Cancer Super-Survivors Use Their Own Bodies To Fight The Disease
Cancer Super-Survivors Use
Their Own Bodies To Fight The Disease
Their Own Bodies To Fight The Disease
Updated 8-21-2016
Collaborations Provide Major Advance in Cancer Treatment
Researchers may have solved a puzzle about which patients will
benefit from immunotherapy
A collaboration between an immunologist helping his stepmother fight cancer and the oncologist who treated her led to a discovery that could help many more patients benefit from a transformative new therapy.
A new class of drugs called checkpoint inhibitors works by releasing a molecular brake that stops the immune system from attacking tumors. So-called immunotherapy has been approved for several types of cancers and found to extend lives of patients with advanced disease for many years. The problem is that for most patients immunotherapy
doesn't work.
The researchers, from University of California, San Francisco, said
they identified a unique type of immune-system cell that "robustly"
predicts whether patients will respond to one of the medicines-an
achievement has the potential to significantly expand the number of
cancer patients who benefit from checkpoint inhibitors.
The new discovery is based on a high-tech analysis of melanoma tissue from 40 patients treated with a checkpoint inhibitor from Merck And Co. called Keytruda, which targets an immune-system brake called PD-1. Although researchers say it will take further research to determine its value in treating patients, the finding offers fresh insight into the complex relationship between the immune system and tumor cells.
"This tells us a lot of important biology," said Jedd Wolchok, chief
of the melanoma and immunotherapies service at Memorial Sloan
Kettering Cancer Center, New York, who wasn't involved with the
research. "It fits with many hypotheses many of us have had about who these treatments work best in." A report on the finding was published online August 15 in the Journal of Clinical Investigation.
The discovery might not have occurred at all had two researchers not met. In 2012, Michael Rosenblum, a physician-scientist who runs a basic-science immunology lab at UCSF, learned his stepmother, Jackie Rosenblum, now 65, had been diagnosed with a rare form of advanced melanoma in her lung, a recurrence of cancer that originally appeared as a skin lesion and had been removed a few years earlier. She was given six months to live.
Dr. Rosenblum had heard about Adil Daud, another UCSF clinical
researcher who was treating patients with skin cancer, and the
exciting results Dr. Daud was seeing in clinical trials with
checkpoint inhibitors. "I cold-called him," Dr. Rosenblum says. The
two men were both in UCSF's dermatology department, although Dr. Rosenblum interest is in inflammatory skin diseases, not cancer.
After initial conversations between the two researchers, Ms.
Rosenblum flew in from her home in North Carolina to see Dr. Daud. He treated her initially with Yervoy, a checkpoint inhibitor marketed by Bristol-Myers Squibb Co. that targets an immune-system brake called CTLA-4. She stopped taking it after developing colitis, one of that drug's potential serious side effects.
In June 2013, Dr. Daud enrolled her in a clinical dose-escalation
trial in which she would be treated with Merck's Keytruda, then known as pembrolizumab.
The two scientists' collaborated on research that focuses on PD-1, a
protein that appears on the surface of immune cells and the target of
the two most popular checkpoint drugs, Keytruda and Bristol-Myers's Opdivo. A biomarker for PD-1 already exists but it has limitations: Patients whose tumors have high levels of a PD-1 related protein called PD-L1 appear to have a better response to therapies targeting PD-1. But some patients with low PD-L1 levels also benefit-meaning that it can help guide some treatment decisions but isn't useful for ruling out anti-PD-1 therapy.
Dr. Rosenblum's lab had developed a technique for analyzing immune cells in tumors and other tissue that he says is more comprehensive than conventional methods. At the beginning of their collaboration he invited Dr. Daud to "send me some samples."
The prevailing theory of how checkpoint inhibitors work is based on evidence that immune-system fighters called CD8 cells, which are normally primed to kill enemy cells, initially see and infiltrate
tumors but can end up in a state of chronic activation, too exhausted to mount an effective attack.
Using the lab's laser-based flow cytometry technology, Dr. Rosenblum and his colleagues identified a candidate CD8 cell that had infiltrated tumors marked by levels of not only PD-1 but also of a second immune-system brake called CTLA-4.
The researchers analyzed results of a study involving Keytruda before it was approved. They looked at the CD8 cells that had infiltrated the melanoma tumors of 20 patients treated with the drug and found that if at least 30% of those cells were marked by PD-1 and CTLA-4, the patient responded to treatment. When fewer than 20% of the infiltrated cells had those markers, not one patient responded.
They did a second similar study on 20 more patients and got the same result. Results varied for patients whose CD8 cells fell between 20% and 30%, making them prime candidates, Dr. Daud suggested, for a combination immunotherapy regimen to potentially increase their chances of a response.
Further analysis showed that the anti-PD1 drug reactivated the
exhausted CD8 cells, and when they were in sufficient numbers, they were able to mount an effective attack on the tumor.
Memorial Sloan Kettering's Dr. Wolchok called the study "a really
important piece of work," but cautioned that among other things, it
needs to be further validated in more patients. Dr. Rosenblum
acknowledged that few hospitals or labs are equipped to perform the analysis, suggesting further work is necessary for it to be easily
adapted to patient care.
But the findings did show that the particular CD8 cells identified
"are the guys that are doing all the work to kill the tumor," Dr.
Rosenblum noted. Researchers are already exploring whether it's
possible to retrieve such cells from the tumor, expand them into huge quantities outside the body and infuse them back into
patients-possibly using a PD-1 inhibitor-to increase the number of
patients who respond.
As for Ms. Rosenblum, 12 weeks after she began treatment with
Keytruda, a CT scan showed that her tumors had shrunk by 70%. She recalls Dr. Daud delivering the news to her by phone while she was on a train. He told her she was "a golden child"; she burst into tears. Her tumors ultimately disappeared. She stopped treatment in June of 2014, about a year after she started, and remains free of any
evidence of disease.
