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Rodeo Competitors Fight Smokeless Tobacco Use at Laramie Jubilee Days

Source: www.y95country.com
Author: Nick Learned

Cody Kiser and Carly Twisselman

Two professional rodeo contestants will ride exclusively for the Oral Cancer Foundation this weekend as part of Laramie Jubilee Days with a goal of preventing young fans from using smokeless tobacco.

Cody Kiser and Carly Twisselman each aim to show rodeo fans, particularly the younger ones, chewing or using other forms of smokeless tobacco isn’t what makes them who they are. They promote the Foundation’s campaign which uses the slogan “Be Smart. Don’t Start.”

Their approach is anything but confrontational or aggressive. Rather than encouraging people to quit, they hope to encourage young fans to never pick up the habit in the first place. And where some rely on statistics to make the point, Kiser and Twisselman take a different approach. Simply giving attention to young rodeo fans is a big part of getting their message across.

“Its not the facts that they’re going to take home,” Kiser says. “Everybody knows that tobacco’s bad; you can get cancer and you can die. But the biggest impact that I see is just acknowledging those kids or acknowledging those people in the audience that want to know more, and you can show them what you can do without tobacco.”

“I’m not out there to tell anybody how to live their life or preach to them about needing to quit,” Kiser says.

“It’s not our place to do that,” Twisselman says. “People most of the time aren’t going to listen when you tell them something like that anyway.”

The pair will be wearing Oral Cancer Foundation gear and handing out buttons, wristbands and bandanas bearing campaign messaging.

As they travel the rodeo circuit, Kiser and Twisselman each say they often see other riders use various types of smokeless tobacco such as chew and snuff.

“It’s very common,” says Kiser. “You see it everywhere.”

“One of my traveling partners, he started when he was in high school. He was just around it all the time,” says Kiser. “It was just the ‘cowboy’ thing to do, I guess.”

“A lot of people are very respectful about it,” Twisselman says. “They’ll see me in my shirt and be like ‘oh yeah, you represent the Oral Cancer Foundation’ and they’ll spit their chew out. I think that in itself is a positive side effect of it.”

“I think a large part of a lot of these cowboys is, it’s the cowboy thing to do, so they start doing it,” Kiser says. “And that’s where I want to step in and show the younger generation that you don’t have to chew to be a cowboy. You can be a cowboy athlete and not chew and treat your body as best you can, because what we do is very difficult and it’s hard on the body.”

“A lot of folks started when they young,” Kiser says. “And I’ve talked to guys who started chewing later in life and they can’t quit, or it’s hard for them. It’s a vicious thing.”

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

Rodeo outreach program fights oral cancer

Source: www.olivesoftware.com
Author: Stewart M. Green

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Carly Twisselman, a spokesperson with the Oral Cancer Foundation’s rodeo outreach program, and her horse Chanel travel the Western rodeo circuit and talk with kids about the dangers of using spit tobacco. Photo by Stewart M. Green

Carly Twisselman brushed her horse Chanel outside a stall at the Norris-Penrose Event Center, home of the Pikes Peak or Bust Rodeo, which will roll into town July 13-16. “I’ve been rodeoing my whole life,” she said. “Now I do it at the professional level. This is my rookie year so I’m going really hard. I want to win the rookie title.”

Summer is the busiest time of the year for cowgirls and cowboys. “We call it Cowboy Christmas, the 4th of July run,” she said. Twisselman and her travel partner have recently competed in Utah, Nevada, Arizona, New Mexico, and just drove up from Pecos, Texas, to Colorado Springs for qualifiers. “It’s a crazy time,” she said. “Lots of traveling, but lots of money to be won.”

Twisselman, a 30-year-old barrel racer, grew up on a ranch near San Luis Obispo on the central California coast. “My family’s been ranching there for seven generations,” she said. “I was on the back of a horse all the time. I was riding before I could walk.”

While growing up in the Western ranching and rodeo culture, Twisselman was aware of the widespread use of spit tobacco by cowboys. “I’ve been around it my whole life and seen a lot of things that were negative and I was affected by it.”

Rodeo and tobacco have a long history together. Starting in 1986, the U.S. Smokeless Tobacco Company sponsored the Professional Rodeo Cowboys Association until the association ended its partnership with tobacco advertisers in 2009. Tobacco use, however, still thrives with cowboys and spectators at rodeos.

In 2014, the Oral Cancer Foundation, a nonprofit organization that supports prevention, education and research of oral cancer, reached out to pro rodeo athletes to spread the word about the dangers of tobacco use, with Cody Kiser, a bareback bronc rider, as their first rodeo spokesperson. This past year they added Carly Twisselman to continue creating awareness in the rodeo community.

“Honestly, it was God that they came to me,” said Twisselman. “Their goal was to reach rodeo people, people in the Western culture and people that were horse lovers because tobacco is a huge problem in rodeo.” The foundation asked Twisselman to be a spokesperson and she gladly accepted. “It’s an amazing thing to represent such a great organization. I can take this rodeo platform where I’m in front of thousands of people and use it for good.” While the Oral Cancer Foundation wants to help adults with tobacco problems, its rodeo focus is on children. According to The Centers for Disease Control and Prevention, 9.9 percent of high school-age boys use spit tobacco nationwide, while 10.5 percent of men ages 18-25 use it. Usage is higher in rural states like Wyoming, Montana and West Virginia. A can of spit tobacco packs as much nicotine as 40 cigarettes, and a 30-minute chew is like smoking three cigarettes, making addiction to spit tobacco one of the hardest to break. Spit tobacco, including smokeless tobacco, dip, snuff, chew and chewing tobacco, can cause gum disease, tooth decay and oral cancer. Almost 50,000 people will be diagnosed with oral cancer in 2016.

“We aren’t telling people they should stop,” Twisselman said, “but we show people why it’s not good to use tobacco. If someone is chewing, I’m not going to go lecture them.”

Twisselman and Kiser focus on helping kids make positive choices about tobacco use. “Kids look up to us as idols and if they see us doing good and not chewing tobacco then maybe they won’t either,” Twisselman said. “Our message is: ‘Be Smart, Don’t Start.’”

