Man who lost nose to cancer may get new one grown on his arm Read more: http://www.nydailynews.com/news/world/man-lost-nose-cancer-new-article-1.1247336#ixzz2IeJvj8Zf

ADAM GAULT/GETTY IMAGES

Scientists will create two prototypes in case someone drops one.

A man who lost his nose to cancer plans on getting it back by having doctors grow another one on his arm.

British scientists are taking a shot at the groundbreaking procedure by using the man’s bone marrow cells to grow the new nose, which they will then implant under skin in the man’s arm, in a highly controlled laboratory.

Doctors will initially grow two noses “just in case someone drops one,” using molds taken of the patient’s original nose before it was surgically removed, according to Dr. Alex Seifalian of University College London.

For two weeks, two prototypes will be maintained in a bioreactor with the heat set to approximate human body temperature, which helps the cells to multiply.

Simultaneously, Seifalian explained, doctors will insert a small balloon under the skin of one of the patient’s arms and inflate it little by little over weeks to help the skin stretch.

Once the facial features take shape, surgeons will implant one of them in the skin on one of the 53-year-old man’s arms. The unusual process will allow the new nose to grow its own skin and develop a normal blood supply.

"We can make the nose, but we can't make the skin," Seifalian told the Belfast Telegraph.

The made-from-scratch sniffer will remain in the man’s arm for four to six weeks as it continues to develop. After this period, doctors will then sew the nose to the patients face, open the nostrils and implant cells that allow for the secretion of mucus.

The exciting regenerative procedure is unprecedented, according to Seifalian. Doctors at University College London did not respond to a request for comment.

Read more: 

adenocarcinoma prostate

Study Shows ID Errors in Prostate Biopsies

As many as 3.5% of prostate biopsy specimens were contaminated or inadvertently switched with that of another patient, according to a review of 13,000 samples from 54 laboratories.

The overall error rate was less than 1%, but rates among different types of labs ranged as high as 3.51%. No laboratory included in the study had an error-free performance record.

Institutional approval for the study required investigators to remove all identifying information from the specimens. Consequently, the impact of the laboratory errors could not be assessed, as reported online in the American Journal of Clinical Pathology.

"It is possible that in a subset of cases, the adenocarcinoma from the foreign patient that was the source of the extraneous tissue exhibited sufficiently similar characteristics of the target patient such that either patient's diagnosis would have resulted in the same course of therapy," John D. Pfeifer, MD, PhD, and Jingxia Liu, PhD, of Washington University in St. Louis, wrote of their findings.

"Regardless of the portion of cases in which patients may have, by chance, received the correct treatment despite the specimen identity error, the fact remains that ... a diagnosis was assigned to the wrong patient with no knowledge or even suspicion of the error that had occurred."

The study examined the frequency of occult "specimen provenance complications" (SPCs), errors that occur without any indication of a problem. SPCs arise when specimens are matched to the wrong patients (type 1 error) or when one patient's specimen is contaminated by tissue from one or more other patients (type 2 error).

SPCs have obvious implications for patient safety and medicolegal actions, the authors noted in their introduction. However, the frequency with which these errors occur has remained unclear.

To describe the rates of both types of SPCs, Pfeifer and Liu analyzed data for 13,000 prostate biopsy specimens obtained in routine clinical practice. The specimens were processed by a variety of surgical pathology and urology group practice laboratories.

Data for the study came from Strand Analytical Laboratories, an Indianapolis company that has developed a DNA-based test for occult SPCs. The test employs short tandem repeat (STR) analysis, originally developed by the FBI.

"STR analysis has been shown to be particularly useful in identifying occult specimen identity errors," the authors noted in their introduction.

The investigators grouped the 54 laboratories into five categories based on work flow, location, and management structure: physician-owned labs within a group-practice setting, independent reference labs, hospital labs, nonphysician owned labs located in facilities shared with group practices, and labs that have the technical histopathology and professional pathology in separate facilities, necessitating transport of specimen slides.

The error rate for all labs combined was low: 0.26% for type 1 errors and 0.67% for type 2 errors. However, the authors pointed out, each SPC involved at least two patients, "the target patient and the foreign patient (or patients) whose tissue was misidentified as originating from the target patient."

Reference laboratories had the highest rate of SPCs: 0.37% for type 1 and 3.14% for type 2, resulting in an overall error rate of 3.51%.

