Never Smoked. Lived Right. Died of Lung Cancer.

Avrum Spira’s aunt died of lung cancer almost 20 years ago. She was a nonsmoking exercise buff in her 40s who hadn’t been exposed to any known toxins; she worked in a government office, not a coal mine. “One of the healthiest people you could imagine, did everything right,” says Spira (ENG’02), who at the time was an internal medicine resident at the University of Toronto.

The one thing she didn’t do right wasn’t her fault: she’d been born to a nonsmoking mother who had died from the same illness. “I’m absolutely convinced she had a genetic predisposition” to lung cancer, says Spira, a School of Medicine professor and chief of computational biomedicine. That conviction set him on a quest for the genetic key to a medical mystery: why some people who have never smoked fall victim to this scourge of cigarette users.

Lung cancer kills more Americans than any other cancer, and twice as many women die from it than from breast cancer, although the latter gets greater public attention, says Spira. In 2008, the last year for which data was available, more than 208,000 Americans were diagnosed with lung cancer and almost 158,600 died from it. Spira says between 10 and 15 percent of these annual victims are nonsmokers (the percentage has been edging up slowly in recent years) with no apparent exposure to other toxins—a crucial caveat. “How do you know someone has been or has not been exposed to something in the environment?” he asks. Some potential toxins, like radon, are invisible, he notes, “so people who we’re seeing now, with higher rates of nonsmoking lung cancer—is it because they were exposed to radon 20 years ago?”

It’s true that worldwide, the rise in the incidence of lung cancer—from the eighth leading cause of death in 1990 to fifth in 2010—is mostly a function, perversely, of good news: as living standards have improved in the developing world, more people survive into adulthood, meaning a decline in childhood deaths from malnutrition and infectious diseases. That has brought an accompanying uptick in the number of people dying from diseases mostly found in wealthier countries, among them cancer. Moreover, air pollution in industrializing countries has resulted in more lung cancer in nonsmokers there, Spira says.

But in the United States, he says, doctors believe there’s a similar spurt in lung cancers in nonsmokers who’ve had no apparent contact with other toxins. The most extensive studies, incorporating detailed questionnaires and visits to peoples’ homes to see their environment, show that “there hasn’t been a clear association among nonsmokers who are getting lung cancer with exposures to other things.”

An ongoing, as-yet-unpublished study by a team that includes Spira is looking at tumor tissue and adjacent, noncancerous tissue from the lungs of 32 subjects with lung cancer: 8 smokers, 11 former smokers, and 13 who never smoked and had no apparent exposure to other toxins. The researchers ran the samples through a gene sequencer at MED, which “can give us unprecedented insight into the genomic changes leading to lung cancer” in nonsmokers, says Rebecca Kusko (MED’14), a graduate student spearheading the study in Spira’s lab.

With the sequencer, “we study the normal cells from each person as a control,” says Spira, “and then what happens in their tumor right next door, and say, what’s changed?” Preliminary results suggest that in the smokers, “a huge number of cancer pathways are activated,” as genes controlling cell growth in the tumors turned on. But those pathways weren’t necessarily activated in the nonsmokers, who showed different gene changes between their healthy lung tissue and their tumorous tissue. The researchers’ hypothesis is that the nonsmokers had a genetic predisposition, a pathway, to cancer that was activated by something in their environment.

That trigger, Spira theorizes, may be a viral infection (cervical, liver, and head and neck cancers are all caused by viruses, he says). The researchers are now sequencing the tumor tissue of the nonsmokers to try and find any viral genes. “Even if there’s one viral gene per million human genes, we might pick it up, we believe,” he says. The work will take a year or two.

Potential therapies—which are many more years away, he warns—might include screening people with the genetic predisposition and then giving those with the predisposition regular lung scans to catch cancers early. Another possibility would be drugs that could turn off uncontrolled growth in cancerous cells. (Spira got attention in 2010 for research suggesting that the natural compound myo-inositolcould turn off incipient lung cancer in smokers.)

Those who walk Commonwealth Avenue and have to dodge fumes from smokers on break may wonder about secondhand smoke. Research is mixed, but Spira, who researches the amount of smoke necessary to change gene expression and possibly lead to lung cancer, believes that it takes a big dose—perhaps exposure over months or years.

