Hunt for HIV cure turns to cancer drugs


ntiretroviral drugs are currently used in HIV treatment to kill any active virus

The outstanding progress in boosting the immune system to treat cancer may help unlock a cure for HIV, according to scientists meeting in Paris.

The body’s normal defences struggle to clear the body of HIV and cancer.

But the rapidly emerging field of immunotherapy has seen some patients with terminal cancer go into complete remission.

The hope is that a similar approach could clear someone of HIV, although some experts have urged caution.

HIV treatment requires daily antiretroviral drugs to kill any active virus. Left unchecked, HIV can destroy the immune system, causing Aids.

A cure is currently impossible because drugs and the immune system fail to detect the sleeping or “latent” HIV hiding in the body’s cells.

Nobel Prize winner and co-discoverer of HIV, Francoise Barre-Sinoussi, told the BBC: “One of the mechanisms why [latently infected cells] persist is the fact they are proliferating very similar to tumour cells.

‘It’s huge’

“Those cells are expressing molecules that are the same molecules that are expressed on tumour cells.

“So that raises the question whether we could develop a strategy for HIV-cure similar to the novel treatment in the field of cancer.”

She is one of the scientists attending the HIV and Cancer Cure Forum in Paris.

Prof Sharon Lewin, the director of the Doherty Institute in Australia, agrees there is much to learn from cancer.

She said: “There are a lot of parallels… I think it’s huge.”

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Cancers evolve tricks to survive an assault by the immune system.

They can produce proteins on their surface, such as PD-L1, which disable immune cells attacking the tumour.

A new class of immunotherapy drugs called “checkpoint inhibitors” allow the immune system to keep on fighting and the results have been remarkable.

In one trial, a fifth of patients with terminal melanoma had no sign of the disease after immunotherapy.

However, only about 50 people with HIV have been given immunotherapy to treat their cancer.

Little evidence

So there is little evidence of immunotherapy drugs and their effect on HIV.

Prof Lewin has started doing the research in the laboratory and thinks immunotherapy drugs could reinvigorate an immune system that has become tired of fighting HIV.

She said: “The parts of the immune system that recognise HIV are often exhausted T-cells, they express immune checkpoint markers.

“In the laboratory, if you then put those cells in with an immune checkpoint blocker, the T-cells do regain function.”

HIV drug efavirenz - used as part of antiretroviral therapy treatmentImage copyrightSCIENCE PHOTO LIBRARY
Image captionAntiretroviral therapy combines three or more drugs which stop the HIV virus from progressing

She said there was emerging evidence that the drugs also activated HIV lying dormant inside immune cells.

Prof Lewin said: “We want the virus to wake up, any virus that wakes up gets killed [by antiretroviral drugs].”

However this is a new concept in HIV that has so far delivered nothing for patients.

And there are important differences between the challenges of cancer and HIV immunology.

‘So different’

In cancer, the immune system can recognise the threat but is not powerful enough to do anything about it, but the immune system does not recognise latently infected HIV cells at all.

Dr Anthony Fauci, the head of the US National Institute of Allergy and Infectious Diseases, said the area is “very hot” right now in cancer.

But he cautioned: “We have to be careful we don’t assume that things that work in cancer are going to work in HIV.

“HIV is so different, that even though it’s worth exploring, I wouldn’t want people to think this is going to be equally successful in HIV.”


Cancer patients’ grey hair unexpectedly darkens in drug study

Fourteen patients in the study found that their grey hair darkened after taking the new drugs. Photograph: Barry Diomede/Alamy

A group of cancer patients’ grey hair has unexpectedly darkened after they took new types of drugs, researchers have revealed.

Chemotherapy is known to make patients’ hair fall out, but the 14 people involved were all being treated with new immunotherapy drugs that work differently and have different side effects from chemotherapy. A Spanish study suggests those may include restoring hair pigment, at least in patients with lung cancer.

Noelia Rivera, a dermatologist at Autonomous University of Barcelona, said they thought it could be an isolated case when it happened with the first patient. But the research team found the same thing when they asked other patients for photographs of themselves from before treatment.

The 14 people were among 52 patients with lung cancer being followed to see whether they developed bad side effects from the drugs — Keytruda, Opdivo and Tecentriq.

While most patients did not have a hair colour change, the 14 cases suggest it is not an isolated finding. In 13 patients, hair turned darkish brown or black; in one patient, it turned black in patches.

The same drugs have been linked previously with hair losing colour in patients with another cancer, melanoma.

All but one of the 14 patients in the Spanish study responded better to treatment than other patients, suggesting that hair darkening might be an indication that the drugs are working, the researchers said.

Rivera said they were continuing with the study to search for an explanation.

“It’s a fascinating report – one of those things that comes out of the blue,” said June Robinson, a Northwestern University research professor in dermatology. Robinson is also editor of the medical journal JAMA Dermatology, which published the study online this month.

She said the results deserved a deeper look but cautioned that it was too soon to suggest that they might lead to new treatments for unwanted grey hair.

Rivera noted that the drugs used in the study had serious side effects that made them unsafe for healthy people. But if it is confirmed that they do change hair colour, a different drug could be developed to treat grey hair, she said.

The pharmaceutical industry has previously capitalised on unexpected drug side effects. Examples include the male pattern baldness drug Propecia, the eyelash growing drug Latisse, and Botox anti-wrinkle injections. Active ingredients in these drugs were initially approved to treat enlarged prostates, eye pressure problems, and eye muscle spasms.