Only one clinical trial has attempted to document SPCs, according to the authors. The Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial took steps to measure the rate of SPCs after three cases of occult biopsy specimen misidentification occurred during the first 2 years.

The rate of type 1 errors was 0.4% during the first 2 years of the REDUCE trial and declined to 0.02% in the final 2 years, after investigators implemented changes in specimen-handling procedures. A type 1 error rate of 0.5% persisted throughout the trial for blood samples that served as reference specimens.

Based on their study, the authors suggested that prospective DNA testing to confirm the identity of prostate biopsies that show adenocarcinoma may be useful for preventing treatment errors stemming from misidentification.

Strand Analytical Laboratories, which developed a test for STR analysis, provided the data for the study.

The authors had no relevant disclosures.

Primary source: American Journal of Clinical Pathology
Source reference:
Pfeifer JD, Liu J "Rate of occult specimen provenance complications in routine clinical practice" Am J Clin Pathol2013; DOI: 10.1309/AJCP50WEZHWIFCIV.

New cancer therapy program opens at Children’s Healthcare of Atlanta

Last week, Erin and Stephen Chance of Druid Hills returned to the place where their son Patrick died from neuroblastoma, a solid tumor of the sympathetic nervous system.
It was one of the hardest things they’ve ever done.



But for years before Patrick’s death last January, the Chances, who are both lawyers, had resolved to be in this fight for the long haul. From the moment they learned of his diagnosis, they began raising money to fund new treatments for neuroblastoma and in 2007 joined forces with CURE Childhood Cancer Inc. to make their efforts official.

And so here they were, back at the Aflac Cancer Center of Children’s Healthcare of Atlanta at Egleston, to talk about Patrick and the center’s new MIBG (metaiodobenzylguanidine) radiation therapy room named in his honor.

Before the therapy room was built, metro Atlanta families like the Chances had to seek MIBG treatment far from home. The new radiation therapy room at Children’s is one of only about eight in the nation, a scarcity caused by cost and a lack of clinical expertise.

“We’d experienced firsthand how hard it was to travel for treatment, to be separated from family, your emotional support and your hospital,” Erin Chance, 39, said. “So, we wanted to provide a place where families in the Southeast could come without traveling so far.”

MIBG treatment has a distinct advantage over traditional radiation.

“Many patients with cancer, when they receive radiation, lay on a table and a beam is focused on them. … A problem with that treatment is while it’s focused on the tumor itself, it hits other parts of the body. It works, but it has some collateral damage,” said Dr. Howard Katzenstein, director of the Innovative Therapy Program for cancer at Children’s Healthcare.

“This MIBG treatment allows the patient to be injected with the radioactive drug that targets the cancer cells directly. The radiation goes inside the tumor and the cells die. There’s a lot less surrounding damage,” Katzenstein said.

Talks to bring the treatment to the Aflac Cancer Center began six months ago when the CHOA Foundation requested a grant from the Chances.

“Stephen and I talked about it for about 30 seconds before we decided to fund the project,” Erin Chance said.

Because of their personal experience with the therapy, they also volunteered to help with the design. Instead of one room, they decided they needed two. One for the patients and one for the family.

When Patrick received MIBG treatment in Philadelphia, for instance, Erin Chance said he had to be isolated from them because he was literally radioactive. They were separated by lead shields, unable to safely touch or see him for days.

“If Patrick would fall asleep or was watching a movie, Stephen and I sat in the hallway to limit radiation exposure,” she said.

Stephen Chance, 44, said they decided to install televisions in each room along with three-way video and microphones, one for the nurses, and the others for the parent and child so that they can see each other on the monitors, talk to each other and actually play video games with one another.

“The parent is protected (from radiation) but has improved access to the child,” he said. “And the nurses can see the child on the monitor without exposure to radiation as well.”

The cost to build the connected rooms was more than $200,000.

Although the therapy room was built with neuroblastoma in mind, Katzenstein said it will also allow for similar treatment for thyroid cancer patients.

“If other drug treatments become available for other types of cancers, the room is built and we’re good to go,” he said.

Patrick Chance was 3 years old when he woke up one morning in 2006, unable to walk.

“From the moment he was diagnosed, it was obvious that there was a need for less toxic, more effective childhood cancer therapy,” Erin Chance said.