How the Promise of Immunotherapy Is Transforming Oncology
Updated 4-17-2016
More than one-third of advanced melanoma patients treated in a study of Bristol-Myers Squibb Co.’s Opdivo have survived at least five years, researchers said, providing fresh evidence of the durable benefit cancer immunotherapy agents have for some patients.
The study followed 107 patients who were enrolled in an early trial of the drug, which was approved for melanoma by the U.S. Food and Drug Administration in 2014. Thirty-four percent of the participants, all of whom had failed on other drugs, were still alive five years after treatment.
“This is a new benchmark for melanoma,” said F. Stephen Hodi, director of the Melanoma Center at Dana-Farber Cancer Institute, Boston, and an investigator at Harvard Medical School’s Ludwig Center.
Dr. Hodi presented the findings at the annual meeting of the American Association for Cancer Research in New Orleans. The AACR said a National Cancer Institute database shows that the five-year survival rate for patients diagnosed with advanced melanoma between 2005 and 2011 was 16.6%.
Opdivo is one of three so-called checkpoint inhibitors currently on the market. Blocking the checkpoints releases molecular brakes, thus allowing immune system cells called T cells to attack cancer. Opdivo, and a rival called Keytruda from Merck & Co. target a brake called PD-1. (Both are approved for melanoma and for lung cancer.)
The first checkpoint inhibitor to reach the market was Yervoy, also from Bristol-Myers. It targets a brake known as CTLA-4 and in a previous analysis was shown to result in long-term survival in about 22% of melanoma patients.
The Yervoy results, and now the new findings for Opdivo, are especially significant, oncologists said, because they suggest, in each case, patients who survive a certain length of time—three years for Yervoy and about four years for Opdivo—are highly unlikely to relapse. That is essentially an unheard-of result in advanced cancer. The treatments appear to have enabled their immune systems to eradicate or take control of their tumors.
“People who have good responses really seem to be protected against their disease returning in many cases,” said Louis M. Weiner, director of the Georgetown Lombardi Comprehensive Cancer Center, Washington, D.C., who wasn’t involved in the studies. “This is a mark of distinction in immunotherapy.”
Still, two-thirds of melanoma patients aren’t as lucky. But the success that has been achieved has sparked a wave of interest in cancer immunotherapy treatments among drug companies. Hundreds of clinical trials involving such agents, either alone or in combination with other drugs, are under way. The aim is to try to extend survival in more patients and find effective regimens against more types of cancer.
The new study is the first to look at long-term survival for an anti-PD-1 agent. Common side effects included a rash, a cough, and in serious cases, immune system attacks on healthy organs such as a the lung and the colon.
When school let out, though, Mr. Telford looked forward to relaxing on a 25th anniversary cruise with his wife. But once in the Caribbean, he struggled to swim and climbing from one deck to another exhausted him. Back at home, he collapsed while running a TV cable in his bedroom.
His family doctor told him he had lost two pints of blood. Further tests revealed a tumor the size of a quarter on his small intestine. He had surgery at Memorial Sloan Kettering Cancer Center, followed by months of chemotherapy. But the disease spread to his liver and kidneys. The diagnosis: Stage 4 melanoma, a skin cancer typically fatal within a year.
“Death is not an option,” he told his doctor.
Nine years later, against all odds, Mr. Telford is still alive. What saved him was an experimental immunotherapy drug—a medication that unleashes the body’s own immune system to attack cancer.
When his tumors began melting away more than eight years ago, Mr. Telford’s good fortune was largely an anomaly amid a mostly dreary landscape for advanced cancer. But his remarkable survival caught the attention of researchers, who began to realize that the way immunotherapy drugs were affecting tumors was unlike almost anything seen with conventional treatments.
Today Mr. Telford is among a growing group of super-survivors who are transforming the world of oncology. In both total numbers and duration of survival, they are charting new territory. And they are reviving hopes that the long-maligned idea of enlisting the power of the immune system against cancer may help to turn the tide against some of the most lethal and resistant forms of the disease.
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“It’s the most exciting thing I’ve ever seen,” says David Lane, scientific director of New York’s Ludwig Institute for Cancer Research. “It’s the long-term survival of people who have advanced disease. This is very unusual.”
Cancer immunotherapy comes in several forms. The drugs sparking the most interest are called checkpoint inhibitors. They work by releasing the natural brakes on the immune system, enabling its foot soldiers, called T cells, to attack tumors.
It is hard to know how many patients whose cancers have metastasized, or spread, have enjoyed sustained survival following immunotherapy treatment. An analysis of 4,846 advanced melanoma patients treated with one checkpoint inhibitor— Bristol-Myers Squibb Co. ’s Yervoy—found that 21% were still alive three years later. That amounts to more than 1,000 people, most of whom experts say almost certainly would have died otherwise. Especially striking is how good the long-term prospects were for people who survived at least three years.
“The people that make it after three years don’t die of melanoma,” says James Allison, head of immunology at MD Anderson Cancer Center in Houston, whose seminal discovery about the immune system and cancer in the mid-1990s laid the groundwork for many of the current advances.
Newer drugs that work similarly to Yervoy, but on different immune-system brakes, are getting even better early results and are extending the benefits beyond melanoma to other cancers.
Immunotherapy is still in its early stages, and more rigorous studies are needed. Oncology is filled with tales of advances that held promise only to be thwarted by cancer’s uncanny ability to develop resistance to medicine’s attacks. There isn’t any assurance that the new immunotherapy will be different.
Researchers and drug makers are striving to overcome huge obstacles to a lasting cure. For one, most patients don’t respond the way the super-survivors have, and researchers are just beginning to understand why. Another mystery is why some patients relapse while remaining on therapy while others go into prolonged remission after undergoing just one course of treatment.
Most experts believe it will take combinations of immunotherapy drugs—or combinations of immunotherapy with other cancer treatments—to optimize their impact. But finding safe and effective combinations is a daunting undertaking.
While side effects of the new drugs are relatively mild for some patients, others have developed potentially devastating complications caused by an out-of-control immune system. Some patients have died as a result. Researchers are devising ways to minimize such problems.