Twisselman also attends junior rodeos where she hands out wristbands, bandanas, pins, and buttons. “Kids love the freebies,” she said. She also wears Oral Cancer Foundation logos on her competition shirts.

Surprisingly, some rodeo women chew tobacco. “It’s not the problem it is with the men,” Twisselman said, “but I do see it. I find it really repulsive. Sometimes women who chew will see me and say, “Oh, you work with oral cancer” and they’ll take their chew out and throw it away because they don’t want to be disrespectful to me.”

Twisselman said she and Kiser are making a difference, noting people are becoming more educated about the dangers of throat cancer from chewing tobacco and learning that it’s not a healthy habit. “We’ve only been doing this for a year now and we’re still getting our feet wet,” she said. “It’s hard to know if fewer kids are chewing now but I’m getting the word out and interacting with them. Because we take the time to talk with kids and give them the little gifts, it has a huge impact on them.”

To learn more about oral cancer and its prevention, medical research, education and for patient support, then visit oralcancer.org.

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

Rodeo rider partners with nonprofit group to fight smokeless tobacco use

Source: www.fox13now.com
Author: Rebecca Cade
 

SALT LAKE CITY — Oral cancer is becoming an epidemic in the U.S., and has been in the news in the last year with the loss of major league baseball hall-of-famer, Tony Gwynn, who died at 54 from smokeless tobacco use.

Rodeo has a historic tie to smokeless tobaccos, and Oral Cancer Foundation, has teamed up with Bareback Rider Cody Kiser to draw awareness to, and prevent, this growing epidemic where it thrives – the rodeo circuit.

Smokeless/spit tobacco is one of the historic causes of deadly oral cancers, and is more addictive than other forms of tobacco use.

The nonprofit is seeking to spread awareness of oral cancer and the dangers of starting terrible tobacco habits. While others are focused on getting users to quit, The Oral Cancer Foundation is reaching out to young people to not pick up the habit that they may see one of their rodeo “heroes” engage in.

Their message is simple, “Be Smart. Don’t Start.”

With the strong addictive powers of smokeless tobacco, the foundation and Kiser aim to engage fans early.

At the rodeos, Kiser will be solely wearing OCF logos and wording, while handing out buttons, wristbands and bandanas with the campaign messaging on them. The bareback rider hopes this will make him an alternative positive role-model for the adolescent age group whose minds are so easily molded.

“It’s something I’ve always been passionate about, so when I got into the partnership with OCF, it was no big deal to be able to say ‘I don’t smoke or chew, never have, and it’s easy not to,'” Kiser said.

Kiser added it all starts with kids.

“Most of these guys I ride with started smoking and chewing in sixth or seventh grade,” he said. “So, if we can get to those kids now, and tell them ‘you don’t have to do this to be cool or be a cowboy’ and show them what you can do without it.”

More information on the campaign can be found at www.oralcancer.org

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

Aspen Dental Practices Donate More Than $20,000 To The Oral Cancer Foundation For Oral Cancer Awareness Month

Source: www.pharmiweb.com.org
Author: Aspen Dental
 

SYRACUSE, N.Y., May 31, 2016 /PRNewswire/ — Aspen Dental–branded practices will donate $22,375 to The Oral Cancer Foundation (OCF) as part of a program that contributed $5 for each ViziLite® oral cancer screening conducted during April for Oral Cancer Awareness Month. In total, more than 4,000 patients were screened across more than 550 practices in 33 states.

Since 2010, Aspen Dental-branded practices have donated more than $105,000 to OCF.

“Approximately 48,250 people in the U.S. will be diagnosed with an oral or oropharyngeal cancer this year; and of those only about 57% will be alive in five years,” said Natalie Riggs, Director of Special Projects for The Oral Cancer Foundation. In 2016 we estimate that 9500 individuals will lose their lives to oral cancers and we are grateful for the support from Aspen Dental practices in helping us raise awareness and aiding in our efforts to fight this disease.”

Oral cancer is frequently preceded by visible pre-malignant lesions and can be diagnosed at a much earlier stage (I or II) with ViziLite® Plus, a specially designed light technology.  When caught early and treated, the survival rate is 80 to 90 percent.

“We’re working to educate our patients about the risk factors, warning signs and symptoms associated with oral cancer so that we can help them catch the disease before it progresses,” said Dr. Murali Lakireddy, a general dentist who owns Aspen Dental offices in Ohio. “Many of our patients do not think about oral cancer when they go to the dentist, but in fact, oral cancer screenings are just as much a part of your routine dental visit as a deep clean from the hygienist.”

To learn more about oral cancer screenings, visit the OFC website at http://www.oralcancerfoundation.org/dental/how_do_you_know.html.

About Aspen Dental Practices
Dentists and staff at Aspen Dental practices believe everyone has the right to quality, affordable oral health care. As one of the largest and fastest-growing networks of independent dental care providers in the U.S., local Aspen Dental practices – more than 550 of them across 33 states – offer patients a safe, welcoming and judgment-free environment to address their dental challenges. Every Aspen Dental-branded practice offers a full range of dental and denture services – including comprehensive exams, cleanings, extractions, fillings, periodontal treatment, whitening, oral surgery, crown and bridge work – allowing patients to have the peace of mind that they are taken care of and protected, so they can focus on getting the healthy mouth they deserve. In 2015, Aspen Dental-branded practices recorded more than 3.7 million patient visits and welcomed nearly 785,000 new patients.

Nivolumab Demonstrated Survival Benefit, Good Tolerance in Refractory HNSCC

Source: www.asco.org
Author: Tim Donald, ELS
 

In the phase III comparative CheckMate 141 trial, nivolumab demonstrated a “significant improval in survival” in patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC), compared with therapy of the investigator’s choice, according to Robert L. Ferris, MD, PhD, FACS, of the University of Pittsburgh Cancer Institute (Abstract 6009). There were fewer treatment-related adverse events with the PD-1 inhibitor than with investigator’s choice therapy, Dr. Ferris said, and nivolumab stabilized patient-reported quality-of-life outcome measures, whereas the investigator’s choice therapy led to meaningful declines in function and worsening of symptoms.