It was then that the couple began raising money to fund those new therapies and donating the proceeds to Children’s Healthcare of Atlanta.

In June 2007, they began collaborating with CURE Childhood Cancer, a nonprofit that funds research and provides support to patients and their families. The Chances formed Press On to CURE Childhood Cancer with another family to fund therapies for neuroblastoma and acute myeloid leukemia, two of the deadliest pediatric cancers in the country.

CURE provides them administrative support, a board of directors and a scientific advisory council.

“Their support enables us to do what we do best, which is fundraise,” Erin said.

Over the next five years, all the while caring for Patrick and his two sisters, they pressed on. Patrick died Jan. 9, 2012, his ninth birthday.

On Jan. 9, 2013, the Chances, Kristin Connor, executive director of CURE Childhood Cancer, and other dignitaries celebrated the grand opening of the new therapy room.

“In a lot of cultures, if you die on your birthday, it’s a sign you perfectly completed your mission on earth,” Erin Chance said. “For me, dedicating this room a year after he died was another completion of that circle. It was part of fulfilling what I believe was his mission on earth: touching people’s lives and changing the course of childhood cancer treatment.”

To date they have raised more than $1.5 million and have donated the money to leading childhood cancer hospitals across the country.

“We’re not done,” Stephen said. “We want to bring more resources to CHOA to help improve childhood cancer therapy. There are lots of January 9s yet to come.”

Drug Is Shown to Help Pancreatic Cancer Cases

Celgene’s drug Abraxane prolonged the lives of patients with advancedpancreatic cancer by almost two months in a clinical trial, researchers reported Tuesday, signifying an advance in treating a notoriously difficult disease but not as big a leap as some doctors and investors had hoped.

“It was not the breakthrough we were anticipating,” said Dr. Andrea Wang-Gillam, an assistant professor and pancreatic cancer specialist at Washington University in St. Louis, who was not involved in the trial.

Still, Dr. Wang-Gillam and others said any progress was welcome against metastatic pancreatic cancer, which has defied most treatments, with patients tending to live only about six months after diagnosis.

Pancreatic cancer is the fourth most common cause of cancer death, with 38,000 Americans expected to die this year, almost as many deaths as from breast cancer, according to the American Cancer Society. Yet there are only 45,000 new cases of pancreatic cancer a year compared with more than 230,000 new breast cancer cases.

“This is a disease that gave oncology a bad name,” said Dr. Robert Mayer, a professor at Harvard and the Dana-Farber Cancer Institute in Boston, who was not involved in the study. Now, he said, Abraxane, as well as another treatment combining four generic drugs, are showing some promise.

In Celgene’s trial, patients who received Abraxane plus gemcitabine, the standard drug for pancreatic cancer, lived a median of 8.5 months, compared with 6.7 months for those who received gemcitabine alone.

At the end of one year, 35 percent of those getting Abraxane were alive, compared with 22 percent of those getting only gemcitabine. After two years, the figures were 9 percent for those getting Abraxane and 4 percent for those who received gemcitabine.

The results of the study, which involved 861 patients, were released by Celgene and by the American Society of Clinincal Oncology in advance of a presentation of the data Friday at the Gastrointestinal Cancers Symposium in San Francisco.

The results were roughly in line with investors’ expectations, according to a recent survey by ISI Group.

Celgene’s stock closed at $99.31 on Tuesday and moved slightly lower in after-hours trading. The study results were released after the close of trading.

Abraxane is a novel form of the widely used cancer drug paclitaxel, also known by the brand name Taxol. In Abraxane, the paclitaxel is bound to albumin, a human protein in tiny particles. That is said to enhance delivery of the drug to tumors and reduce side effects.

Abraxane was approved to treat advanced breast cancer in 2005 and to treat non-small-cell lung cancer in October. Sales in the first nine months of 2012 were $320 million, a small percentage of Celgene’s revenues of $4.1 billion in that period, much of it from the multiple myeloma drug Revlimid.

Abraxane was developed by Abraxis BioScience, which Celgene acquired for $2.9 billion in 2010. Abraxis stockholders also received a security entitling them to additional cash payments if Abraxane won approval for pancreatic cancer. Celgene said Tuesday it would apply for such approval in the first half of this year.

A big impediment to future Abraxane sales in pancreatic cancer could be that its median survival was almost three months less than that of Folfirinox, a combination of four generic cancer drugs.