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McCain’s cancer diagnosis jolts Senate

Sen. John McCain, R-Ariz., arrives ...In this July 11, 2017, file photo, Sen. John McCain, R-Ariz., arrives on Capitol Hill in Washington. McCain has been diagnosed with a brain tumor after a blood clot was removed.

WASHINGTON — Sen. John McCain’s diagnosis of brain cancer jolted the Senate where Republicans and Democrats offered prayers and words of encouragement for a six-term lawmaker with a war hero past.

“The outpouring of bipartisan respect and love for John McCain as he faces this cancer battle reminds us that after all the meanness there is a human side to politicians,” said Sen. Dick Durbin, D-Ill., said Thursday. “Count this Democrat in John McCain’s corner.”

Said Sen. David Perdue, R-Ga.: “John McCain is a friend, a mentor and a true patriot. If anyone can tackle a challenge like this, it’s him.”

The 2008 Republican presidential nominee and Vietnam prisoner of war who has spent more than three decades in Congress was diagnosed with an aggressive type of brain cancer. The 80-year-old Arizona lawmaker has glioblastoma, according to doctors at the Mayo Clinic in Phoenix, where McCain had a blood clot removed above his left eye last Friday. He and his family are considering further treatment, including chemotherapy and radiation.

“Subsequent tissue pathology revealed that a primary brain tumor known as a glioblastoma was associated with the blood clot,” his office said in a statement late Wednesday.

According to the American Brain Tumor Association, more than 12,000 people a year are diagnosed with glioblastoma, the same type of tumor that struck McCain’s close Democratic colleague in legislative battles, the late Ted Kennedy of Massachusetts. The American Cancer Society puts the five-year survival rate for patients over 55 at about 4 percent.

The senator and chairman of the Armed Services Committee had been recovering at his Arizona home. His absence forced Majority Leader Mitch McConnell, R-Ky., to delay action on health care legislation.

South Carolina Sen. Lindsey Graham said he spoke to McCain Wednesday evening and that McCain said: “Yeah, I’m going to have to stay here a little bit longer, take some treatments. I’ll be back.”

In a statement on Twitter, his daughter, Meghan McCain, spoke of the shock of the news and the anxiety over what happens next. “My love for my father is boundless and like any daughter I cannot and do not wish to be in a world without him. I have faith that those days remain far away,” she said.

As word spread of his diagnosis, presidents past and present along with McCain’s current and former Senate colleagues offered support in an outpouring rarely seen in Washington.

“Senator John McCain has always been a fighter. Melania and I send our thoughts and prayers to Senator McCain, Cindy, and their entire family. Get well soon,” President Donald Trump said.

Barack Obama, who dashed McCain’s dreams of the presidency, said in a tweet: “John McCain is an American hero & one of the bravest fighters I’ve ever known. Cancer doesn’t know what it’s up against. Give it hell, John.”

McCain has a lifetime of near-death experiences — surviving the July 1967 fire and explosion on the USS Forrestal that killed 134 sailors; flying into power lines in Spain; the October 1967 shoot-down of his Navy aircraft and fall into Truc Bach Lake in Hanoi; and 5 1/2 years in a North Vietnamese prison.

“The Hanoi Hilton couldn’t break John McCain’s spirit many years ago, so Barbara and I know — with confidence — he and his family will meet this latest battle in his singular life of service with courage and determination,” said former President George H.W. Bush.

Politics aside, McCain and Bill Clinton developed a strong friendship, and the former president said: “As he’s shown his entire life, don’t bet against John McCain. Best wishes to him for a swift recovery.”

The junior senator from Arizona, Republican Jeff Flake, said Thursday that McCain told him about his tumor only at the end of a telephone conversation, saying he was “feeling fine, but I might have some chemotherapy in my future.” Flake said on ABC’s “Good Morning America” that his colleague is “optimistic, obviously. He’s John McCain. That’s what we’d expect.”

In the past, McCain had been treated for melanoma, but a primary tumor is unrelated. Doctors said McCain is recovering from his surgery “amazingly well” and his underlying health is excellent.

With his irascible grin and fighter-pilot moxie, McCain was elected to the Senate from Arizona six times, most recently last year, but twice thwarted in seeking the presidency.

An upstart presidential bid in 2000 didn’t last long. Eight years later, he fought back from the brink of defeat to win the GOP nomination, only to be overpowered by Obama. McCain chose a little-known Alaska governor as his running mate in that race, and helped turn Sarah Palin into a national political figure.

After losing to Obama in an electoral landslide, McCain returned to the Senate, determined not to be defined by a failed presidential campaign. And when Republicans took control of the Senate in 2015, McCain embraced his new job as chairman of the powerful Armed Services Committee, eager to play a big role “in defeating the forces of radical Islam that want to destroy America.”



Puma Biotech Jumps On Breast Cancer Drug Approval

Leerink’s Michael Schmidt and Varun Kumarreiterated an Outperform rating on the stock today, writing that while the approval isn’t a surprise, it has removed an overhang for the stock, and it came in earlier than expected to boot.