AM16.6009-Ferris2Dr. Robert L. Ferris

“Nivolumab is a new standard-of-care option for patients with refractory or metastatic HNSCC after platinum-based therapy,” Dr. Ferris said.

Dr. Ferris presented the trial results at the “Harnessing the Immune System in Head and Neck Cancer: Evolving Standards in Metastatic Disease” Clinical Science Symposium on June 6. He noted that in this trial of patients whose disease had progressed after platinum-based therapy, nivolumab doubled the 1-year overall survival (OS) rate, with 36.0% OS for the immunotherapeutic drug compared with 16.6% for the investigator’s choice therapy. These top-line results were presented at the 2016 American Association of Cancer Research meeting1; Dr. Ferris presented data the additional endpoints of quality of life, correlative biomarkers, and safety.

There is an extremely poor prognosis for patients with platinum-refractory recurrent or metastatic HNSCC, with median OS of 6 months or fewer. Previous research, by Dr. Ferris and others, has shown that HNSCC can express T-cell suppressive ligands, such as PD-L1, thereby evading host immune response. PD-L1 is frequently expressed on HNSCC cells, both HPV-positive and -negative.

The phase III CheckMate 141 study enrolled patients with HNSCC aged 18 and older with ECOG status 0 or 1, and with disease progression within 6 months after the most recent dose of platinum-based therapy. Patients were enrolled regardless of PD-L1 status and irrespective of number of previous lines of therapy. Immunohistochemistry testing for p16 was performed to determine HPV status. Patients were randomly assigned 2:1 to nivolumab (3 mg/kg intravenous [IV] every 2 weeks) or investigator’s choice of single-agent therapy with methotrexate (40 mg/m² IV weekly), docetaxel (30 mg/m² IV weekly), or cetuximab (400 mg/m² IV once, then 250 mg/m² weekly).

OS was compared between arms and by PD-L1 expression and HPV (p16) status. Nivolumab demonstrated a survival benefit in the overall study population, regardless of PD-L1 expression or p16 status, Dr. Ferris said. The magnitude of the OS benefit of nivolumab was greater in patients expressing PD-L1 at 1% or more (HR 0.55, 95% CI [0.36, 0.83]) compared with those expressing PD-L1 at less than 1% (HR 0.89, 95% CI [0.54, 1.45]). However, increasing levels of PD-L1 expression ( ≥ 5%, ≥ 10%) did not result in further OS benefit.

The OS benefit was greater with nivolumab than investigator’s choice therapy in both patients who were p16 positive (HR 0.56, 95% CI [0.32, 0.99]) and p16 negative (HR 0.73, 95% CI [0.42, 1.25]). When OS was analyzed for both PD-L1 expression and p16 status, the hazard ratios favored nivolumab for all subgroups.

Treatment-related adverse events of any grade were lower in the nivolumab arm (58.9%) than the investigator’s choice therapy arm (77.5%). Serious (grade 3 or 4) treatment-related adverse events were also lower in the nivolumab arm (13.1%) than in the investigator’s choice therapy arm (35.1%). Patient-reported outcome measures for quality of life were assessed based on two EORTC scales. Treatment with nivolumab stabilized the outcome measures of physical function, social function, absence of sensory problems, and absence of trouble with social contact, whereas the investigator’s choice therapy led to meaningful declines in function and worsening of symptoms.

AM16.6009-Uppaluri_0Dr. Ravindra Uppaluri

Discussant Ravindra Uppaluri, MD, PhD, of Washington University School of Medicine, said that the CheckMate 141 trial “continues to highlight the use of PD-L1 status as a stratifier.” The trial results “offer hope for patients with refractory or metastatic HNSCC,” he said. “Obviously better biomarkers are needed, and, ultimately, a composite immune profile may be required.”

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

June, 2016|Oral Cancer News|

HPV is changing the face of head and neck cancers

Source: www.healio.com
Author: Christine Cona
 

A drastic increase in the number of HPV-associated oropharynx cancers, particularly those of the tonsil and base of tongue, has captured the attention of head and neck oncologists worldwide.

In February, at the Multidisciplinary Head and Neck Cancer Symposium in Chandler, Ariz., Maura Gillison, MD, PhD, professor and Jeg Coughlin Chair of Cancer Research at The Ohio State University in Columbus, presented data that showed that the proportion of all head and neck squamous cell cancers that were of the oropharynx — which are most commonly HPV-positive cancers — increased from 18% in 1973 to 32% in 2005.

9ea467bbf8646a69da2a432f8fcc5452Maura Gillison, MD, PhD, Jeg Coughlin Chair of Cancer Research at The Ohio State University, said screening for HPV in the head and neck is years behind cervical screening for HPV.

 

In addition, studies from the United States, Europe, Denmark and Australia indicate that HPV-positive patients have a more than twofold increased cancer survival than HPV-negative patients, according to Gillison.

With the rising incidence of HPV-related oropharynx cancers, it will soon be the predominant type of cancer in the oral or head and neck region, according to Andy Trotti, MD, director of radiation oncology clinical research, H. Lee Moffitt Cancer Center & Research Institute, in Tampa, Fla.

“We should be focusing on HPV-related oropharyngeal cancer because it will dominate the field of head and neck cancers for many years,” he said during an interview with HemOnc Today. “It is certainly an important population for which to continue to conduct research.”

Because HPV-associated oropharyngeal cancer is emerging as a distinct biological entity, the recent rise in incidence will significantly affect treatment, and prevention and screening techniques, essentially reshaping current clinical practice.

Social change driving incidence

In the analysis performed by Gillison and colleagues, trends demonstrated that change in the rates of head and neck cancers was largely due to birth cohort effects, meaning that one of the greatest determinants of risk was the year in which patients were born.

The increased incidence of HPV-related oropharyngeal squamous cell carcinoma started to occur in birth cohorts born after 1935, indicating that people who were aged in their teens and twenties in the 1960s were demonstrating increased incidence, Gillison said.