Results of a clinical trial published in 2011 showed that pancreatic cancer patients getting Folfirinox had a median survival of 11.1 months compared with 6.8 months for those getting gemcitabine.

Experts cautioned that it was difficult to draw conclusions since Abraxane and Folfirinox were not compared directly in the same trial. Nonetheless, doctors are going to make treatment decisions based on the separate results.

Abraxane, which Celgene says will cost $6,000 to $8,000 a month for a pancreatic cancer patients, is likely to be more expensive than Folfirinox. However, Folfirinox is hard to tolerate and requires the patient to wear an infusion pump.

“The simplicity of Abraxane plus gemcitabine may be attractive to physicians and patients,” said Dr. Neal J. Meropol, chief of hematology and oncology at University Hospitals and Case Western Reserve University in Cleveland. Abraxane does cause low white blood cell counts and nerve damage.

How much of an extension of life is meaningful to patients is a matter of some debate, especially with cancer drugs costing thousands of dollars a month.

In 2005 the Food and Drug Administration approved Tarceva, now sold by Roche and Astellas, to treat pancreatic cancer. In a clinical trial, those who got Tarceva plus gemcitabine had a median survival only 12 days longer than those who received a placebo plus gemcitabine.

This article has been revised to reflect the following correction:

Correction: January 22, 2013

An earlier version of this article misstated the specialty of Dr. Andrea Wang-Gillam, an assistant professor at Washington University in St. Louis. She is a specialist in pancreatic cancer, not prostate cancer.

By ANDREW POLLACK

Published: January 22, 2013

Sam Callahan faced cancer and lived his life to the fullest

Sam Callahan was a fighter and those who knew the 17-year-old say they'll remember him as an inspiration.

Sam died peacefully in the bedroom of his Campbell home on Jan. 14 after a 3 1/2-year battle with Ewing's sarcoma. He is survived by his mother Suzy Callahan van Bronkhorst, father Kenn Callahan, brother Joseph Callahan, stepfather Derek van Bronkhorst and grandfather Don Callahan, a lifelong resident of Los Gatos.

"He fought so hard," his stepfather said. "He really put up a battle. He never complained, never asked, 'Why me?' He took it head-on.

"He had his goals and he achieved those goals. But words can't express the effect he had on other people in the way he lived his life while he was here."

Sam's family will host a celebration of his life at Bellarmine College Preparatory, 960 W. Hedding St. in San Jose, on Jan. 24 beginning at 11:15 a.m. Sam was a junior at Bellarmine Prep.

Sam's life--along with the lives of his family members--changed forever in September 2009 when he was rushed to the hospital with a 102-degree fever and a pain in his side. After a series of tests doctors learned that it was Ewing's sarcoma, a rare type of cancer that frequently strikes teenage boys.

Doctors said that Sam's chances of living past a year were slim, van Bronkhorst said. But that didn't seem to shake Sam's confidence that he would not just live that long, van Bronkhorst said, but beat the deadly disease.

He was treated at Stanford University for about nine months, and then began flying to the University of Texas' MD Anderson Cancer Center in Houston for weekly treatments and then eventually to Santa Monica, his stepfather said.

Whether it was chemotherapy or clinical trials, he never talked too much to his friends about his illness. In fact, van Bronkhorst said, the teenager went out of his way to "just be Sam."

Although he lived a relatively short life, he made an impact on others, including Major League Baseball player Darnell McDonald.

Sam, an outstanding baseball player in his own right before he was stricken with the disease, met McDonald while the teenager and his family visited AT&T Park in San Francisco for a Giants-Red Sox game in 2010. As McDonald was saying goodbye, a family friend handed him a blue "Sam's Team" wrist band and said if he wore it during the game he would hit a home run.

McDonald, not known as a home run hitter, did wear the band and hit a ball into the stands.

"I thought of it as I was rounding second base," McDonald told the Boston Globe at the time. "I remember that they said I was going to hit a homer. And then I did. It made me feel blessed."

Sam and McDonald were able to meet a couple of more times and had "an amazing relationship," van Bronkhorst said.

It wasn't just McDonald who was inspired by Sam, van Bronkhorst added. He seemed to have a similar effect on many he came to know. Part of it may have been that he seemed mature beyond his years, both before and after his diagnosis.