More detail from their note:

The product label looks broad, not restricting use to specific patient populations (e.g., hormone-receptor [HR] positive patients) and there is no black box warning. The prescribing information contains fairly detailed information about the use of antidiarrheal prophylaxis measures, providing specific information on how to manage the drug’s main side effect. Information on pricing and launch timing is not available yet; PBYI previously guided to a cost of therapy that is similar to that of other breast cancer drugs. We’d expect a US launch not immediately given that PBYI has hired a US sales force only contingent on obtaining regulatory approval. A recommendation from the European CHMP is still pending and expected later this month or next. We currently model $1.3Bn US Nerlynx peak sales in the extended adjuvant treatment setting based on relatively conservative assumptions and believe 2018E Street consensus of $215M should be achievable.


Forget lifestyle – we need to end poverty to combat cancer

The Minister for Health, Simon Harris, and Minister of State for Health Promotion, Catherine Byrne, during the launch of a new ‘National Cancer Strategy 2017-2026’ at Iveagh House, Dublin. Photograph: Gareth Chaney Collins

From the point of view of early diagnosis, treatment, and support for survivors, the new National Cancer Strategy 2017-2026 is an excellent document. However, the prevention section is a big disappointment. According to the foreword by the Minister for Health, Simon Harris, “cancer prevention is a cornerstone of this strategy as it offers the most cost-effective, long-term approach for cancer control”.

Prof John Kennedy, chairman of the steering group that put the strategy together, also stresses the need for prevention and aggressive programmes of public education and “that the most strenuous efforts must be made to target more deprived populations in cancer prevention”.

Although recognising the “incontrovertible evidence of the enormous impact of socioeconomic status and deprivation on death rates from some cancers Ireland”, he blames smoking and poor diet. In fact, the prevention chapter is all about the promotion of healthy lifestyles. This approach will not prevent cancer or reduce inequalities.

Did the members disregard the evidence that inequality and health inequality are the main cancer risk factors? No, they knew about the health impact of inequality. “Reducing health inequalities is a priority of this strategy, as lifestyle risk factors generally follow social, deprivation, gender, and age patterns.” The steering group included a representative from the National Cancer Registry which produced a report on cancer inequalities last year titled Cancer Inequalities in Ireland by deprivation, urban/rural status and age: A National Cancer Registry Report 2016.

This report showed that not only was there a higher incidence of cancer in deprived populations but these populations had much lower survival rates. “Strong patterns of inequality . . . are documented for most of the measures examined [nine major cancer types].” None of the proposed prevention actions in the new cancer strategy will reduce inequality and may widen the health gap between socioeconomic groups. It is more likely that the steering group recognised the impact of inequality but did not know what to do about it.

There is overwhelming evidence that focusing on getting the lifestyle message across and public health education does not prevent cancer or any other disease. Prevention groups know that poor people get sick more often than those who are better off but do not analyse the problem. They assume it is a health education issue and believe that if only “the poor” realised that smoking, drinking, and being overweight was bad for their health they would change their behaviour. Because of this erroneous belief, health professionals, the Department of Health and the HSE rely on health information campaigns. They believe that if they say it often enough people will change.

For example, Goal 1 in the National Cancer Strategy is directed at reducing the cancer burden by focusing on health inequalities through information campaigns. “A significant effort is required to ensure that prevention and awareness campaigns have a particular focus on addressing health inequalities” and “it is vital that we are effective in getting the message across to the population that each person can impact significantly on their own level of risk of developing cancer.” This is so stupid.

According to Margaret Whitehead, a World Health Organisation expert on the social determinants of health and health inequalities, “the solutions may seem so complex that people can easily become frozen into inaction” leading to “lifestyle drift.” In 1988, she wrote The Health Divide which analysed the huge differences in health between socioeconomic groups.

According to a 2016 paper by Whitehead, the reason poor people do not adopt healthy lifestyles is because they do not control their own destiny. “Being in a low social position; living in a disadvantaged environment with a sense of collective threat and powerlessness and the degree to which people are discriminated against and excluded from the society in which they live”, means that people are more likely to develop cancer and other chronic diseases.

According to the new cancer strategy, “As more evidence emerges regarding the development of cancer . . . there will be a need to identify the most effective prevention methods.” We already know the most effective method which is to reduce or, as far as possible, eliminate inequalities and thus health inequalities. Unless this happens the numbers of people with cancer will not just double by 2040, as predicted in the National Cancer Strategy, but treble.


Is this the key to stopping cancer from spreading?

Cancer cells dividing

Divide and conquer – can metastasis be controlled?
When a tumor migrates to another part of the body, it makes cancer much more difficult to beat. A recently published study, investigating a metabolite called 20-HETE, gives new insight into this process and how it might be stopped.

Cancer’s ability to metastasize – move through the body and take root in a distant location – is a thorn in the side of cancer treatments.

A localized tumor is much easier to treat, and chances of survival are greater. Once the tumor has moved on, it can be harder to control. Around 30 percent of people with breast cancer experience metastasis, commonly affecting the lymph nodes, bones, brain, lungs, and liver.

Understanding how a tumor sets up shop in distant parts of the body is an important area of study. The trouble is, cancer is incredibly adept at finding a new location; in fact, tumors constantly send out cells into the bloodstream to see if they take hold and flourish. They are also experts at recruiting cellular assistance and making their new home perfect for supporting their continued growth.

New research, looking at a metabolite called 20-HETE, hopes to learn how we can disrupt cancer’s ability to succeed in distant tissues.

What is 20-HETE?

20-HETE (20-Hydroxyeicosatetraenoic acid) is a breakdown product of arachidonic acid, a fatty acid used widely throughout the body. 20-HETE carries out a number of useful roles, including the regulation of vascular tone, blood flow to organs, and sodium and fluid transport in the kidney. The metabolite also plays a role in inflammation, helping the body fight off infections and other diseases.