“Two important and probably related events happened in the 1960s. In 1964, the surgeon general published a report citing smoking as a risk factor for lung cancer, and public health policy began promoting smoking cessation along with encouragement not to start smoking,” she told HemOnc Today.

If you were 40 years old between 2000 and 2005, your risk for having HPV-related cancer is more than someone who was between the age of 40 and 45 years in 1970, according to Gillison. Social changes that occurred among people born after 1935, for example, a reduction in the number of smokers, is consistent with the increasing proportion of oropharyngeal cancers that were HPV-related.

“The rates for HPV-related cancers began to increase and the rates for HPV-unrelated cancers started to decline, consistent with the known decline in tobacco use in the U.S. population,” she said.

Now, most cases of head and neck squamous cell carcinoma in non-smokers are HPV-related; however, oral HPV infection is common and is a cause of oropharyngeal cancer in both smokers and non-smokers, research shows.

In addition to a decrease in tobacco use reducing HPV-unrelated oral cavity cancers, the number of sexual partners may have increased during this time and have helped to increase HPV-related oropharyngeal cancers, according to Gillison.

Determining the cause of the elevated incidence is only a small piece of the puzzle. Screening, establishing who is at risk, and weighing vaccination and treatment options are all relevant issues that must be addressed.

Screening is problematic

A critical area for examination and research is the issue of screening for oral cancers. In contrast to cervical cancer, there is no accepted screening that has been shown to reduce incidence or death from oropharyngeal cancer, according to Gillison.

Not many studies have examined the issue of screening for HPV-unrelated oral cancers, and the few that have, tend to include design flaws.

Gillison said there is a hope that dentists would examine the oral cavity and palpate the lymph nodes in the neck as a front-line screen for oral cancer; however, in her experience, and from her perspective as a scientist, this has never been shown to provide benefit for oral cancer as a whole.

Another caveat with regard to HPV detection is that head and neck HPV screening is about 20 years behind the cervical field.

“Clinicians screening for HPV in the field of gynecology were incredibly fortunate because Pap smear screening was already an accepted cervical cancer screening method before HPV was even identified,” she said. “There was already a treatment algorithm: If there were cytologic abnormalities, patients were referred to the gynecologist, who in turn did a colposcopy and biopsy.”

A similar infrastructure does not exist for oropharyngeal cancer. People with HPV16 oral infection are at a 15-fold higher risk for oropharynx cancer and a 50-fold increased risk for HPV-positive head and neck cancer, yet there is no algorithm for treatment and management of these at-risk individuals, Gillison said.

In 2007, WHO said there was sufficient evidence to conclude that HPV16 was the cause of oropharynx cancer, but with no clinical algorithm already established, progress in this area is much further behind.

Another problematic aspect of HPV-related oropharyngeal cancer screening is that the site where the cancer arises is not accessible to a brush sampling, according to Gillison.

“To try to find this incredibly small lesion in the submucosal area that you cannot see and cannot get access to with a brush, highlights that we need to develop new techniques, new technologies and new approaches,” she said.

The near future consists of establishing the actual rates of infection in the oral cavity and oropharynx, and then screening for early diagnosis, according to Erich Madison Sturgis, MD, MPH, associate professor in the department of head and neck surgery and the department of epidemiology at The University of Texas M.D. Anderson Cancer Center.

“I am not extremely hopeful because the oropharyngeal anatomy makes screening complicated, and these cancers likely begin in small areas within the tonsils and the base of the tongue,” Sturgis told HemOnc Today. “I am hopeful, however, that preventive vaccines will eventually, at a population level, start to prevent these cancers by helping people avoid initial infection by immunity through vaccination earlier in life.”

Much of the currently known information surrounding the issue of HPV-related oral cancers is new, so researchers continue to conduct research in various relevant areas. One key question to answer is who may be at higher risk for HPV-related oropharynx cancers.

Who is at risk?

As mentioned earlier, the number of oral sex partners seems to play a role in the risk for contracting the HPV virus.

In one study published in The New England Journal of Medicine in 2007, findings demonstrated that a high lifetime number of oral sex partners (at least six partners) was associated with an increased risk for oropharyngeal cancer (OR=3.4; 95% CI, 1.3-8.8).

In addition to a higher number of oral sex partners, other still unknown factors may be contributing to risk. This is an area that needs further research, according to Barbara Burtness, MD, chief of head and neck oncology, and professor of medical oncology at Fox Chase Cancer Center in Philadelphia.

The effect of smoking status is another area that needs further research. According to Burtness, smokers with HPV-associated oropharynx cancer have less favorable outcomes.

When discussing the prognosis of HPV-associated cancers, Sturgis said low risk is defined as low or no tobacco exposure and positive HPV status, and intermediate risk is defined as significant tobacco exposure but an HPV-positive tumor, and the highest risk group appears to be the HPV-negative group.

Although HPV-negative cancers are overwhelmingly tobacco-related cancers and tend to have multiple mutations, it appears that HPV-positive cancers, particularly those in patients with low tobacco and alcohol exposure, tend to lack mutations and to have a better prognosis, and this may ultimately help to guide treatment practices, according to Sturgis. Yet, there is still much to learn about HPV-related oropharyngeal cancers on various fronts.

Vaccination a hopeful ally

In HPV-related head and neck cancer, particularly oropharynx cancers, more than 90% of patients who have an HPV-type DNA identified, have type 16, according to Sturgis.

The two current HPV vaccines, Gardasil (Merck) and Cervarix (GlaxoSmithKline), which are approved for cervical cancers, include HPV types 16 and 18; therefore, in theory, they should be protective against the development of infections in the oropharynx and protective at preventing these HPV-associated cancers from occurring.

The presumption is that if there was a population-wide vaccination against HPV, there would be less person-to-person transmission, and this would lead to fewer oropharynx cancers, according to Burtness, who said this theory still needs further research.

There is excitement at the possibility that therapeutic vaccines could be developed, and various groups are investigating this, Burtness added.