Sam was asked, and eventually accepted the invitation, to speak at his eighth-grade graduation from St. Lucy Parish School. What he told his young peers could have been said to college graduates.

"No matter what the odds are against you, the human will is the strongest force in the world," Sam said. "In each of us we possess a drive that can move mountains and achieve anything we focus on."

Sam focused on living. And that's just what he did.

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

NI hospital offers new procedure for diagnosing lung cancer

A new technique for detecting lung cancer without the need for surgery is helping patients in Enniskillen, County Fermanagh.

A thin flexible telescope, called an endobronchial ultrasound, is inserted through the patient's mouth and provides camera pictures and ultrasound images.

Samples can also be taken which can lead to faster diagnosis.

Dr Terence McManus uses the device in the South West Acute Hospital.

The 30-minute procedure is carried out under local anaesthetic and patients can normally return home the same day.

Dr McManus, a respiratory consultant, said: "It's a new technique that allows us to biopsy and diagnose conditions at an earlier stage.

"It can, in some cases, avoid the need for more invasive surgery techniques.

"Using this technique we can diagnose conditions such as cancer, inflammatory conditions, and sometimes infections as well."Lung disease

He said it allowed doctors to "establish a diagnosis and then determine what is the most appropriate treatment for a patient as quickly as possible".

Approximately 900 people in Northern Ireland are diagnosed with lung cancer each year.

It is the second most common cancer among men and the third most common among women.

Stephen Hogan from Florencecourt, County Fermanagh, has lung disease and has undergone the procedure.

He described it as very simple and added it had no unpleasant side effects.

"The big difference for me is knowing where I'm at with the diagnosis and the referral on to the oncologist and then I know what my treatment options are. So, it actually gives you a sense of relief and it saves a lot of time.

"I'm dependent on some degree of oxygen so travelling between A and B is a bit of an issue and we're very lucky to have this brand new facility, so it's brilliant."

The South West Acute Hospital, which opened its doors six months ago, is the first in Northern Ireland to offer this service.

Joe Lusby, deputy chief executive of the Western Health Trust, said it demonstrated how the latest technology is benefiting patients in the new state-of-the-art hospital.

"Anything that provides a faster and more accurate diagnosis of lung disease is bound to be good for the patient," he said.

"This hospital is built for the next 60 years at least so what we were doing is not just transferring services across from the former Erne Hospital.

"We were determined to add services that were appropriate to provide locally so that people don't have to travel great distances to access these services."

About 90% of lung cancer cases are caused by smoking cigarettes and Dr McManus has also seen patients getting the disease at a younger age.

He said: "It can affect any age. Smoking is certainly the biggest risk factor so we would always emphasise the importance of stopping smoking as soon as possible, it's never too late to stop smoking."

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treatment of lung cancer (Adenocarcinoma Lung )

In the treatment of lung cancer. Depends on the stage of the cancer and the patient's condition. As well as the lungs. And other factors.

If cancer is detected. Has not spread anywhere.the ideal treatment is surgery to remove skin cancer from fresh.the three options are as follows.

Wedge resection is surgery to remove part of the lung.lobectomy was cut out of one lung lobe (lobe).pneumonectomy is cut out all the lung.

Surgery is required to remove the lymph nodes.
Check the spread of cancer cells to the lymph nodes as well.

Some doctors may use. video-assisted thoracoscopy (VATS) surgery.
The tumor is small. The initial phase. Especially in the border area.
The output of the lungs, called VATS has been used for the diagnosis.
Of lung cancer as well.

The surgery to remove the lung. Can cause respiratory problems in the second.
Especially in patients with severe emphysema. Before surgery, your doctor should monitor their lung function before and.Expect. After surgery, the result would be?
In some cases, surgery may be impossible.

If the cancer has spread. Treatment may include "chemical treatment".
And "radiotherapy", which may be earlier. Or after the surgery.

In cases where the tumor has already spread. The way in which chemotherapy.
Select to slow the growth of cancer. 

Do not expect to be cured.
Treatment with chemical treatment. Can cause the symptoms of the disease can do better.The lives of patients with lung cancer live longer than I have.

And radiation. Enable to reduce the symptoms of lung cancer.
It will be used in cases where the cancer has spread to the bone and cause.
Bone pain. It can be used in combination with a chemical treatment.
Tumor confined to the breast.