“It’s extremely exciting that so many patients are responding” to checkpoint inhibitors, says Bert Vogelstein, director of the Ludwig Center at Johns Hopkins Kimmel Cancer Center in Baltimore. “But the reality is that most are not.”
The drugs, which are costly to develop, are certain to fuel the debate about the cost of innovative drugs. Yervoy costs more than $120,000 for a four-course treatment, while Merck & Co’s Keytruda, approved in September for advanced melanoma, costs $12,500 a month, or $150,000 for a year.
More than 25 companies ranging from the pharmaceutical industry’s biggest names to a group of startups are pursuing some form of immunotherapy.
Bristol-Myers’s drug Yervoy, which is based on Dr. Allison’s discoveries, blocks an immune system brake called CTLA-4. Merck’s Keytruda inhibits a brake called PD-1. Bristol, Roche Holding AG and AstraZeneca PLC are among several companies also testing agents against checkpoint targets.
Another approach involves genetically modifying certain T cells outside the body, creating what are called CAR T cells, and infusing them back to attack targets on the surface of cancer cells.
Novartis AG , closely held Juno Therapeutics Inc., Kite Pharma Inc., and a collaboration between Bluebird bio and Celgene are pursuing this strategy. Amgen Inc. is developing yet another T-cell approach while several other companies are reviving efforts to develop cancer vaccines.
The efforts are a departure from most current cancer treatments, including chemotherapy, radiation and the new crop of medicines that target genetic mutations underlying a tumor’s growth. These strategies take direct aim at the tumor—generally to only limited effect in patients with advanced cancer. Even the recent excitement about genetically targeted drugs has been tempered by the ability of tumors to mutate and grow resistant to tailored attacks.
With immunotherapy, “We’re treating the immune system, not the cancer,” says Dr. Allison.
Richard Logan, a 59-year-old veterinarian in Ozark, Ala., embraced the alternative approach in 2009, soon after melanoma that had started as a bleeding mole on his back progressed to his lung and liver. He already had endured about a year of treatment with interferon, an immune-system booster with harsh side effects that left him exhausted.
In addition, his father had recently died of melanoma, succumbing about six months after the cancer had spread from its original site. “I pretty much knew the old treatments weren’t going to be much help,” he says.
An Internet search led him to the melanoma center at Boston’s Dana Farber Cancer Institute. In July 2009 he enrolled in a trial there for a drug that later became Yervoy. Within two months, his tumors started shrinking and by that December, he says, “I felt pretty confident I was going to have extended relief from this disease.”
Now nearly five years later, Dr. Logan says his cancer has stabilized. He remains on Yervoy, flying regularly to Boston for infusions. He rates the side effects on Yervoy as a “two or three” compared with a 10 on interferon. He continues to run his veterinary practice, saw his son graduate from college and recently remarried.
He doesn’t use the word “cure” to describe his status, saying only that he is “confident” in how he is doing on the drug. “If this starts to pale, I’m keeping aware of whatever else is available out there,” he says. “I’m pretty even-keel and take it as it comes.”
Getting the immune system to “see” and attack tumors has stymied researchers for decades. Unlike, say, a flu virus—an invader that quickly catches the immune system’s attention—a tumor cell may reflect only “modest changes in cells that the body has been taught to leave alone and tolerate,” says Walter J. Urba, director of cancer research at Providence Cancer Center in Portland, Ore. Moreover, he says, “cancer cells are pretty smart and they change in ways that can avoid the immune system.”
For years, scientists thought the immune system didn’t recognize tumors at all. Then research on biopsy specimens revealed that T cells often succeed in infiltrating the environment around tumors, but either fail to mount an adequate response or hold the cancer at bay for years before finally being overmatched.
When the T cell does recognize the tumor, it amounts to an ignition switch for the immune response. But just “turning the key” isn’t enough. T cells generally need a second so-called co-stimulatory signal to become activated against the cancer. That is the gas pedal.
For two to three decades, immunotherapy efforts have focused on the gas pedal. Researchers and companies have tested vaccines that educate T cells to find cancer cells and developed treatments to boost activated T cells and direct them at vulnerable targets on tumors. Despite some success against relatively rare cancers, results have proved lackluster.
Sharon Belvin was diagnosed with advanced melanoma 10 years ago, two weeks before her wedding. After chemotherapy, radiation and drug therapy failed to stop the cancer, she enrolled in a clinical trial for a new immunotherapy drug, now known as Yervoy. One year later, all evidence of her cancer had disappeared from scans. She now has two children and is a personal trainer.
“No matter what you did, only 10% to 15% of patients seemed to get a benefit,” says F. Stephen Hodi, director of the melanoma center at Dana Farber.
Getting the immune system to “see” and attack tumors has stymied researchers for decades. Unlike, say, a flu virus—an invader that quickly catches the immune system’s attention—a tumor cell may reflect only “modest changes in cells that the body has been taught to leave alone and tolerate,” says Walter J. Urba, director of cancer research at Providence Cancer Center in Portland, Ore. Moreover, he says, “cancer cells are pretty smart and they change in ways that can avoid the immune system.”
For years, scientists thought the immune system didn’t recognize tumors at all. Then research on biopsy specimens revealed that T cells often succeed in infiltrating the environment around tumors, but either fail to mount an adequate response or hold the cancer at bay for years before finally being overmatched.
When the T cell does recognize the tumor, it amounts to an ignition switch for the immune response. But just “turning the key” isn’t enough. T cells generally need a second so-called co-stimulatory signal to become activated against the cancer. That is the gas pedal.
For two to three decades, immunotherapy efforts have focused on the gas pedal. Researchers and companies have tested vaccines that educate T cells to find cancer cells and developed treatments to boost activated T cells and direct them at vulnerable targets on tumors. Despite some success against relatively rare cancers, results have proved lackluster.
Sharon Belvin was diagnosed with advanced melanoma 10 years ago, two weeks before her wedding. After chemotherapy, radiation and drug therapy failed to stop the cancer, she enrolled in a clinical trial for a new immunotherapy drug, now known as Yervoy. One year later, all evidence of her cancer had disappeared from scans. She now has two children and is a personal trainer.