“There is reason to think that the vaccines may be helpful; however, when HPV infects the tonsillar tissues, it exerts control in the host cells by making two proteins: E6 and E7; so another potentially exciting therapeutic avenue would be to target those specific viral proteins,” she told HemOnc Today.

Anxiety about protection from the HPV virus is palpable, according to Sturgis. He described the worry that many patients experience about contracting and transmitting HPV infection.

“Many patients are concerned they will put their spouses and/or children at risk in ways such as kissing them; and we need to tone down those worries until we have better data,” he said.

Screening and vaccination are fundamental aspects of current ongoing research, but of equal importance is determining what clinicians should do to treat a population of patients with HPV-related oropharyngeal cancers.

HPV status may influence treatment

With rates of HPV-related cancers escalating, determining the appropriate treatment for these patients is crucial.

During the past 10 years, findings from retrospective studies have shown that patients with HPV-related cancers have a much better prognosis than patients who test negative for HPV. Findings from several retrospective analyses from clinical trials conducted during the past 2 years have come to the same conclusion, according to Gillison: HPV-positive patients have half the risk for death compared with patients negative for HPV.

Therefore, there may be several alternative treatment options, including the possibility of reducing the dose of radiation given to patients after chemotherapy, thereby reducing toxicity.

Comparing HPV-negative and HPV-positive patients may not be enough to determine proper treatment, researchers said. Data between different cohorts of HPV-positive patients also needs to be examined. Smoking, for example, may play a role in patient outcome.

In a prospective Radiation Therapy Oncology Group clinical trial (RTOG 0129), presented by Gillison at the 2009 ASCO Annual Meeting and recently published in The New England Journal of Medicine (see page 53), researchers conducted a subanalysis of the effect of smoking on outcome in uniformly staged and treated HPV-positive and HPV-negative patients while accounting for a number of potential confounders. HPV-positive patients who were never smokers had a 3-year OS of 93% compared with heavy smoking HPV-negative patients who had an OS of 46%.

The study found that smoking was independently associated with OS and PFS. Patients had a 1% increased risk for death and cancer relapse for each additional pack-year of smoking. This risk was evident in both HPV-positive and HPV-negative patients. Gillison said smoking data must be paid attention to, and she encouraged cooperative group research on the topic.

Most of the findings demonstrate improved outcomes for patients with HPV-positive oropharyngeal cancers vs. patients with HPV-negative oropharyngeal cancers, according to the experts interviewed by HemOnc Today.

Dose de-intensification for less toxicity

To date, there is no evidence that HPV-related cancers should be managed differently than HPV-unrelated cancers, but it is a hot topic among clinicians in the field, according to Burtness.

The superior outcomes for HPV-associated oropharynx cancer have suggested the possibility of treatment de-intensification. The use of effective induction chemotherapy may permit definitive treatment with a lower total radiation dose. In theory, this would reduce the severity of late toxic effects of radiation, such as swallowing dysfunction. Such a trial is being conducted by the Eastern Cooperative Oncology Group. Burtness said this is currently pure research question.

“There is still much research that needs to be done before clinicians can safely reduce the dose of radiation administered to HPV-positive patients,” Burtness said.

Currently, she and colleagues in the ECOG are conducting a study of patients with HPV-associated stage III or IV oropharynx cancers to examine the possibility of tailoring therapy to these patients. Patients are assigned to one of two groups: low-dose intensity-modulated radiotherapy 5 days per week for 5 weeks (27 fractions) plus IV cetuximab (Erbitux, ImClone) once weekly for 6 weeks, or standard-dose intensity-modulated radiotherapy 5 days per week for 6 weeks (33 fractions) plus IV cetuximab once weekly for 7 weeks.

If patients have a very good clinical response to chemotherapy, which is likely to happen with HPV-associated cancers, they are eligible to receive a reduced dose of radiation, and hopefully, they would experience less adverse effects, Burtness said.

“Patients who are treated with the full course of radiation for head and neck cancer are now getting 70 Gy, and they are often left with dry mouth, and speech and swallowing difficulty,” she said. “We are hopeful that if these particular cancers are treatment responsive to chemotherapy, we may be able to spare the patient the last 14 Gy of radiation.”

Immunotherapy a viable treatment

Another possible treatment technique that may benefit patients with HPV-related cancers is immunotherapy. One form of immunotherapy uses lymphocytes collected from the patient, and training the cells in the laboratory to recognize in this case a virus that is associated with a tumor and consequently attack it. This approach potentially may be used to treat HPV-related oropharynx cancers, according to Carlos A. Ramos, MD, assistant professor at the Center for Cell and Gene Therapy at Baylor College of Medicine, Houston.

“With some infections that lead to cancer, even though the virus is present in the tumor cells, the proteins shown to the immune system are limited; therefore, they do not drive a very strong immune response,” Ramos told HemOnc Today. “Training the immune system cells, T lymphocytes, may make them respond better to antigens.”

Data from ongoing trials that are taking T lymphocytes from patients and educating them to recognize antigens in patients with the Epstein-Barr virus associated tumors have shown some activity against them, according to Ramos. This adoptive transfer appears to be safe and may have the same effect on the HPV virus associated tumors. Immunotherapy does not cause the usual toxicities associated with chemotherapy, he said.

“There are currently no trials showing whether we can prevent more recurrences with this approach, but the results of trials examining viruses such as Epstein-Barr are good so far, in both patients who have no evidence of disease and in those who still have disease,” he said.

Even patients with active disease who have not responded to other therapies have responded to this therapy, Ramos said. He and colleagues are working toward compiling preclinical data to study the possibility of using immunotherapy to treat patients with HPV-related cancers.

Journey is just beginning

Much of what is known about risk, screening, prevention and treatment of HPV-related oropharynx cancers is in the early stages of discovery and much is still theoretical, according to Sturgis.

“As far as we can tell, these infections are transmitted sexually; the hope is that as we have better vaccines for prevention of cervical dysplasia, the downstream effect will help prevent other HPV-related cancers, such as anal cancers and penile cancers and oropharyngeal cancers,” he said.

Several recent studies examining new therapies that may reduce the intensity of traditional treatments while maintaining survival rates would have a major effect on the field, according to Sturgis.

