient? As Vogelstein recalls, "We all said in unison, 'He must have MMR deficiency!' " because such a genetic glitch would spawn even more mutations.

When the patient's tumor tissue was tested, it was indeed positive for the defect.

The researchers decided to run a small trial, led by Hopkins immunologist Dung Le and geneticist Diaz, to determine whether the defect could predict a patient's response to immunotherapy. The pharmaceutical company Merck provided its still-experimental drug pembrolizumab. Three groups of volunteers were recruited: 10 colon cancer patients whose tumors had the genetic problem; 18 colon cancer patients without it; and 7 patients with other malignancies with the defect.

The first results, published in 2015 in the New England Journal of Medicine, were striking. Four out of the 10 colon cancer patients with the defect and 5 out of the other 7 cancer patients with the abnormality responded to the drug. In the remaining group, nothing. Since then, updated numbers have reinforced that a high proportion of patients with the genetic feature benefit from the drug, often for a lengthy period. Other trials by pharmaceutical companies have shown similar results.

The Hopkins investigators found that tumors with the defect had, on average, 1,700 mutations, compared with only 70 for tumors without the problem. That confirmed the theory that high numbers of mutations make it more likely the immune system will recognize and attack cancer if it gets assistance from immunotherapy.

For Joho, now 27 and living in suburban Philadelphia, the hard lesson from the past few years is clear: The cancer field is changing so rapidly that patients can't rely on their doctors to find them the best treatments.

"Oncologists can barely keep up," she said. "My sister found a trial I was a perfect candidate for, and my doctors didn't even know it existed."

Her first several weeks on the trial were rough, and she still has some lasting side effects today joint pain in her knees, minor nausea and fatigue.

"I have had to adapt to some new limits," she acknowledged. "But I still feel better than I have in five years."

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IT'S A START: Newly approved gene therapy may help 4 percent of cancer patients - Sarasota Herald-Tribune

Scientist in Baltimore has discovered a catfish gene that, when activated in a rodent brain, can sense electromagnetic fields. There are numerous animals, throughout all types and species, expect humans (supposedly), that can sense the feeble network of Earths electromagnetic global field. The glass catfish is one of those animals and Galit Pelled, the lead researcher and associate professor at John Hopkins University School of Medicine and Kennedy Kreiger Institute, plus his team are hoping its electromagnetic perceptive gene (EPG) will one day be used to manipulate heart and brain cells. This non-evasive wireless technique of controlling human cells could replace pacemakers, treat epilepsy, or even help create an interface between the human brain and a machine.

Previously, researchers discovered similar genes in bacteria and birds but those created a chemical compound responsible for sensing the magnetic fields. This recent discovery, which was presented by Pelled at the 2017 International IEEE EMBS Conference on Neural Engineering, is different since the gene works alone for function and is, therefore, simpler to manipulate.

By injecting different strands of the catfish gene into frog eggs, Pelled and his lab mates were eventually able to discover which eggs responded to magnets and which bits of DNA were responsible for the electromagnetic perception.

While Assaf Gilad, co-author of the study and an associate professor of radiology at Johns Hopkins Medicine, says We dont know exactly what the protein is doing, they do know the end result. The responsible protein adheres to a cell surface and then the cell is filled with calcium. In heart cells and neurons, a sudden flush of calcium turns the cell on, so it begins to beat or fire. By expressing the genes in a group of brain cells, and later, a living rat brain, the team of researchers could activate the neural cells with only an electromagnetic field and no other devices.

Currently, doctors are able to treat conditions such as epilepsy and depression, ailments related to misfiring neurons, using invasive deep brain stimulation. Gilad hopes that with EPGs, delivered by gene therapy or transplants, these illnesses could be eased through wireless manipulation instead. Similarly, electromagnetic genes have the likelihood to be useful for heart conditions too, replacing traditional pacemakers with a biological one made EPGs. The ability to remotely control neuronal activity is big, says Gilad. But its still in the early, experimental stages.

At the moment, researchers have only identified one part of the glass catfishs electromagnetic sensing abilities and their current focus is understanding the system in general with immediate medical applications as their goal.

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