“No matter what you did, only 10% to 15% of patients seemed to get a benefit,” says F. Stephen Hodi, director of the melanoma center at Dana Farber.
The insight that changed the equation came from Dr. Allison. In the early 1990s, researchers racing to unravel how T cells function homed in on a molecule called CTLA-4. They had suspected it was a “gas pedal” that activated the immune system. Dr. Allison, then at University of California Berkeley, was among those who determined that it actually inhibited the immune response—it was a brake.
That led him to a question: Would blocking CTLA-4 with a drug—in effect, suppressing the suppressor—unleash the immune system to attack cancer?
He and his colleagues fashioned an antibody to CTLA-4. In a study published in Science in 1996, they showed that the strategy, which prevented the immune system from turning off, led to the eradication of tumors in mice.
Translating that discovery into an FDA-approved medicine took 15 years. After shopping the antibody to skeptical drug companies for two years, Dr. Allison joined forces with a small company called Medarex Inc., then in Princeton, N.J. The initial human studies were encouraging enough to draw Bristol-Myers into a collaboration with Medarex to mount a large-scale study.
Early results were less than impressive. Tumors shrank sufficiently in only about 10% of patients—no better than was seen in other forms of immunotherapy, raising doubts the drug could be approved.
But researchers also noticed something unusual: Some patients were living much longer than expected, including some who had gone off therapy. Others reported feeling better even though their tumors hadn’t quickly responded by conventional measures.
One of them was Mr. Telford, the high-school teacher with advanced melanoma. In June 2006, with the encouragement of Jedd Wolchok, chief of melanoma and immunotherapy at Sloan Kettering, he enrolled in a study of the Bristol-Medarex anti-CTLA-4 drug. The protocol called for four treatments, one every three weeks. The goal: tumor shrinkage at 12 weeks.
It didn’t work. After Mr. Telford’s last infusion, his scans showed tumors in his liver had gotten much larger. Dr. Wolchok prepared to deliver the message oncologists dread: The drug wasn’t working and there weren’t any other options.
But in the exam room, Mr. Telford told the doctor: “This is the best I’ve felt in months.”
That led him to a question: Would blocking CTLA-4 with a drug—in effect, suppressing the suppressor—unleash the immune system to attack cancer?
He and his colleagues fashioned an antibody to CTLA-4. In a study published in Science in 1996, they showed that the strategy, which prevented the immune system from turning off, led to the eradication of tumors in mice.
Translating that discovery into an FDA-approved medicine took 15 years. After shopping the antibody to skeptical drug companies for two years, Dr. Allison joined forces with a small company called Medarex Inc., then in Princeton, N.J. The initial human studies were encouraging enough to draw Bristol-Myers into a collaboration with Medarex to mount a large-scale study.
Early results were less than impressive. Tumors shrank sufficiently in only about 10% of patients—no better than was seen in other forms of immunotherapy, raising doubts the drug could be approved.
But researchers also noticed something unusual: Some patients were living much longer than expected, including some who had gone off therapy. Others reported feeling better even though their tumors hadn’t quickly responded by conventional measures.
One of them was Mr. Telford, the high-school teacher with advanced melanoma. In June 2006, with the encouragement of Jedd Wolchok, chief of melanoma and immunotherapy at Sloan Kettering, he enrolled in a study of the Bristol-Medarex anti-CTLA-4 drug. The protocol called for four treatments, one every three weeks. The goal: tumor shrinkage at 12 weeks.
It didn’t work. After Mr. Telford’s last infusion, his scans showed tumors in his liver had gotten much larger. Dr. Wolchok prepared to deliver the message oncologists dread: The drug wasn’t working and there weren’t any other options.
But in the exam room, Mr. Telford told the doctor: “This is the best I’ve felt in months.”
When Dr. Wolchok insisted the scans showed no improvement, Mr. Telford recalls saying, “I don’t care what your scans say, I feel better.” His energy levels were up and his night sweats had stopped.
A mystified Dr. Wolchok told him to come back for another checkup in two months. This time, the tumors were getting smaller. By May 2007, his scans showed no evidence of cancer.
Mr. Telford remained on the drug until last December. He is essentially free of disease. Now 60 years old, he is still teaching and coaching baseball.
So exceptional was Mr. Telford’s case that he became known among immunotherapy researchers as “the liver guy,” Dr. Wolchok says. His experience “was a pivotal moment” that helped prompt Medarex and Bristol-Myers to change the primary measurement of the trial, Dr. Wolchok says. Instead of looking at how long the therapy kept cancer from progressing, a measure that can lead to approval of drugs for metastatic cancer, they opted to test for overall survival.
It took some 700 patients and extended the trial to 2010. In the end, fewer than 10% met standard criteria for tumor shrinkage. But 23% survived at least three years, making the drug the first to ever show a survival benefit in patients with advanced melanoma. The drug, now owned by Bristol-Myers and known as Yervoy, was approved in 2011.
The challenge was to widen the benefit to more patients and more cancers.
For reasons of biology, melanoma is more vulnerable than most other tumor types to attacks by the immune system. For immunotherapy to become a mainstay of cancer treatment, it needs to prove effective against more tumors.
A mystified Dr. Wolchok told him to come back for another checkup in two months. This time, the tumors were getting smaller. By May 2007, his scans showed no evidence of cancer.
Mr. Telford remained on the drug until last December. He is essentially free of disease. Now 60 years old, he is still teaching and coaching baseball.
So exceptional was Mr. Telford’s case that he became known among immunotherapy researchers as “the liver guy,” Dr. Wolchok says. His experience “was a pivotal moment” that helped prompt Medarex and Bristol-Myers to change the primary measurement of the trial, Dr. Wolchok says. Instead of looking at how long the therapy kept cancer from progressing, a measure that can lead to approval of drugs for metastatic cancer, they opted to test for overall survival.