Gillison said the rise in the number of cases of HPV-related cancers is changing the patient population considered to be at risk, and more research is vital.

“The most important thing for clinicians to do is be aware that trials are being developed and strongly encourage their patients to participate,” she said.  Christen Cona

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

June, 2016|Oral Cancer News|

Rodeo rider raising awareness of chewing tobacco and oral cancer

Source: www.krcrtv.com
Author: Danielle Radin

 

chewing-JPG

REDDING, Calif. – The Redding Rodeo kicked off Wednesday night with events like barrel racing, cattle roping and mutton busting.

Professional barrel racer, Carly Twisselman said chewing tobacco is prominent at rodeos. She’s teamed up with the Oral Cancer Foundation to try to change that.

“We want to show children that you can follow your dreams, be who you want to be, pursue being a rodeo athlete and not chew tobacco,” said Twisselman.

Twisselman competes in rodeos across the country and sees chewing tobacco time and time again.

She’s teaching children chewing tobacco is not the ‘cool thing to do.’ She also wears letting on her sleeves every race that reads, “Be smart, don’t start.”

She also has a brother who chews and had a health scare from it.

“My brother’s had signs of cancer of the mouth from chewing,” said Twisselman. ”  “I just think that’s the wrong message we should be sending to this children.”

According to the oral cancer foundation, there will be about 48,000 new cases of oral cancer in 2016 in the United States. 75 percent of all oral cancer patients use tobacco.

They estimate nearly 10,000 people in the United States will die from oral cancer in 2016.

 

In an era of rapidly proliferating, precisely targeted treatments, every cancer case has to be played by ear.

Source: www.nytimes.com
Author: Sidhartha Mukherjee

 

15oncologist1-superJumbo-v5Illustration by Cristiana Couceiro. Photograph by Ansel Adams, via the National Archives, College Park, Md.

 

The bone-marrow biopsy took about 20 minutes. It was 10 o’clock on an unusually chilly morning in New York in April, and Donna M., a self-possessed 78-year-old woman, had flown in from Chicago to see me in my office at Columbia University Medical Center. She had treated herself to orchestra seats for “The Humans” the night before, and was now waiting in the room as no one should be asked to wait: pants down, spine curled, knees lifted to her chest — a grown woman curled like a fetus. I snapped on sterile gloves while the nurse pulled out a bar cart containing a steel needle the length of an index finger. The rim of Donna’s pelvic bone was numbed with a pulse of anesthetic, and I drove the needle, as gently as I could, into the outer furl of bone. A corkscrew of pain spiraled through her body as the marrow was pulled, and then a few milliliters of red, bone-flecked sludge filled the syringe. It was slightly viscous, halfway between liquid and gel, like the crushed pulp of an overripe strawberry.

I had been treating Donna in collaboration with my colleague Azra Raza for six years. Donna has a preleukemic syndrome called myelodysplastic syndrome, or MDS, which affects the bone marrow and blood. It is a mysterious disease with few known treatments. Human bone marrow is normally a site for the genesis of most of our blood cells — a white-walled nursery for young blood. In MDS, the bone-marrow cells acquire genetic mutations, which force them to grow uncontrollably — but the cells also fail to mature into blood, instead dying in droves. It is a dual curse. In most cancers, the main problem is cells that refuse to stop growing. In Donna’s marrow, this problem is compounded by cells that refuse to grow up.

Though there are commonalities among cancers, of course, every tumor behaves and moves — “thinks,” even — differently. Trying to find a drug that fits Donna’s cancer, Raza and I have administered a gamut of medicines. Throughout all this, Donna has been a formidable patient: perennially resourceful, optimistic and willing to try anything. (Every time I encounter her in the clinic, awaiting her biopsy with her characteristic fortitude, it is the doctor, not the patient, who feels curled and small.) She has moved nomadically from one trial to another, shuttling from city to city, and from one drug to the next, through a landscape more desolate and exhilarating than most of us can imagine; Donna calls it her “serial monogamy” with different medicines. Some of these drugs have worked for weeks, some for months — but the transient responses have given way to inevitable relapses. Donna is getting exhausted.

Her biopsy that morning was thus part routine and part experiment. Minutes after the marrow was drawn into the syringe, a technician rushed the specimen to the lab. There he extracted the cells from the mixture and pipetted them into tiny grain-size wells, 500 cells to a well. To each well — about 1,000 in total — he will add a tiny dab of an individual drug: prednisone, say, to one well, procarbazine to the next and so forth. The experiment will test about 300 medicines (many not even meant for cancer) at three different doses to assess the effects of the drugs on Donna’s cells.

Bathed in a nutrient-rich broth suffused with growth factors, the cells will double and redouble in an incubator over the course of the following two weeks, forming a lush outgrowth of malignant cells — cancer abstracted in a dish. A computer, taught to count and evaluate cells, will then determine whether any of the drugs killed the cancerous cells or forced them to mature into nearly normal blood. Far from relying on data from other trials, or patients, the experiment will test Donna’s own cancer for its reactivity against a panel of medicines. Cells, not bodies, entered this preclinical trial, and the results will guide her future treatment.

I explained all this to Donna. Still, she had a question: What would happen if the drug that appeared to be the most promising proved unsuccessful?

“Then we’ll try the next one,” I told her. “The experiment, hopefully, will yield more than one candidate, and we’ll go down the list.”

“Will the medicine be like chemotherapy?”

“It might, or it might not. The drug that we end up using might be borrowed from some other disease. It might be an anti-inflammatory pill, or an asthma drug. It might be aspirin, for all we know.”

My conversation with Donna reflected how much cancer treatment has changed in the last decade. I grew up as an oncologist in an era of standardized protocols. Cancers were lumped into categories based on their anatomical site of origin (breast cancer, lung cancer, lymphoma, leukemia), and chemotherapy treatment, often a combination of toxic drugs, was dictated by those anatomical classifications. The combinations — Adriamycin, bleomycin, vinblastine and dacarbazine, for instance, to treat Hodgkin’s disease — were rarely changed for individual patients. The prospect of personalizing therapy was frowned upon: The more you departed from the standard, the theory ran, the more likely the patient would end up being undertreated or improperly managed, risking recurrence. In hospitals and clinics, computerized systems were set up to monitor an oncologist’s compliance with standard therapy. If you chose to make an exception for a particular patient, you had to justify the choice with an adequate excuse. Big Chemo was watching you.