Aside from its natural and positive effects, 20-HETE appears to have a darker, more sinister side; these murky depths are currently being plumbed by postdoctoral fellow Dr. Thaiz F. Borin and his team at Augusta University, GA. His latest findings are published this week in PLOS ONE.

Co-author Dr. B.R. Achyut, assistant professor in the MCG Department of Biochemistry and Molecular Biology, explains 20-HETE’s Jekyll and Hyde personality:

“There is normal function, and there is tumor-associated function. Tumors highjack our system and use that molecule against us.”

According to recent studies, 20-HETE provides the cancer with virtually everything that it needs; it forms part of the “seed and soil” hypothesis. For a cancer cell to up sticks and move, it needs all of its ducks in a row. It must detach from its position and become aggressive enough to survive the journey; then, once it has found a new site, it needs to recruit supporting tissue and blood vessels.

According to Dr. Ali S. Arbab, leader of the Tumor Angiogenesis Initiative at the Georgia Cancer Center, recent studies show that 20-HETE prepares the new site in a number of ways. The metabolite activates helpful protein kinases and growth factors that encourage cells to grow in size, proliferate, and differentiate.

To flourish, tumors are also dependent on the creation of new blood vessels, and 20-HETE can help in this regard. Additionally, 20-HETE turns up inflammation, a hallmark of many diseases, including cancer. It manages this

Disrupting the tumor microenvironment

In Dr. Arbab’s studies on metastasis and the processes behind it, he and his team are focused on “going after that tumor microenvironment.” In the most recent study, they used a molecule called HET0016, which inhibits the actions of 20-HETE.

To test HET0016’s ability to scupper 20-HETE’s homemaking powers, they inserted cancer cells in the mammary fat pad of mice. Once the cancer had set down roots and begun to spread, they injected the mice with HET0016. The drug was given for 5 days a week for 3 weeks.

After just 48 hours, cancer cells were less able to move freely around their test tube.

The drugs also reduced levels of metalloproteinases in the lungs; these enzymes destroy protein structures, allowing cancer cells to penetrate and new blood vessels to grow.

Similarly, other molecules useful to cancer cells, such as growth factors and myeloid-derived suppressor cells, were reduced. As Arbab says, “It gets rid of one of the natural protections tumors use, and tumor growth in the lung goes down.”

Although HET0016 is not ready for use in humans, the study demonstrates that 20-HETE could be a useful target for preventing cancer’s spread. Arbab notes that there are already certain drugs on the market – including some over-the-counter anti-inflammatory drugs – that might also inhibit this hijacked molecular pathway.

The team plans to continue looking for ways to prevent cancer from coercing 20-HETE into playing the bad guy. Preventing breast cancer from metastasizing would be a huge step forward because, as the authors write, “Distant metastasis is the primary cause of death in the majority of breast cancer types.”


Sam Johnson wants us to rethink the way we look at cancer

With sister Connie in the final stages of advanced cancer, actor Samuel Johnson has once again expressed his frustration that there is still no cure for the hideous disease.

And while his latest Instagram post could be considered offensive to some, we’re positive that was not his intention.

Johnson, 39, shared his thoughts on the Love Your Sister social media page today, starting by saying, “If cancer wore a burqa would we have cured it already?”


Image: Instagram @loveyoursister

What we think he meant by that comment is that if cancer were vilified the way those who wear burquas are WRONGLY targeted, if we focused all that energy wasted on mistakenly assuming all Muslims are terrorists, then cancer would probably have been eradicated by now.

His message seeming to be: Stop inventing fake problems and focus on targeting the real ones, like cancer.

The actor writes, “We want all the freedoms and we want them all now. We hate and kill other humans, for freedom from each other.

“For a freedom cancer doesn’t permit.

“75% of us live in real fear of a home-grown terrorist attack, while cancer will detonate and kill 50,000 of us this year. In our own backyard. Not in some province we can’t pronounce, let alone point to on a map.

“Rather than chanting for death, I choose to fight for life. Ideological rant over. xsam”

Followers of the cancer fundraising page have chosen to accept Johnson’s comments in the spirit in which they were intended, with @maso_chick who has experience with breast cancer saying, “Nope .. a burqa hides everything.”

The actor responded, “Cancer cares not of burquas or bikinis…”.

Connie before her final public appearance. Image: Instagram @loveyoursister

@amelie73 also chose to take his comments at face value, saying, “I know of no-one personally that has been killed by terrorism, but have lost two relatives, two colleagues, a dear neighbour, and one sweet young man to cancer.

“My father-in-law lost all his eight siblings to cancer.

“I live every day with the feeling that if I get it, it won’t be a huge shock. Governments please fund our defence against this actual menace, that’s killing thousands of Australian’s each year.

“Help us.”

Sam and Connie promote a fundraising drive. Image: TODAY

Samuel Johnsons’ sister Connie, 40, is dying from an aggressive form of cancer, her third experience with the disease since the age of 12.

Initially diagnosed with bone cancer, she recovered and lead a normal life until being diagnosed with uterine cancer at 22, and then breast and liver cancer at age 33.

Since her most recent cancer battle, brother Sam has dedicated his life to raising money for cancer research, establishing the charity Love Your Sister which has raised $5 million to date.