It took some 700 patients and extended the trial to 2010. In the end, fewer than 10% met standard criteria for tumor shrinkage. But 23% survived at least three years, making the drug the first to ever show a survival benefit in patients with advanced melanoma. The drug, now owned by Bristol-Myers and known as Yervoy, was approved in 2011.
The challenge was to widen the benefit to more patients and more cancers.
For reasons of biology, melanoma is more vulnerable than most other tumor types to attacks by the immune system. For immunotherapy to become a mainstay of cancer treatment, it needs to prove effective against more tumors.
That is beginning to happen. Data presented at the American Society of Clinical Oncology meeting in June and at the European Society of Medical Oncology in September offered encouraging results for bladder, head and neck, kidney and other cancers. Checkpoint inhibitors are being tested in breast and pancreatic cancers, and Hodgkin lymphoma, multiple myeloma and other cancers.
The disease attracting intense interest is lung cancer, which causes more than 200,000 deaths a year in the U.S.
David Gobin, a retired Baltimore policeman, was diagnosed with lung cancer at 58. He lost much of his right lung to surgery and much of his spirit to aggressive chemotherapy, which failed.
In late 2010, he joined a trial at Johns Hopkins for an experimental Bristol-Myers drug that blocks the immune system brake called PD-1. The protocol called for a one-hour infusion every two weeks for two years.
Four months later, a scan showed his tumor had significantly improved. Remnants of the tumor still showed up on scans when his treatment ended after two years, but it hasn’t grown since.
“Every time we scanned him, things were decreasing,” says Julie Brahmer, his oncologist at Hopkins. “With the rate his disease was progressing back when I first met him, he shouldn’t be around.”
Mr. Gobin gets short of breath because of the lung surgery, and he needs to take frequent rests. He isn’t complaining.
Before being treated with the drug—now called nivolumab—he was twice told he had less than a year to live. He hasn’t taken the drug for 23 months.
“I still have a little cancer. It’s still sitting there,” he says. “It’s not doing anything.”
Most researchers believe that the key to expanding immunotherapy lies in combination treatments.
A 53-patient Bristol-Myers study combining Yervoy and nivolumab resulted in a two-year melanoma survival rate of 79%, but that came at a cost of serious side effects.
Researchers also are experimenting with pairing such drugs with vaccines or with treatments such as chemotherapy, radiation and genetically targeted drugs. The hope is that attacking the tumor with these approaches will make it more visible to T cells, a necessary step if releasing the brakes is to have a significant effect on the cancer.
“Almost every combination is appealing in some way,” says Roy Herbst, chief of medical oncology at Yale Cancer Center, but “how to sort through all that is incredibly difficult.”
The disease attracting intense interest is lung cancer, which causes more than 200,000 deaths a year in the U.S.
David Gobin, a retired Baltimore policeman, was diagnosed with lung cancer at 58. He lost much of his right lung to surgery and much of his spirit to aggressive chemotherapy, which failed.
In late 2010, he joined a trial at Johns Hopkins for an experimental Bristol-Myers drug that blocks the immune system brake called PD-1. The protocol called for a one-hour infusion every two weeks for two years.
Four months later, a scan showed his tumor had significantly improved. Remnants of the tumor still showed up on scans when his treatment ended after two years, but it hasn’t grown since.
“Every time we scanned him, things were decreasing,” says Julie Brahmer, his oncologist at Hopkins. “With the rate his disease was progressing back when I first met him, he shouldn’t be around.”
Mr. Gobin gets short of breath because of the lung surgery, and he needs to take frequent rests. He isn’t complaining.
Before being treated with the drug—now called nivolumab—he was twice told he had less than a year to live. He hasn’t taken the drug for 23 months.
“I still have a little cancer. It’s still sitting there,” he says. “It’s not doing anything.”
Most researchers believe that the key to expanding immunotherapy lies in combination treatments.
A 53-patient Bristol-Myers study combining Yervoy and nivolumab resulted in a two-year melanoma survival rate of 79%, but that came at a cost of serious side effects.
Researchers also are experimenting with pairing such drugs with vaccines or with treatments such as chemotherapy, radiation and genetically targeted drugs. The hope is that attacking the tumor with these approaches will make it more visible to T cells, a necessary step if releasing the brakes is to have a significant effect on the cancer.
“Almost every combination is appealing in some way,” says Roy Herbst, chief of medical oncology at Yale Cancer Center, but “how to sort through all that is incredibly difficult.”
Richard Murphy, a father of three from Marshfield, Mass., didn’t know what a biopsy was when he was diagnosed in 2008, at 43, with a rare form of melanoma. He underwent two surgeries and several bouts of radiation and chemotherapy, but his tumors spread to his lung and surrounded his spine. He enrolled in a study of Yervoy in February 2011.
After his fourth treatment at Dana Farber, scans showed his tumors had shrunk. But by August, he says, “everything kind of had grown.” Dr. Hodi soon concluded the drug wasn’t working and took him off the study.
Dr. Hodi had another idea. His colleagues at Dana Farber had played key roles in identifying PD-1 as an immune checkpoint, and a slot opened up in a study of an anti-PD-1 agent being developed by Merck that became known as Keytruda. In March 2012, Mr. Murphy had his first dose.
The day of his scheduled sixth treatment in June, a blood test showed “off-the-chart” levels of an enzyme that suggested possible muscle damage. He was hospitalized out of concern for possible kidney failure. Whether the PD-1 drug was responsible isn’t certain, but Dr. Hodi took him off the study.
The next day, an ultrasound to check his kidneys revealed something else: Mr. Murphy’s tumors were shrinking. By the end of August 2012, there wasn’t any evidence of disease on his scans, just shadows where tumors had been. His checkup this October showed the same.
Mr. Murphy, a real-estate agent, stages and participates in triathlons to raise money for cancer research.
“I was on two clinical trials and I was kicked off two clinical trials,” he says. “I don’t think you’d expect the outcome that we have. You wouldn’t expect that would be the pot of gold.”