Almost half a century after the surgeon general first warned of smoking’s dangers, Spira says that even Hollywood is catching on that not all cancer victims heedlessly bring the disease on themselves. In 2011, he was a presenter at the Prism Awards, given for accurate portrayals of illness in entertainment media. He handed an award to an actress whose character on the soap opera The Bold and the Beautifulhad lung cancer.

The character was a nonsmoker.

Tumors Evolve Rapidly in a Childhood Cancer, Leaving Fewer Obvious Treatment Targets

An extensive genomic study of the childhood cancer neuroblastoma reinforces the challenges in treating the most aggressive forms of this disease. Contrary to expectations, the scientists found relatively few recurrent gene mutations -- mutations that would suggest new targets for neuroblastoma treatment. Instead, say the researchers, they have now refocused on how neuroblastoma tumors evolve in response to medicine and other factors.

"This research underscores the fact that tumor cells often change rapidly over time, so more effective treatments for this aggressive cancer will need to account for the dynamic nature of neuroblastoma," said study leader John M. Maris, M.D., director of the Center for Childhood Cancer Research at The Children's Hospital of Philadelphia (CHOP).

Striking the peripheral nervous system, neuroblastoma usually appears as a solid tumor in a young child's chest or abdomen. It comprises 7 percent of all childhood cancers, but causes 10 to 15 percent of all childhood cancer-related deaths. Neuroblastoma is notoriously complex, with a broad number of gene changes that can give rise to the disease.

Maris headed the multicenter research collaborative, the TARGET (Therapeutically Applicable Research to Generate Effective Treatments) initiative, which released its findings January 20 in Nature Genetics. This largest-ever study genomic study of a childhood cancer analyzed DNA from 240 children with high-risk neuroblastomas. Using a combination of whole-exome, whole-genome and transcriptome sequencing, the study compared DNA from tumors with DNA in normal cells from the same patients.

Researchers at CHOP and other centers previously discovered neuroblastoma-causing mutations, such as those in the ALK gene. In the subset of patients carrying this mutation, oncologists can provide effective treatments tailored to their genetic profile.

"A few years ago, we thought we would be able to sequence the genomes of individual patients with neuroblastoma, detect their specific cancer-causing mutations, and then select from a menu of treatments," said Maris. The oncology researchers designed the TARGET study to perform genomic analyses of a large cohort of high-risk neuroblastoma patients, with the goal of mapping out a limited number of treatment strategies. This approach would represent a significant step forward in personalizing neuroblastoma therapy.

However, while the researchers confirmed that roughly 10 percent of the study's neuroblastoma patients had ALK mutations, and found that a handful of other gene mutations each accounted for percentages in the single digits, there were relatively few recurrent mutations in somatic (non-germline) cells. "The relative paucity of recurrent mutations challenges the concept that druggable targets can be defined in each patient by DNA sequencing alone," wrote the authors.

In the absence of frequently altered oncogenes that drive high-risk neuroblastomas, the authors concluded that most such cases may result from other changes: rare germline mutations, copy number variations and epigenetic modifications during tumor evolution.

"Personalized medicine is more complex than we had hoped," said Maris. "While there are successes such as those in treating patients whose tumors harbor ALK mutations, this study implies that we must think very differently about how we'll use genomics to define treatment." Maris added that neuroblastoma researchers may need to turn to functional genomics, learning which tumors will or won't respond to treatments, as well as going beyond a static picture of a cancer cell with fixed genetic contents, to devising interventions to deal with dynamic tumor cells that evolve during nervous system development.

Co-corresponding authors with Maris are Matthew Meyerson, M.D., Ph.D., of the Broad Institute, Harvard Medical School and Dana-Farber Cancer Institute, and Marco A. Marra, Ph.D., of the University of British Columbia. In addition to his position at Children's Hospital, Maris also is on the faculty of the Perelman School of Medicine at the University of Pennsylvania.