Last week the devastated actor wrote a love letter to his sister who is suffering through the final stages of the cruel disease, saying, “I wish I could soften your pain, or lessen your fear, or give you something tangible, but tangible clearly isn’t in season.

“I’m proud to walk you to the hardest part of the road. The end. The only part of the road in your life that must sadly be traveled alone.”


How does a high-fat diet raise colorectal cancer risk?

Image result for How does a high-fat diet raise colorectal cancer risk?A new study suggests a molecular explanation for the link between a high-fat diet and colorectal cancer.
While the evidence of a link between an unhealthful diet and colorectal cancer is robust, the underlying mechanisms for this association have been unclear. A new study, however, may have uncovered an explanation.

Researchers from the Cleveland Clinic in Ohio have identified a cellular signaling pathway, called JAK2-STAT3, that drives the growth of cancer stem cells in the colon in response to a high-fat diet.

What is more, the researchers found that blocking the JAK2-STAT3 pathway in mice fed a high-fat diet halted the growth of these stem cells, a finding that might fuel the development of new drugs to treat colorectal cancer.

Study co-author Dr. Matthew Kalady, co-director of the Comprehensive Colorectal Cancer Program at the Cleveland Clinic, and colleagues recently reported their findings in the journal Stem Cell Reports.

After skin cancer, colorectal cancer – a cancer that begins in the colon or rectum – is the third most commonly diagnosed cancer in the United States.

The American Cancer Society estimate that there will be 95,520 new cases of colon cancerdiagnosed in the U.S. this year, as well as 39,910 new cases of rectal cancer.

In recent years, a wealth of studies have suggested that a high-fat diet is a risk factor for colorectal cancer. However, the precise mechanisms behind this association have been ambiguous.

With the hope of shedding light on such mechanisms, Dr. Kalady and colleagues investigated how a high-fat diet influences JAK2-STAT3, a cellular signaling pathway known to promote tumorgrowth.

Findings may fuel new treatments

To reach their findings, the researchers used microrarray analysis to assess primary and metastasized tumors in mouse models of colorectal cancer.

When the mice were fed a high-fat diet, the growth of cancer stem cells in the colon increased. Studies have indicated that cancer stem cells are a key driver in the growth and metastasis of tumors.

On further investigation, the team found that blocking the JAK2-STAT3 cellular signaling pathway in the rodents reversed the increase in cancer stem cell growth triggered by a high-fat diet.

When analyzing the effects of a high-fat diet in colorectal cancer mouse models that were obesity-resistant, the researchers were able to replicate their findings.

Dr. Kalady says that this study is the first to demonstrate how a specific molecular pathway might mediate the link between a high-fat diet and colorectal cancer, a discovery that could yield new treatments for the disease.

We can now build upon this knowledge to develop new treatments aimed at blocking this pathway and reducing the negative impact of a high-fat diet on colon cancer risk.”

Dr. Matthew Kalady

“These findings also provide a new way in which cancer stem cells are regulated and provide insight into how environmental influences, such as diet, can alter cancer stem cell populations in advanced cancers,” adds study co-author Justin D. Lathia, Ph.D., of the Lerner Research Institute at Cleveland Clinic.


Athlete gets cancer. Athlete fights cancer. Repeat, again and again…

Image result for Athlete gets cancer. Athlete fights cancer. Repeat, again and again...It was on the morning of Good Friday in 2009 when the runner first met her cancer. She was a fifth-year senior at Minnesota, sitting in the lobby of a hotel in Tempe, Ariz., one day before a college track meet. The runner was born Gabriel Anderson, because her mom liked Biblical names and thought Gabriel evoked both strength and beauty. Plus, it would work fine for a boy or a girl, though the kids in elementary school ruthlessly truncated it to Gabe, which has stuck. One day she would marry a Gophers distance runner named Justin Grunewald and legally add an “e” to her first name, thus transforming into Gabriele Grunewald—but still Gabe to most outside her family. On this morning in Tempe, however, she was just an anxious 22-year-old waiting for a doctor’s phone call that would alter the course of her life.

Several days earlier she’d noticed a tiny bump below her left ear, and a doctor had performed a fine-needle aspiration to remove fluid. Grunewald remembers that procedure to this day because even with everything she has endured since, nothing has been more painful. The fluid was sent out for a biopsy, and Gabe kept training with her teammates, eventually flying off to Arizona. She was in good shape, ready at 22 to start a crowning college season in which she would finally win a Big Ten title, finally earn All-America, finally put up the numbers to launch a professional running career. Plus, it couldn’t be cancer. Just a few weeks earlier her mother, Laura, endured exploratory surgery for what doctors believed was advanced uterine cancer…only to learn post-surgery that she didn’t have cancer after all. The family had escaped. “I went from thinking my wife was going to die to everything is fine and dandy, all right there in a hospital waiting room,” says Gabe’s father, Kim. Life couldn’t be so cruel as to test them again—not this soon.

It was cancer. Gabe’s doctors told her she had adenoid cystic carcinoma (ACC), a rare form found primarily in the salivary glands that occurs in 3.5 out of every million cancer patients. (While there will be an estimated 255,180 new cases of breast cancer in 2017, only 1,200 to 1,300 people will be diagnosed with ACC.) “It’s a cancer most oncologists will never see,” says Naomi Fujioka, now Gabe’s primary oncologist at University of Minnesota Health.