I memorized the abbreviated names of combination chemo — the first letter of each drug — for my board exams, and I spouted them back to my patients during my clinic hours. There was something magical and shamanic about the multiletter contractions. They were mantras imbued with promise and peril: A.B.V.D. for Hodgkin’s, C.M.F. for breast cancer, B.E.P. for testicular cancer. The lingo of chemotherapists was like a secret code or handshake; even the capacity to call such baleful poisons by name made me feel powerful. When my patients asked me for statistical data, I had numbers at my fingertips. I could summon the precise chance of survival, the probability of relapse, the chance that the chemo would make them infertile or cause them to lose their hair. I felt omniscient.

Yet as I spoke to Donna that morning, I realized how much that omniscience has begun to wane — unleashing a more experimental or even artisanal approach in oncology. Most cancer patients are still treated with those hoary standardized protocols, still governed by the anatomical lumping of cancer. But for patients like Donna, for whom the usual treatments fail to work, oncologists must use their knowledge, wit and imagination to devise individualized therapies. Increasingly, we are approaching each patient as a unique problem to solve. Toxic, indiscriminate, cell-killing drugs have given way to nimbler, finer-fingered molecules that can activate or deactivate complex pathways in cells, cut off growth factors, accelerate or decelerate the immune response or choke the supply of nutrients and oxygen. More and more, we must come up with ways to use drugs as precision tools to jam cogs and turn off selective switches in particular cancer cells. Trained to follow rules, oncologists are now being asked to reinvent them.

The thought that every individual cancer might require a specific individualized treatment can be profoundly unsettling. Michael Lerner, a writer who worked with cancer patients, once likened the experience of being diagnosed with cancer to being parachuted out of a plane without a map or compass; now it is the oncologist who feels parachuted onto a strange landscape, with no idea which way to go. There are often no previous probabilities, and even fewer certainties. The stakes feel higher, the successes more surprising and the failures more personal. Earlier, I could draw curtain upon curtain of blame around a patient. When she did not respond to chemotherapy, it was her fault: She failed. Now if I cannot find a tool in the growing kit of drugs to target a cancer’s vulnerabilities, the vector feels reversed: It is the doctor who has failed.

Yet the mapless moment that we are now in may also hold more promise for patients than any that has come before — even if we find the known world shifting under our feet. We no longer have to treat cancer only with the blunt response of standard protocols, in which the disease is imagined as a uniform, if faceless, opponent. Instead we are trying to assess the particular personality and temperament of an individual illness, so that we can tailor a response with extreme precision. It’s the idiosyncratic mind of each cancer that we are so desperately trying to capture.

Cancer — and its treatment — once seemed simpler. In December 1969, a group of cancer advocates led by the philanthropist Mary Lasker splashed their demand for a national war on cancer in a full-page ad in The New York Times: “Mr. Nixon: You Can Cure Cancer.” This epitomized the fantasy of a single solution to a single monumental illness. For a while, the centerpiece of that solution was thought to be surgery, radiation and chemotherapy, a strategy colloquially known as “slash and burn.” Using combination chemotherapy, men and women were dragged to the very brink of physiological tolerability but then pulled back just in time to send the cancer, but not its host, careering off the edge.

Throughout the 1980s and 1990s, tens of thousands of people took part in clinical trials, which compared subjects on standard chemo combinations with others administered slightly different combinations of those drugs. Some responded well, but for many others, relapses and recurrences were routine — and gains were small and incremental for most cancers. Few efforts were made to distinguish the patients; instead, when the promised cures for most advanced malignancies failed to appear, the doses were intensified and doubled. In the Margaret Edson play “Wit,” an English professor who had ovarian cancer recalled the bewildering language of those trials by making up nonsensical names for chemotherapy drugs that had been pumped into her body: “I have survived eight treatments of hexamethophosphacil and vinplatin at the full dose, ladies and gentlemen. I have broken the record.”

To be fair, important lessons were garnered from the trials. Using combinations of chemotherapy, we learned to treat particular cancers: aggressive lymphomas and some variants of breast, testicular and colon cancers. But for most men and women with cancer, the clinical achievements were abysmal disappointments. Records were not broken — but patients were.

A breakthrough came in the 2000s, soon after the Human Genome Project, when scientists learned to sequence the genomes of cancer cells. Cancer is, of course, a genetic disease at its core. In cancer cells, mutated genes corrupt the normal physiology of growth and ultimately set loose malignant proliferation. This characteristic sits at the heart of all forms of cancer: Unlike normal cells, cancer cells have forgotten how to stop dividing (or occasionally, have forgotten how to die). But once we could sequence tens of thousands of genes in individual cancer specimens, it became clear that uniqueness dominates. Say two identical-looking breast cancers arise at the same moment in identical twins; are the mutations themselves in the two cancers identical? It’s unlikely: By sequencing the mutations in one twin’s breast cancer, we might find, say, 74 mutated genes (of the roughly 22,000 total genes in humans). In her sister’s, we might find 42 mutations, and if we looked at a third, unrelated woman with breast cancer, we might find 18. Among the three cases, there might be a mere five genes that overlap. The rest are mutations particular to each woman’s cancer.

15oncologists4-master675-v2-1Dr. Azra Raza, left, speaking to Donna M., a patient who travels from Chicago for treatment for myelodysplastic syndromes, in a waiting room at NewYork-Presbyterian/Columbia. Credit Kirsten Luce for The New York Times

 

No other human disease is known to possess this degree of genetic heterogeneity. Adult-onset diabetes, for example, is a complex genetic disease, but it appears to be dominated by variations in only about a dozen genes. Cancer, by contrast, has potentially unlimited variations. Like faces, like fingerprints — like selves — every cancer is characterized by its distinctive marks: a set of individual scars stamped on an individual genome. The iconic illness of the 20th century seems to reflect our culture’s obsession with individuality.