Support for this study came from the National Institutes of Health (grants CA98543, CA98413, MD004418, CA124709, CA060104, and HG003067), the Canada Research Chair in Genome Science, the Giulio D'Angio Endowed Chair, the Alex's Lemonade Stand Foundation, the Arms Open Wide Foundation, and the Cookies for Kids Foundation.

http://www.sciencedaily.com/releases/2013/01/130120145816.htm

Fighting cancer with a healthy lifestyle

Carmen Tafolla, San Antonio’s first poet laureate, signs copies of her books in November. Tafolla is battling breast cancer with chemotherapy and lifestyle changes.

Photo: File Photo, San Antonio Express-News
Dear Pueblo de San Antonio:

I have profoundly enjoyed living and writing the role of poet laureate for this city — infusing a middle school's halls with poetry, speaking to young artists from Syria about the role of the arts in conflict resolution, collaborating with musicians to turn lines of poetry into great works by the San Antonio Composers' Association.

But this letter is not about poetry. It's about life, and what's more poetic than life itself — full of ironies, beauty and harsh surprises?

This letter is about a disease — one bigger and harder to heal than a cold or a flu. This letter is about cancer — a word I do not find devastating, but challenging.

I've never quite had the blanket-grief reaction to the word some do, because I grew up with this word. When I was 3 years old, my mother had cancer and was told she would not make it through the night. That was 58 years ago and today, she is 95, cancer-free and thriving. I know the limitations of medical knowledge. I know the power, too, of faith and healthy emotions.

But now, the battle is personal. In June I was diagnosed with a fast-growing, invasive breast cancer. The recommendation was six months of chemotherapy, followed by surgery, followed by more chemotherapy and radiation. I began poring through all the medical research I could access. I found a cancer researcher at M.D. Anderson whose work showed turmeric, a common spice, to be more effective than most chemo drugs. I also discovered the huge role that diet plays in creating cancer in the first place. Cancer cells are sugar junkies. Our modern diet is, basically, a cancer-producing diet.

So, I became a “mas o menos vegan,” relying on herbs and raw vegetables to empower the body's own natural cancer defenses. I eliminated all sugars and chemicals, most starches and most animal products from my diet. I say “mas o menos” vegan because I did allow a tiny amount of organic fish and meat. I don't want to imply that after cancer has gotten a stronghold, one can easily reverse it all through diet. I sought factors that oxygenated the cancer cells to kill them — daily exercise, ozone therapy and the avoidance of carcinogens and hormone additives in meats and milk.

While this slowed the growth of the cancer, it didn't stop it. Finally, I submitted to chemotherapy, and found it difficult, but doable. I'm now five weeks into a six-month chemotherapy treatment plan and, thanks to wonderful friends and health practitioners, I have found ways to work and write and even do performances around the chemo schedule, planning ahead for the weeks I know are at low resistance.

I still intend to keep all of my scheduled readings, but there will be weeks when my blood count is low that I will avoid receptions, crowds and hand-shaking. But I'll keep on writing; for a poet, that's like breathing or drinking water!

The chemo, as tough as it is on my immune system, has now shrunk the tumor to about 60 percent of its size.

But my goal is not just to eliminate this tumor. My goal is to keep from regrowing cancer, and for that, lifestyle changes are necessary.

There is one thing I can tell you, mi querido pueblo, and that is that cancer is easier to avoid than it is to heal. We each have a choice about what we feed our bodies. It's not that hard to establish new food traditions, centering meals on fresh fruits and vegetables and focusing on raw, healthy snacks — seeds, nuts, things not from a can or doused with sugar.

Let's lead the healthy life Native San Antonians led here 10,000 years ago, built on exercise, sunshine, fresh air, natural foods and the “good medicine” of respeto and love for the universe around you. To a new year of good health — for all of us!

http://www.mysanantonio.com/opinion/commentary/article/Fighting-cancer-with-a-healthy-lifestyle-4206308.php

'Microbeads' May Boost Survival in Advanced Colon Cancer Patients

Jan. 19 (HealthDay News) -For advanced colon cancer patients who have developed liver tumors, so-called "radioactive beads" implanted near these tumors may extend survival nearly a year longer than among patients on chemotherapy alone, a small new study finds.

The same study, however, found that a drug commonly taken in the months before the procedure does not increase this survival benefit.

The research, from Beaumont Hospitals in Michigan, helps advance the understanding of how various treatment combinations for colorectal cancer -- the third most common cancer in American men and women -- affect how well each individual treatment works, experts said.