She would need surgery to remove the tumor. In tears, Gabe told her coach, Gary Wilson, that she would seek another year of eligibility to achieve her goals, bureaucratic wrangling be damned. She then gathered her teammates by the hotel pool and shared the news. Ladia Albertson-Junkans, who 16 months earlier had lost her 49-year-old stepfather to Hodgkin’s lymphoma, was so shaken that she ran from the hotel in tears, a reaction she regrets to this day. Most of the others experienced it as a sudden first brush with mortality. “For those women,” says Wilson, “it was like hearing that one of [their] sisters had cancer.”

Gabe went back to her room and Googled ACC, and from dense paragraphs of scientific jargon one truth jumped off the screen: There is no standard of care. There are treatments and there is research, but there is nothing resembling a silver bullet. It is a whack-a-mole cancer that can be repeatedly swatted back into its hole, only to return in the same hole—or somewhere else—sometimes quickly or other times many years later. “It’s characterized by coming back,” says Fujioka. Gabe read all of this as “incurable.” She remembers that word; maybe it was on one of the web pages. “I thought, Well, that’s not good. What happens? People get this disease and just succumb to it?” She would later learn that curability is not binary, but something more nebulous, more intimate. She still applies the term incurable, but mostly as a means of dumbing down the complexity of her illness for laypeople, often media.

That weekend in Tempe, Gabe stayed with her team and 24 hours later ran a personal best of 4:22.87 in the 1,500 meters because it would have been a shame to let all that training go to waste. Later, back in Minnesota, she underwent a grueling six-hour surgery to remove the tumor and one of her six salivary glands, followed by two months of daily radiation treatments. It all marked the beginning of Gabe’s life with cancer, not the end. She couldn’t have known then just how challenging, how painful, how rewarding, how terrifying…how important that life would be.


Grunewald’s last-place finish in the 1,500 national championship in June can less than a week after she spent four hours in the ER with a fever.
Rich Pedroncelli/AP

More than eight years later, on the evening of June 10, Gabe was one of 15 women fanned out across the pale-orange surface of the track at Vanderbilt University in Nashville, host of the Music City Distance Carnival meet. They stood at the top of the backstretch, where the 3¾ laps of the 1,500 meters begin, but a grove of live oak trees blotted out light from the towers that rose above the track, leaving the racers in a fuzzy half-darkness just before the gun. They would come off the line like ghosts emerging from the cornstalks in Field of Dreams. The day’s 87-degree heat had given way to a pleasant stillness, so sweet for racing. Grunewald lined up fourth from the inside, wearing a yellow racing top and a blue bottom.

Since that morning in Tempe, cancer had come back three times. First there was thyroid cancer in 2010, just a year after her initial diagnosis. This was an entirely different kind of cancer, which at first confused everybody (but which now seems like a footnote). In the days between those first two cancers, Gabe, now 31, had lived—and run—voraciously. She learned that ACC five-year survival rates are very high (approximately 89%), and she attacked those five years. “Just fit in everything I can,” Gabe says. She procured that extra year of eligibility and took a whopping 10 seconds off her 1,500-meter PR, down to 4:12.06. She finished second at the Big Ten championship, second at the NCAAs and scored a modest pro contract with Brooks. Justin was away at medical school, in Duluth, so she also stayed out a little later, drank a little more beer and a little more red wine, escaping and experiencing a life she’d avoided in her past. “Sometimes those nights ended in tears and drama,” she says, “because I would get emotional about everything.” She had surgery on the thyroid cancer that fall, followed by one treatment with radioactive iodine, and then she bounced back quickly.

The big cancer, ACC, stayed away for seven years, and in that time Gabe carved out a career as a solid professional middle-distance runner. She finished fourth in the 1,500 meters at the 2012 Olympic trials, ran a personal best in the same event in ‘13 (4:01.48; only 10 American women have ever run faster) and won the indoor 3,000-meter national title in ‘14.

Then the ACC came back last summer in the form of a cantaloupe-sized tumor that absorbed two thirds of her liver. Doctors took it out, leaving a 13-inch, purple fishhook-shaped scar on Gabe’s abdomen. Six months later, the ACC came back again, this time in the form of 12 small tumors on her liver. Multiple treatment options were considered, and rejected, before doctors prescribed a course of chemotherapy. Gabe delayed treatment to try to achieve the qualifying standard, 4:09.52, for last month’s U.S. national championships—that would be her goal for the year. Her season’s training had started late because of the abdomen surgery, but she was in respectable shape. Now she would have to hurry to qualify before chemo. “We were going to have to cram a lot of training into a short time, which is never a good thing,” said Gabe’s longtime professional coach, Dennis Barker.

She ran 4:20.17 in a May 5 race at Stanford, and then two weeks later, in Southern California, 4:12. It was as fast as she would run this year.

But Gabe did something else, too: She began to talk about her cancer with anyone who asked. She developed a short, digestible version of a long, complex story for reporters. She sat for hours for a mini-documentary funded in part by Brooks and in part by the American Cancer Society. She shared endlessly on Instagram and Twitter. (She also devoted multiple days to this story.) All of this was exhausting and did nothing to help Gabe in her pursuit of 4:09. “It was so far out of my comfort zone, and it was overwhelming,” Gabe would say later. “I was conflicted about how much I wanted to share, like if I didn’t talk about my cancer maybe it wouldn’t come back. But a lot of people are suffering from this. It was totally worth it.”