Patients who can not tolerate surgery because of this.
Patients may receive radiation. With chemical treatment. O alone.
For the tumor reduced.

As the treatment of cancer has evolved very ...
Some cancer treatment centers. Check for any abnormalities.
Specific genes (mutations) and treatment of cancer.
The process is called "targeted therapy".

Directing therapy to inhibit the growth of tumor cells in the wave.
By chemical reaction. Focusing on the transformation of the Alliance.
For example, gene therapy can targetedterapy something.
Prevent cancer has been a growing wave of orders ...

Knowledge. Genetic variation (specific genetic mutation).We can provide that. Patients should be treated every battle.For example, women with adenocarcinoma. Those who have never smoked before

Prognosis (prognosis).
Appearance of lung cancer. adenocarcinoma. Report directly to global health.
The patients themselves. In general, cancer has a poor prognosis.In particular, the cancer has spread outside the breast or.The cancer spread to lymph nodes. That is in both lungs.


Possibility of treating lung cancer is cured. There was only one case is cut.
Cancer out. Or kill cancer cells outside.Of lung cancer, but a doctor. Has spread to the waste.Likely to be cured, it can be difficult.Only one out of five patients only. This can survive up to five years.

After completion of the procedure then.
Patients should be monitored periodically.Although the results of treatment in the early stages, it seems. Cancer is already lost.However, cancer is seen once again during the month or year

Immune Cells, Cytokines Predict Recurrence in Stage I Lung Adenocarcinoma

Expression of certain immune markers in tumor and surrounding cells can help predict probabilities of recurrence in patients with stage I lung adenocarcinoma, according to new work by researchers at Memorial Sloan-Kettering Cancer Center in New York.

According to senior author Prasad S. Adusumilli, MD, the presence of a “good” immune response can apparently help prevent the cancer’s recurrence. In the new study, Adusumilli and colleagues looked for eight tumor-infiltrating immune cells as well as five cytokines in 956 patients with stage I lung adenocarcinoma; the first 478 patients were considered a training cohort, and the second group of 478 was a validation cohort. The results were published online ahead of print on December 26 in the Journal of Clinical Oncology.

Among the immune cells, a high density of FoxP3-positive cells in the tumor-associated stroma was significantly associated with recurrence (P = 0.43 vs low density). The ratio of FoxP3 to CD3 cells was an even stronger predictor, however; the 5-year recurrence-free probability was 85% for those with a high ratio and 77% for those with a low ratio (P = 0.004). This result was replicated from the training cohort to the validation cohort.

High magnification micrograph of a primary lung adenocarcinoma showing nuclear staining with a TTF-1 immunostain; source: Nephron, Wikimedia Commons

Of the cytokines tested, several were found to have prognostic value. Higher expression levels of interleukin-12 receptor beta-2 (IL-12RB2) was associated with better recurrence rates than lower expression, with a 5-year recurrence-free probability of 90% for the former and 80% for the latter (P = 0.026). In contrast, high expression of tumor IL-7R yielded a poorer 5-year recurrence-free probability of 76% vs 86% for those with lower expression of the cytokine (P = 0.001). These results were also replicated in the validation cohort after first appearing in the training cohort. The other three cytokines tested—CCR7, CXCL12, and CXCR4—showed no significant associations with recurrence.

Multivariate analysis showed that these three immune markers—stromal FoxP3-CD3 ratio, IL-12RB2, and IL-7R—are independently associated with recurrence. The FoxP3-CD3 ratio had a hazard ratio (HR) for recurrence of 2.00 (95% CI, 1.22–3.27; P = 0.006). The two cytokines had HRs of 2.24 (95% CI, 1.02–4.95; P = 0.045) and 1.65 (95% CI, 1.02–2.68; P = 0.45), respectively.

The authors wrote that the current system for evaluating of stage I disease relies only on anatomic factors. “In fact, for stage I lung adenocarcinoma, tumor size is the only standard prognosticator available,” they wrote. “In our study, we have demonstrated the prognostic power of immunologic parameters for stage I lung adenocarcinoma.”

Notably, when overall survival was used as an endpoint rather than recurrence, only IL-7R remained a significant prognosticator (P = 0.007). “The ability of IL-7R to prognosticate both recurrence-free and overall survival merits further investigation of its biologic role,” the authors wrote.

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