"I definitely think there's a lot of room for studying the associations between different types of treatments," said study author Dr. Dmitry Goldin, a radiology resident at Beaumont. "There are constantly new treatments, but they come out so fast that we don't always know the consequences or complications of the associations. We need to study the sequence, or order, of treatments."

The study is scheduled to be presented Saturday at the International Symposium on Endovascular Therapy in Miami Beach, Fla. Research presented at scientific conferences has not been peer-reviewed or published and should be considered preliminary.

Goldin and his colleagues reviewed medical records from 39 patients with advanced colon cancer who underwent a procedure known as yttrium-90 microsphere radioembolization. This nonsurgical treatment, approved by the U.S. Food and Drug Administration, implants tiny radioactive beads near inoperable liver tumors.

Thirty of the patients were pretreated with the drug Avastin (bevacizumab) in periods ranging from less than three months to more than nine months before the radioactive beads were placed.

The liver is a common site for the spread of colorectal cancer, which, according to the U.S. Centers for Disease Control and Prevention, is diagnosed in about 137,000 Americans and kills about 52,000 each year. Many of the liver tumors are inoperable, leaving doctors fewer choices to help prolong patients' lives.

Avastin is commonly prescribed for colon cancer that has spread ("metastatic" cancer) because the drug hinders the growth of new blood vessels that feed tumors.

With the yttrium-90 procedure, which has been in use at major U.S. medical centers for more than a decade, a catheter is inserted into a small incision near the groin and threaded through arteries until it reaches the hepatic artery in the liver, where millions of microbeads are released near tumor sites. These beads emit high-dose radiation directly to cancerous cells, sparing damage to healthy cells.

Goldin's team found that 40 percent of the 17 patients with shorter intervals -- less than three months -- since their last Avastin dose before receiving the microbeads needed their microbead infusion stopped early due to slow blood flow near the tumors, a much higher number than patients whose last Avastin dose was further in the past. This was expected, Goldin said, because the main effect of Avastin is to cut tumors' blood supply.

Additionally, treatment with Avastin didn't increase the survival benefit of the microbeads, which added 10 to 12 months to patients' life spans compared to chemotherapy alone, Goldin said -- a survival of 34.5 months after the diagnosis of metastatic colon cancer, compared with 24 months.

"If you look at those [survival] numbers, there's a promising benefit" to using microbead radiation, he said. But the cost of both treatments is high -- in the tens of thousands of dollars per patient, he noted.

Dr. Felice Schnoll-Sussman, a gastroenterologist and director of research at the Jay Monahan Center for Gastrointestinal Health at New York-Presbyterian Hospital/Weill Cornell Medical Center in New York City, said the study won't change her clinical approach to treating metastatic colon cancer. But "it's important for us to try to tease through the different treatment recommendations and understand how one treatment affects another," she said.

"Maybe it helps you understand timing, which is never a terrible thing," she added. "This is the art of treatment of metastatic colorectal cancer -- it's in the tweaking of the treatments."

The U.S. National Cancer Institute has more about metastatic cancer.

'Microbeads' May Boost Survival in Advanced Colon Cancer Patients

Smartphone Apps Can Fall Short in Detecting Skin Cancer, Study Finds

Relying on health-care smartphone apps to detect skin cancer can postpone diagnosis and cause harm, a new study has found.

When researchers at the University of Pittsburgh Medical Center tested four popular apps for detecting melanoma -- the most serious form of skin cancer -- they found that on average three of them incorrectly classified 30 percent or more melanomas. The findings were published Wednesday in the Journal of the American Medical Association-Dermatology.

Of the 188 moles the researchers studied, 60 of them had already been diagnosed as melanoma by a board-certified dermatologist. The study found that the accuracy of the apps varied drastically -- the best-performing apps diagnosed cancerous moles correctly 98.1 percent of the time, while the worst-performing detected melanoma only 6.8 percent of the time.

Typically, in employing these apps, users photograph the skin lesions they would like analyzed, and the app generates a response.