Cancer has outwitted scientists and doctors for decades. More than 1,500 people still die of the disease every day in this country. But scientists will tell you they have learned more about cancer in the last five years than ever before. And no one is more optimistic about what that will mean for patients than Dr. Patrick Soon-Shiong. He's been called a genius, a showman, an innovator and a hypester. He's also the richest man in Los Angeles, a doctor and entrepreneur who is worth an estimated $11 billion.
Soon-Shiong was a respected surgeon before making his name in the cancer world by developing a multibillion dollar drug that few initially thought would work. He now wants to disrupt the conventional way we treat cancer and Soon-Shiong is overflowing with ideas on how to do it.
Give Dr. Patrick Soon-Shiong a white board and a few markers, and like a mad scientist he'll diagram how he thinks cancer can be beaten. He wants to attack on multiple fronts and is confident there is a pathway to the cure. For 45 minutes, he outlined his vision from beginning to end.
Sanjay Gupta: This is a crazy looking board (laughter)...
Patrick Soon-Shiong: This is what goes on in my head you know, this is, it's like bursting. It just has to get this stuff out right?
Sanjay Gupta: Are we looking inside your head?
Patrick Soon-Shiong: Yeah, I think so, a little bit (laughter)...
Sanjay Gupta: How long before we get to here?
Patrick Soon-Shiong: I'm incredibly encouraged to say that we are on the path. And the technology to actually do all these things is not just hypothetical.
Technology is the main weapon Soon-Shiong is deploying against cancer. In October, at his company's headquarters in Los Angeles, final tests were being run on high-speed tumor genome sequencing machines that Soon-Shiong is convinced will unmask the molecular secrets to cancer.
Patrick Soon-Shiong: And for the first time with this technology we can watch it, catch it, outsmart it, and play chess at this multi-dimensional level.
To understand the significance of what Soon-Shiong is touting, it's important to know what cancer is.
Patrick Soon-Shiong: A cancer is not what people think, cells growing. Cancer is actually the inability of the cells to die.
The key is figuring out the genetic mutation or glitch that prevents cells from dying a natural death. Soon-Shiong's hope is to provide patients with the precise genetic mutations that fuel their cancer regardless of where tumors are found in the body.
Patrick Soon-Shiong: The mutation that happens in lung cancer could be the exact same mutation that happens in the breast cancer. So you need to treat that patient based on its mutation not on its physical, anatomical location.
Sanjay Gupta: That's a big idea. I mean, you know, the idea that the breast cancer specialist, they're looking for breast cancer mutations and they may be missing the ball.
Patrick Soon-Shiong: Absolutely.
A lung cancer drug could work on breast cancer, for instance, if the mutation is the same.
The concept of doing away with labeling the disease by where it's found is not unique to Soon-Shiong, but it is a tectonic shift in the fight against cancer, the notion of classifying a cancer by its mutation.
Patrick Soon-Shiong: Imagine reclassifying cancer. And having people conceive and understand that cancer's a slew of rare diseases. So I am very excited because we are gonna create this revolution.
Sanjay Gupta: And what's it going to mean?
Patrick Soon-Shiong: Well, it's going to mean you have a better shot at having a better outcome and having a quality of life and actually turn the cancer hopefully into a chronic disease.
Sanjay Gupta: That's very optimistic. Realistic as well?
Patrick Soon-Shiong: I think so. Very much so.
Soon-Shiong has appointed himself to lead this revolution. Cancer genome sequencing is not new but what's different about Soon-Shiong's project is the scale. He has spent nearly a billion dollars of his own money to build a massive infrastructure, run by super computers, to find every single genetic mutation that could drive cancer.
This is Soon-Shiong's plan: A patient, anywhere in the world, has his tumor biopsied. The tumor cell's complete genetic map is then created all the way down to the proteins that are produced. What only recently took months can now be done in a day.
Ultimately, personalized information for each cancer patient would show up in the palm of his hand.
Patrick Soon-Shiong: This is the baby...
Sanjay Gupta: That's it, huh?
Patrick Soon-Shiong: It'll be the world's first browser of the cancer genome, so think about that. You'll be able to fly through to get to the single letter that's mutated.
He's teamed with Blackberry to produce a device that will identify for patients and doctors what they need to make more informed decisions.
Sanjay Gupta: At the end of the day, someone has a tumor and they could find out the complete analysis of that tumor and what the perfect drug is to treat it?
Patrick Soon-Shiong: Correct. That's what's exciting. It's not the end of the day. This is what we think we can bring to the world now.
But some in the cancer world fear Soon-Shiong is getting ahead of himself, that he's declaring victory before any of this has been proven to work consistently.
Derek Raghavan: It's show me the money, show me the data. Show me that it's true.
Patrick Soon-Shiong: Correct. That's what's exciting. It's not the end of the day. This is what we think we can bring to the world now.
But some in the cancer world fear Soon-Shiong is getting ahead of himself, that he's declaring victory before any of this has been proven to work consistently.
Derek Raghavan: It's show me the money, show me the data. Show me that it's true.
(Buy/Rent/Layaway)
Dr. Derek Raghavan, a renowned oncologist and researcher, is president of the Levine Cancer Institute in Charlotte, North Carolina.
Sanjay Gupta: Dr. Soon-Shiong says, 'Look, if we can figure out which mutation's driving cancer, we're gonna be able to find the drugs that treat cancer.' Is that a fair theory?
Dr. Derek Raghavan: Yes. That's a fair theory. But to say I can throw a tumor into a gizmo, and that gizmo will tell me the answer in a few minutes, and everything will flow from that, I don't think we're there now. I don't think we'll be there next year. I think there's just too much hard, complex science that has to be done before this is state of the art. But it's a very cool idea for the future.
Sanjay Gupta: Dr. Soon-Shiong says, 'Look, if we can figure out which mutation's driving cancer, we're gonna be able to find the drugs that treat cancer.' Is that a fair theory?
Dr. Derek Raghavan: Yes. That's a fair theory. But to say I can throw a tumor into a gizmo, and that gizmo will tell me the answer in a few minutes, and everything will flow from that, I don't think we're there now. I don't think we'll be there next year. I think there's just too much hard, complex science that has to be done before this is state of the art. But it's a very cool idea for the future.