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Others agree. Alan Ho, a medical oncologist at Memorial Sloan Kettering Cancer Center in New York City, has consulted on Gabe’s case, and he says he’s already seeing more attention paid to ACC “since Gabriele has been so generous in talking about it.” Gabe, meanwhile, has seen dozens of people reach out on social media, including a woman who raced against her in college and whose husband has ACC.

On the night of June 2, Gabe ran 4:17.75 and finished fourth in a 1,500- meter race at the Boston Boost Games in Somerville, Mass. Uneven pacing cost her, but she also felt lousy. She was to begin a first round of weekly chemotherapy for the liver tumors three days later. The window was closing. Minutes after the Somerville race, Gabe stood on the grass next to the track, goose bumps rising on her slender arms in 62-degree chill. “O.K., that’s it,” she said. “Time to for me to start treatment. Time to move on to the next thing.”

But she didn’t. On June 5 she spent four hours in a lounge chair at the Masonic Cancer Clinic at UM Hospital in Minneapolis while bags of Cisplatin and Vinorelbine were dripped into her bloodstream through an intravenous line in her left forearm. (Gabe’s chemotherapy regimen calls for weekly infusions on a three-week, on-on-off cycle; she will get at least four cycles, possibly six.) Then, four days later, she flew to Nashville to take one more crack at 4:09.

It did not go well. Unlike the Boston race, this one was evenly paced and relatively quick: 65 seconds at 400 meters and 2:12 at 800. Gabe stuck her nose in it for half a mile, then she imploded, falling off the back. She staggered across the line in 4:28.88, 12th among the 13 runners who finished; she’d last run that slow when she was a sophomore in college. Afterward, she dropped to all fours on the track and rolled onto her side, crying.

For nearly eight years—but more intensely over the last 10 months—she had woken every morning with voices in her head, defining her mortality. She was sad about exotic vacations she thought might never be taken and weddings that might be missed; she feared she might never be a mother but was grateful for a rich, short life. “I’ve lived my dreams, married my dream guy,” she says. She was by turns resigned (“Modern medicine and my faith will lead me to whatever ends up happening”) and willful (“No one knows how long I can survive this; I take that as a challenge”).

She was enduring it all while living and running, but the chemotherapy was one punch too many, and now she lay on the pebbled surface of Vanderbilt’s track, wasted beneath the lights. Sara Vaughn, one of Gabe’s best friends on the running circuit (where friendships are rare), helped her to her feet. “This is too hard,” Gabe said between sobs. “I can’t do this anymore.”

One day after the race at Vanderbilt, Gabe and Justin run an easy seven miles from their apartment in downtown Minneapolis, just west of the Mississippi River and in the shadow of the Vikings’ hulking new U.S. Bank Stadium. Gabe is still bothered by her performance. “I made an impulsive decision to spend $1,000 to fly to Nashville and [I ran] four twenty- eight,” she says, spitting out the time like it’s bad sushi. “I don’t want to make a joke of my sport. I mean, what am I doing?”

The athlete-with-cancer story is a familiar one. Athlete gets cancer. Athlete fights cancer. Athlete beats cancer. Or: Athlete loses fight and is mourned for battling bravely. But it is always more complicated than that. Gabe remembers the first time she got sick, in 2009, and then ran so fast afterward, with the word cancer in the first paragraph of every story. “I was being such a good cancer-survivor-runner,” she says, a little cynically, because back then she had no idea what lay ahead. All these years later, she is still battling her cancer with chemotherapy while trying to run footraces against fast, healthy opponents because it helps her feel alive and because maybe it will help others feel alive too.

Gabe is 5’ 6”, 110 pounds when she’s racing fit, rail thin and taut. Her face is elastic, twisting and scrunching to fit any mood. She is also feisty. In Nashville, Wilson, her old college coach, tried to console her, saying, “You’re inspiring so many people.” Gabe laughed: “I’m trying to inspire myself to be less of a dips—.” Now she adds, “I have no idea if I’m doing a good job of running on chemo. It’s such a strange, abstract concept.”

It’s another banality that some cancer patients fight harder than others and are rewarded with prolonged life, when in reality some are just less fortunate. That disclaimer aside, Gabe has always been the fighting type. She was raised in Perham, Minn., a town of 3,185 in the middle of the Lakes Region, 180 miles northwest of the Twin Cities. She’s the second of five children—three boys and two girls, the last two, twins—born to Kim and Laura, both 60, who met as teenagers in Grand Forks, N.D., and both graduated from the University of North Dakota.

The Andersons encouraged their children to play sports. Kim had been a state champion high school wrestler—Laura was a cheerleader; “that’s all we had,” she says—and in the winter he would take his kids ice fishing, six holes in the ice house and a bunch of tip-ups outside. Gabe was serious from the start. “I was not a popular kid,” she says. “I never even made homecoming court. It was a cutthroat competition.” Team sports were cutthroat too, and Gabe often saw her brothers succeed or fail based on the venomous whims of small-town sports politics. Running was the key that unlocked her spirit; she made the varsity track and cross country teams as a seventh grader and was competitive with the best small-school runners in the state. “With running, nobody could [choose not to] start me in a big game,” she says. “You got out of it what you put in.”

She didn’t have any boyfriends. “The boys in my town, they weren’t going anywhere,” she says. “They were going to [North Dakota State in] Fargo. Maybe. I didn’t want to go to Fargo.” Laura recalls, “Gabriele was much too strong for high school boys.” The guys on the cross-country team called her Grandma Gabe “because they were afraid to ask her out,” adds Caleb, one of her two older brothers.