"Patients do bring these in and ask about them," Dr. Darrell Rigel, clinical professor of dermatology at NYU Langone Medical Center, told ABC News. "I tell them that the difference between these and 'real' in-office melanoma diagnostic devices is the difference of a toy car versus a real car. One you play with, and the other works."
The app with the highest sensitivity for melanoma detection, the study found, did not use automated algorithms to analyze the images. Instead, the images were sent to board-certified dermatologists, and users received a diagnosis within 24 hours.

None of these apps, though, are not subject to regulatory oversight, and although disclaimers state they are for educational purposes only -- to help users track their lesions, for example -- dermatologists worry that people, particularly those who are lower-income and uninsured, might substitute the apps' findings for medical advice.

"It is very concerning that these apps are used for diagnosis by patients, as it could lead to delay in diagnosis of melanoma, the cancer which is perhaps the most critical in early diagnosis being important for survival," said Rigel.

The U.S. Food and Drug Administration has responded to the explosion of health-related smartphone apps and announced in July 2011 plans to regulate smartphone apps that paired with medical devices the agency already regulates, such as cardiac monitors and radiologic imaging devices. In 2012, Congress passed the FDA Safety and Innovation Act, allowing the FDA to regulate some medical apps on smartphones. But which apps will come under this regulation and which will not remains unclear.

Given their accessibility, these apps could hold tremendous potential once they have been evaluated, said Dr. Meg R. Gerstenblith, an assistant professor in the department of dermatology at Case Western Reserve University.

"If a patient were insistent on using one of these apps," said Gerstenblith, "I would inform him/her that the current study suggests that those apps that involve a board-certified dermatologist evaluating images of lesions may be superior to those that do not employ a board-certified dermatologist to evaluate the lesions."

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Segregation tied to more lung cancer deaths: study

Black lung cancer patients seem more likely to die of the disease than white cancer patients in the U.S., especially those living in segregated counties, according to a new study.

Researchers, who published their findings in JAMA Surgery on Wednesday, found blacks patients living in segregated counties had a lung cancer mortality rate about 10 percentage points higher than those living in diverse neighborhoods during the mid-2000s.

That compared to white lung cancer patients whose lung cancer mortality rate did not seem to change between segregated and diverse areas.

"We first thought it was a mistake. We ran it five times through the program," said the study's lead author Dr. Awori Hayanga, a lung transplant fellow at the University of Pittsburgh Medical Center.

"If you are one color living in one type of neighborhood versus another, 10 percent is huge," he said.

According to the American Cancer Society, lung cancer is the leading cause of cancer deaths for both men and women. It kills more people than colon, breast and prostate cancer combined.

In 2013, the Society projects over 228,000 Americans will be diagnosed with lung cancer, and about 159,500 will die from it.

For the new study, Hayanga and his colleagues used national databases to collect information on lung cancer deaths in U.S. counties between 2003 and 2007. They also classified those counties as low, moderate and high segregated areas based on their concentration of one race versus another.

Nationally, black lung cancer patients had about a 59 percent mortality rate when the researchers accounted for smoking and income, compared to about a 52 percent mortality rate in white patients.

When looking at specific counties, the researchers found white lung cancer patients' mortality rate remained steady between diverse and predominantly white counties - between about 50 percent and 53 percent.

For black lung cancer patients, however, there were larger differences.

Black patients living in diverse counties had a mortality rate of about 52 percent, which was comparable to white patients.

But black patients living in highly segregated counties had a mortality rate of about 63 percent. Black patients living in moderately segregated areas had a mortality rate of 57 percent.

While the study cannot prove living in a segregated community caused the worse mortality rates in black patients, Hayanga said there is probably something different in predominantly black communities.

ENVIRONMENTAL VS. PATIENT FACTORS

"The point I'm trying to make is that neighborhood segregation is not just a proxy for socioeconomic status. We accounted for that," said Hayanga. "That's where we ask ourselves, do we know about the different fabric of different neighborhoods?"

He told Reuters Health that by comparing different counties, a person would find one has resources the other does not, such as hospitals and doctors.

The new study shows there are some health problems that can't be explained by genetics and treated with drugs, said David Chang, who wrote a commentary accompanying the work.

Disparities are "probably one of the issues that it's not the patients that matter but the systems," Chang, from the University of California, San Diego, told Reuters Health.

"Location matters, and one has to be critical about where they live and where they pay taxes," said Hayanga, who worked with Chang on previous research.