The vast majority of mutations are actually not a threat. So to figure out which mutations are dangerous, Soon-Shiong is going back in time.
Patrick Soon-Shiong: This national treasure...
Sanjay Gupta: Wow...
In the basement of the John Wayne Cancer Institute in Santa Monica, California, decades of cancer tissues were stored by scientists in deep freeze vats. Now Soon-Shiong wants to use technology that didn't exist back then to map the genomes of these thousands of tissues in order to look for critical patterns.
Sanjay Gupta: So even after a patient died, their samples were stored here. They can go back, say, "Oh, they had this mutation." And now we can explain that this mutation actually leads to death. And other mutations may not.
Patrick Soon-Shiong: That's exactly right. And ask the question, "Why did this patient live and why did this patient die? Why did this treatment work, why did that not work?"
To make any of this work, Soon-Shiong believes you need to upend the way cancer drugs are developed. He's started a biotech company to try to dramatically ramp up production.
Patrick Soon-Shiong: I know it sounds an audacious goal but you need to actually develop 20 to 30 drugs a year to actually get ahead of this game.
Sanjay Gupta: Right now it takes a few years to create a single drug and you're talking about 30 drugs in, in one year. Is that really feasible?
To make any of this work, Soon-Shiong believes you need to upend the way cancer drugs are developed. He's started a biotech company to try to dramatically ramp up production.
Patrick Soon-Shiong: I know it sounds an audacious goal but you need to actually develop 20 to 30 drugs a year to actually get ahead of this game.
Sanjay Gupta: Right now it takes a few years to create a single drug and you're talking about 30 drugs in, in one year. Is that really feasible?
Soon-Shiong is impatient with the pace of drug approvals. In the early 90s, he invented a drug called Abraxane that treats pancreatic, lung and breast cancer patients. But more than a decade passed before the FDA approved it.
Patrick Soon-Shiong: The problem is for cancer, however, we don't have that time. You know, if you have pancreatic cancer, you have two months, if you have metastases throughout your body. The war against cancer is a war against time.
Soon-Shiong is also frustrated with what he calls the trial and error cycle of cancer care.
(Buy/Rent/Layaway)
Patrick Soon-Shiong: The truth of the matter, we treat cancer today, we guess. We take what we call the average results, put it in you, see if it works. If it doesn't work, oops, we'll try another drug. If it does work, we stop the drug. When you look back 10 years from now, it's almost barbaric.
The 62-year-old native of South Africa can afford to be outspoken because of his immense wealth. He doesn't need to rely on the government or Big Pharma for funding. Soon-Shiong is certain what he terms the Dark Age of cancer treatment is nearly over, and the Enlightened Age is about to begin.
Sanjay Gupta: What will the average person note about the Enlightened Age versus the Dark Age?
The 62-year-old native of South Africa can afford to be outspoken because of his immense wealth. He doesn't need to rely on the government or Big Pharma for funding. Soon-Shiong is certain what he terms the Dark Age of cancer treatment is nearly over, and the Enlightened Age is about to begin.
Sanjay Gupta: What will the average person note about the Enlightened Age versus the Dark Age?
(Buy/Rent/Layaway)
Patrick Soon-Shiong: The treatment doesn't need to be painful. Metastasis doesn't need to be a death sentence. Cancer could be a chronic disease...and treated towards the cure.
While the oncology world may cringe when he boasts, as he's prone to do, patients see him differently.
David Roy: The established community doesn't like false hope. But if you have a terminal disease like I do, you want some hope.
David Roy was diagnosed two years ago with stage four, metastatic pancreatic cancer. He was given four and a half months to live and told to settle his affairs. He called Dr. Soon-Shiong, whom he had met on a plane years before. Soon-Shiong recommended a UCLA oncologist who devised an unusual therapy that combined Abraxane with other cancer drugs. Then Soon-Shiong had Roy's tumor genome sequenced. Based on those results, Roy is now taking part in a clinical trial involving another front in cancer treatment.
(Buy/Rent/Layaway)
Patrick Soon-Shiong: That's the T-cell and that's the cancer cell.
It's called immunotherapy. Soon-Shiong is not the only one working on it, but he was anxious to show us why oncologists believe it's a promising field: a time-lapse demonstration of how T-cells, which our immune systems naturally produce, can attack cancer cells...
Patrick Soon-Shiong: This is a cell that's actually gobbling up the cancer cell. This cell will grow in size and this cell will decrease in size so watch (laughs). So, here's the T-cell gobbling it up. There's the cancer cell. And...
Sanjay Gupta: That's amazing. So you're literally watching cancer cells die here?
Patrick Soon-Shiong: Correct.
Sanjay Gupta: If you find these T-cells and you're able to isolate them, is the idea then, you know they could do the job, you could come out and grow them, proliferate them, and put 'em back in the body.
Patrick Soon-Shiong: Exactly.
Even though it's been two years now since David Roy's original diagnosis, he's realistic about his chances of survival. But he's convinced Soon-Shiong and other scientists are on track to dramatically decrease cancer death rates in the not too distant future.
David Roy: I'm not sure that it'll happen fast enough for me, but I have every confidence that my children and grandchildren won't be concerned about the things that I'm concerned about. We are on the edge here, of going from the oil lamp to electricity. And it is going to happen.
Soon-Shiong's most provocative idea, though, centers on how cancers may become metastatic.
He believes chemotherapy works best when administered in frequent, low doses and that in some cancers the traditional method of blasting a tumor with heavy doses of chemotherapy may be actually be counterproductive - because it could induce cancer cells to escape the hostile environment, enter the bloodstream and find a new home.
Sanjay Gupta: It's on the move.
Patrick Soon-Shiong: It's on the move. And it's looking for another place to land.
Patrick Soon-Shiong: Circulating tumor cells in the blood is the new frontier. Those are the circulating tumor cells.
Sanjay Gupta: That's incredible.