Gabe didn’t win an individual state championship until the 800 meters in 2004, her senior year. In that race she upset the favorite by getting to the front and staying there, setting a three-second PR of 2:14.14. “She dominated that race,” says Jeff Morris, who coached Gabe her last two years at Perham High and saw what others would see later. “The word that describes her is grit. Every day she would push for faster workout paces. In her senior year I had her running with the boys.”

Gabe waffled on where to attend college. Her 2:14 brought late offers from some D-III and small D-I colleges, but she wanted to take a shot at Minnesota. Wilson, who had been coaching the Gophers since 1985, regularly sought to recruit home-state walk-ons with modest high school times, knowing some of them would prosper. He wrote Gabe several letters, inviting her to visit campus, but she kept stubbornly declining. “They were recruiting over me,” says Gabe. “They didn’t make me feel very wanted.” Wilson saw things differently. “I called her four or five times,” he says, “and she didn’t call me back. [Morris] told me to keep trying and I said, ‘No; this kid is a pain in the butt.’” Gabe finally traveled to Minneapolis that summer, spoiling for a fight. “God’s honest truth, before her foot even hit the floor inside my office I was thinking, This kid is tough. She walked in with an attitude, like, I’m gonna knock your head off.”

Gabe walked on at Minnesota with something to prove and she flourished. She ran on two Big Ten-champion cross-country teams and challenged for conference track titles in the 800 and 1,500 meters, before and after her first cancer. Albertson-Junkans remembers doing a workout with Gabe during their freshman year: a five- mile run, with the miles becoming progressively faster, before finishing with an all-out 800 meters on the track. “She would leave it out there in the 800,” says Albertson-Junkans, now an accomplished trail runner. “She had a willingness to dig deep and go to the most painful places. Most people back off. They get frightened. Gabe would embrace that discomfort and uncertainty.”

Wilson says, “I don’t want this to sound wrong, but she was resilient like a guy. Some women—and I love coaching women—will cry and say, ‘I hate you, coach.’ You could get in Gabe’s face, and she would stand there and take it. She was just, ‘O.K., I got it. Let’s go.’” Teammates remember the breadth of Gabe’s spirit. “Such a strong personality,” says Mallory Van Ness, who ran for three years with Gabe at Minnesota. “And a big karaoke fan. She’ll request Whitney Houston’s ‘I Wanna Dance With Somebody’ and get right up there.”

Her tactical strength was her kick. “She’s so fierce, so tough,” says Vaughn. “Not afraid to throw elbows or get gritty. So many times I would see her make a move at the end of a race and think, That’s the move I should have made.” But that strength was also her weakness. She would use her kick as an excuse for sitting just a stride too far out of the real race, or moving a second too late. Barker, her pro coach, says, “Physically, Gabe has everything it takes. The mental part was always a little harder. I’ve tried to get her to be more aggressive [earlier] in her races.”

Gabe made every U.S. championship 1,500-meter final from 2009 through, finishing as high as fourth in ’12 and fifth in ’14. She has had the misfortune of coming along in the same era as two of the best American milers in history: ’16 Olympic 1,500- meter bronze medalist Jenny Simpson and U.S. 1,500-meter record holder Shannon Rowbury. Those two have dominated the championship finals. It’s a tough room.


Spreading cancer caught on film

Image result for Spreading cancer caught on film

The way in which every single cancer cell spreads around the body has been captured in videos by a team in Japan.

The normal body tissues show up as green, while the cancer comes out as intense red spots.

The team, at the University of Tokyo and the RIKEN Quantitative Biology Center, says the technology will help explain the deadly process.

The research is on mice so far, but it is hoped the method could one day help with treatment too.

The spread of cancer around the body is a crucial moment called metastasis.

Before a cancer spreads it is easier to contain and cure, afterwards it is incredibly difficult.

The tumour itself has to evolve so bits of it are able to break free, survive travelling in the blood stream and invade new tissues.

A deeper understanding of how this happens could lead to new ideas for treatment.

See-through animals

The mice were injected with cancerous tissue engineered to fluoresce.

The researchers then let the disease progress before using chemicals that made the mouse’s body and internal organs highly transparent.

It meant the body could be rapidly imaged and the location of any cancerous tissue detected.

The study, published in the journal Cell Reports, details cancers growing in the lungs, intestines, and liver before spreading around the body.

Dr Hiroki Ueda, one of the researchers, said: “The images reveal cancerous colonies in enough detail to calculate their shapes, volumes, and distributions – characteristics critical to distinguishing between patterns of metastasis.

He told the BBC News website: “We are now applying this technology to the human clinical samples.

“I hope this tissue-clearing and 3D imaging of human samples will make diagnosis easier, more objective and accurate in near future.”

Watch an infection take hold in 3D and in real time

Further experiments showed how cancer can get better at spreading.

Dr Kohei Miyazono said: “Most of the cancer cells appear to die during circulation in the bloodstream and fail to metastasise.”

But cancers then start producing chemical signals to help them grow.

The researchers tested the effect of one of them, called TGF-beta, and showed it dramatically improved the chances of cancers colonising the lung tissue.

“[They] are far more likely to survive the journey and form malignant outposts,” Dr Miyazono added.

It is thought the technology could be adapted to other disciplines, including how the body’s cells behave in people with autoimmune diseases.