Dr. Karen Reckamp, a lung cancer specialist at City of Hope in Duarte, California, said there should be a focus on getting cancer care where it's needed.

"There is more technology in our healthcare and it's becoming more complex. People living in more remote areas wouldn't have the knowledge or access to seek out that care," said Reckamp, who was not involved with the new study.

She added that the new research doesn't answer what needs to change in those communities, but may shine a light on where the disparities are coming from.

"What we're seeing is that we can't uproot half of the American population and move them to other counties. What we have to do is take responsibility for those neighborhoods," said Hayanga.

Tiny Tim, Houston's Beloved Fat Cat, Has Cancer

Tiny Tim, the hefty Houston feline that gained national attention for his overweight figure and subsequent strict diet and exercise plan, has been diagnosed with cancer in his leg that could prove fatal.

Dr. Alice Frei, who has been monitoring the 30-pound cat's progress at the Southside Place Animal Hospital, today announced Tiny's "aggressive tumor" on his Facebook fan page, "Tiny Tim at Spah."

"Tiny Tim has cancer," Frei wrote. "There is no radiation or chemotherapy for such an aggressive tumor."

Frei said Tiny was rushed to Texas A&M University School of Veterinary Medicine for treatment on Wednesday after SPAH staff noticed his elbow was swollen and pathology results showed cancer. A&M veterinarians confirmed the pathologist's findings, and "said the cancer was so rapidly growing that they could not define the cell of origin," Frei wrote.

Tiny is scheduled to have a CAT scan on Friday to see how far the tumor has spread. The SPAH staff will then assess a treatment plan, but options for the beloved cat seemed dire.

"If Tiny Tim's CAT scan does not show [the] tumor has invaded his chest, we have decided that the only course of treatment is to have the leg amputated," Frei wrote. "If the tumor has spread to his chest his treatment options are basically zero."

The staff is now waiting to see if Tiny will need surgery, but even that will be a difficult decision.


"Surgery for Tiny Tim is a huge risk because of his size, and if he makes it through the surgery he has a long road back," Frei wrote. "It will be rough. With it he may die. Without it he will die."

Tiny, who's about 9 years old, weighed in at a hefty 35.2 pounds when he arrived at the animal hospital around Christmas 2011, but testing showed that Tiny was otherwise healthy. When a search for his owner proved unsuccessful, the hospital took him in as a permanent resident -- provided he'd lose weight.

By New Year's, the "super sweet cat" had been placed on a strict diet for the year.

"He has been on a very, very regimented diet -- measured meal plans, the whole works, and he is at 28.6 pounds," SPAH manager Debbie Green told ABCNews.com in a recent interview. "He weighs in twice a week, and he gets meals measured in little bags throughout the whole week, so we know exactly what he's eating."

Tiny is fed a precise 307 calories per day, and his team of doctors would be "really, really excited if he got closer to 20 pounds," Green said.

Earlier this year, Tiny seemed to plateau at 30 pounds. The cat, somewhat ironically, lives in a food pantry in the animal hospital because he is too big for the normal cat cages at Southside. A staff member figured out Tiny had clawed a small hole into a bag of food and had been having midnight snacks.

Tiny's doctors make sure Tiny exercises by making him work for his bed and board. He is carried to the front of the clinic at least three times a day, and he has to walk the 50 feet back to his room for meals.

"He doesn't voluntarily walk around the office," Green said. "He used to move 10 steps and then sit down. Now he can get from the front to the back, which is about 50 feet, without much trouble at all."

Tiny's cancer hasn't been the only health concern for the SPAH staff. He is also at risk for feline diabetes or thyroid problems in the future because of his weight, Green said. They believe arthritis could become a problem for him too.

Regardless, the popular feline is usually pretty quiet and prefers the peace of his pantry to the business of the hospital's waiting room, but he enjoys the attention and brushing he receives from friends and fans who often stop by to visit him.

Tonight, he remained at the A&M veterinary hospital, where "he is doing fine, has the entire cat ward to himself and is getting lots of attention," according to his Facebook fan page.

http://abcnews.go.com/US/tiny-tim-houstons-beloved-fat-cat-cancer/story?id=18243559