If cancer spreads the likelihood of survival decreases dramatically. So before individual rogue cancer cells fan out and form new tumors, Soon-Shiong wants to detect them with what are known as liquid biopsies. A person's blood sample is put through this bio-chip that separates normal blood cells from heavier, circulating tumor cells. This is a view inside the bio-chip as the tumor cells are being funneled to the top.
Patrick Soon-Shiong: And if we can now monitor the cancer cell in the blood we then have a path to getting this and winning this war. We never had those paths before.
After pulling out the circulating tumor cells, scientists can take them back to the genome sequencer to look for new mutations that made them resistant to the initial treatment...and hopefully find a new drug to treat it. It's yet another angle Soon-Shiong is taking to disrupt cancer.
Sanjay Gupta: You got genomics. You have circulating tumor cell liquid biopsies. Death by T-cell. Why are you the one taking all this on, I mean these are lots of different types of things...
Patrick Soon-Shiong: You know, somebody once said to me, "You know, Patrick, you're all over the place." And I said, "You have to be all over the place" because I'm trying to fight this war from all over the place. Because you can't, there's no one single magic bullet.
It's called immunotherapy. Soon-Shiong is not the only one working on it, but he was anxious to show us why oncologists believe it's a promising field: a time-lapse demonstration of how T-cells, which our immune systems naturally produce, can attack cancer cells...
Patrick Soon-Shiong: This is a cell that's actually gobbling up the cancer cell. This cell will grow in size and this cell will decrease in size so watch (laughs). So, here's the T-cell gobbling it up. There's the cancer cell. And...
Sanjay Gupta: That's amazing. So you're literally watching cancer cells die here?
Patrick Soon-Shiong: Correct.
Sanjay Gupta: If you find these T-cells and you're able to isolate them, is the idea then, you know they could do the job, you could come out and grow them, proliferate them, and put 'em back in the body.
Patrick Soon-Shiong: Exactly.
Even though it's been two years now since David Roy's original diagnosis, he's realistic about his chances of survival. But he's convinced Soon-Shiong and other scientists are on track to dramatically decrease cancer death rates in the not too distant future.
David Roy: I'm not sure that it'll happen fast enough for me, but I have every confidence that my children and grandchildren won't be concerned about the things that I'm concerned about. We are on the edge here, of going from the oil lamp to electricity. And it is going to happen.
Soon-Shiong's most provocative idea, though, centers on how cancers may become metastatic.
He believes chemotherapy works best when administered in frequent, low doses and that in some cancers the traditional method of blasting a tumor with heavy doses of chemotherapy may be actually be counterproductive - because it could induce cancer cells to escape the hostile environment, enter the bloodstream and find a new home.
Sanjay Gupta: It's on the move.
Patrick Soon-Shiong: It's on the move. And it's looking for another place to land.
Patrick Soon-Shiong: Circulating tumor cells in the blood is the new frontier. Those are the circulating tumor cells.
Sanjay Gupta: That's incredible.
If cancer spreads the likelihood of survival decreases dramatically. So before individual rogue cancer cells fan out and form new tumors, Soon-Shiong wants to detect them with what are known as liquid biopsies. A person's blood sample is put through this bio-chip that separates normal blood cells from heavier, circulating tumor cells. This is a view inside the bio-chip as the tumor cells are being funneled to the top.
Patrick Soon-Shiong: And if we can now monitor the cancer cell in the blood we then have a path to getting this and winning this war. We never had those paths before.
After pulling out the circulating tumor cells, scientists can take them back to the genome sequencer to look for new mutations that made them resistant to the initial treatment...and hopefully find a new drug to treat it. It's yet another angle Soon-Shiong is taking to disrupt cancer.
Sanjay Gupta: You got genomics. You have circulating tumor cell liquid biopsies. Death by T-cell. Why are you the one taking all this on, I mean these are lots of different types of things...
Patrick Soon-Shiong: You know, somebody once said to me, "You know, Patrick, you're all over the place." And I said, "You have to be all over the place" because I'm trying to fight this war from all over the place. Because you can't, there's no one single magic bullet.
Monty Henry, Owner
Additional Resources:
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* Electrical Hyper-Sensitivity: The-Truth!!
* The Creature From Jekyll Island: This Blog And Video Playlist Explains Why The U.S. Financial System is Corrupt and How It Came To Be That Way
* Dropping Off The Grid: A Growing Movement In America: Part I
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Watch your child's caregiver while sitting at a traffic light or lunch meeting, or check on your business security from the other side of the world. Our built-in hidden video features all digital transmissions providing a crystal clear image with zero interference. With the IP receiver stream your video over the internet through your router, and view on either a PC or smart phone. Designed exclusively for DPL-Surveillance-Equipment, these IP hidden wireless cameras come with multiple features to make the user's experience hassle-free.
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• Video is Recorded Locally To An Installed SD Card (2GB SD Card included)
• Email Notifications (Motion Alerts, Camera Failure, IP Address Change, SD Card Full)
• Live Monitoring, Recording And Event Playback Via Internet
• Back-up SD Storage Up To 32GB (SD Not Included)
• Digital Wireless Transmission (No Camera Interference)
• View LIVE On Your SmartPhone!
Includes:
* Nanny Cameras w/ Remote View
* Wireless IP Receiver
* Remote Control
* A/C Adaptor
* 2GB SD Card
* USB Receiver
FACT SHEET: HIDDEN NANNY-SPY (VIEW VIA THE INTERNET) CAMERAS
Specifications:
Receiver Specs:
* Transmission Range of 500 ft Line Of Sight
* Uses 53 Channels Resulting In No Interference
* 12V Power Consumption
* RCA Output
* Supports up to 32gig SD
Camera Specs:
* 640x480 / 320x240 up to 30fps
* Image Sensor: 1/4" Micron Sensor
* Resolution: 720x480 Pixels
* S/N Ratio: 45 db
* Sensitivity: 11.5V/lux-s @ 550nm
* Video System: NTSC
* White Balance: Auto Tracking
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