If each individual cancer has an individual combination of gene mutations, perhaps this variability explains the extraordinary divergences in responses to treatment. Gene sequencing allows us to identify the genetic changes that are particular to a given cancer. We can use that information to guide cancer treatment — in effect, matching the treatment to an individual patient’s cancer.

Many of the remarkable successes of cancer treatments of the last decades are instances of drugs that were matched to the singular vulnerabilities of individual cancers. The drug Gleevec, for instance, can kill leukemia cells — but only if the patient’s cancer cells happen to carry a gene mutation called BCR-ABL. Tarceva, a targeted therapy for lung cancer, works powerfully if the patient’s cancer cells happen to possess a particular mutant form of a gene; for lung-cancer patients lacking that mutation, it may be no different from taking a placebo. Because the medicines target mutations or behaviors that are specific to cancer cells (but not normal cells), many of these drugs have surprisingly minimal toxicities — a far cry from combination chemotherapies of the past.

A few days after Donna’s visit to the clinic, I went to my weekly meeting with Raza on the ninth floor of the hospital. The patient that morning was K.C., a 79-year-old woman with blood cancer. Raza has been following her disease — and keeping her alive — for a decade.

“Her tumor is evolving into acute leukemia,” Raza said. This, too, is a distinctive behavior of some cancers that we can now witness using biopsies, CT scans and powerful new techniques like gene sequencing: We can see the cancers morphing from smoldering variants into more aggressive types before our eyes.

“Was the tumor sequenced?” I asked.

“Yes, there’s a sequence,” Raza said, as we leaned toward a screen to examine it. “P53, DNMT3a and Tet2,” she read from the list of mutant genes. “And a deletion in Chromosome 5.” In K.C.’s cancer, an entire segment of the genome had been lopped off and gone missing — one of the crudest mutations that a tumor can acquire.

“How about ATRA?” I asked. We had treated a few patients carrying some of K.C.’s mutations with this drug and noted a few striking responses.

“No. I’d rather try Revlimid, but at a higher dose. She’s responded to it in the past, and the mutations remain the same. I have a hunch that it might work.”

15oncologist3-superJumbo-v4

Cancer by Genes
Researchers have discovered that cancers they once assumed were quite different might be similar genetically, which means a treatment that used to work for only a small group of patients now might help a much larger group. Mutations in the gene E2F3, for example, are found in breast, lung, bladder and prostate cancers, among others. Knowing this, it’s possible to develop similar drugs that target the gene across different cancers.

 

As Raza and I returned to K.C.’s room to inform her of the plan, I couldn’t help thinking that this is what it had come down to: inklings, observations, instincts. Medicine based on premonitions. Chemo by hunch. The discussion might have sounded ad hoc to an outsider, but there was nothing cavalier about it. We parsed these possibilities with utmost seriousness. We studied sequences, considered past responses, a patient’s recent history — and then charged forward with our best guess. Our decisions were spurred by science, yes, but also a sense for the art of medicine.

Oncologists are also practicing this art in areas that rely less on genes and mutations. A week after Donna’s biopsy, I went to see Owen O’Connor, an oncologist who directs Columbia’s lymphoma center. O’Connor, in his 50s, reminds me of an amphibious all-terrain vehicle — capable of navigating across any ground. We sat in his office, with large, sunlit windows overlooking Rockefeller Plaza. For decades, he explained, oncologists had treated relapsed Hodgkin’s lymphoma in a standard manner. “There were limited options,” O’Connor said. “We gave some patients more chemotherapy, with higher doses and more toxic drugs, hoping for a response. For some, we tried to cure the disease using bone-marrow transplantation.” But the failure rate was high: About 30 percent of patients didn’t respond, and half of them died.

Then a year or two ago, he tried something new. He began to use immunological therapy to treat relapsed, refractory Hodgkin’s lymphoma. Immunological therapies come in various forms. There are antibodies: missile-like proteins, made by our own immune systems, that are designed to attack and destroy foreign microbes (antibodies can also be made artificially through genetic engineering, armed with toxins and used as “drugs” to kill cancer cells). And there are drugs that incite a patient’s own immune system to recognize and kill tumor cells, a mode of treatment that lay fallow for decades before being revived. O’Connor used both therapies and found that they worked in patients with Hodgkin’s disease. “We began to see spectacular responses,” he said.

Yet even though many men and women with relapsed Hodgkin’s lymphoma responded to immunological treatments, there were some who remained deeply resistant. “These patients were the hardest to treat,” O’Connor continued. “Their tumors seemed to be unique — a category of their own.”

15oncologists5-master675Dr. Siddhartha Mukherjee, left, speaking to K.C., who has acute myeloid leukemia, at NewYork-Presbyterian/Columbia. Credit Kirsten Luce for The New York Times

 

Lorenzo Falchi, a fellow training with O’Connor and me, was intrigued by these resistant patients. Falchi came to our hospital from Italy, where he specialized in treating leukemias and lymphomas; his particular skill, gleaned from his experience with thousands of patients, is to look for patterns behind seemingly random bits of data. Rooting about in Columbia’s medical databases, Falchi made an astonishing discovery: The men and women who responded most powerfully to the immune-boosting therapies had invariably been pretreated with another drug called azacitidine, rarely used in lymphoma patients. A 35-year-old woman from New York with relapsed lymphoma saw her bulky nodes melt away. She had received azacitidine as part of another trial before moving on to the immunotherapy. A man, with a similar stage of cancer, had not been pretreated. He had only a partial response, and his disease grew back shortly thereafter.

Falchi and O’Connor will use this small “training set” to begin a miniature trial of patients with relapsed Hodgkin’s disease. “We will try it on just two or three patients,” Falchi told me. “We’ll first use azacitidine — intentionally, this time — and then chase it with the immune activators. I suspect that we’ll reproduce the responses that we’ve seen in our retrospective studies.” In lung cancer too, doctors have noted that pretreating patients with azacitidine can make them more responsive to immunological therapy. Falchi and O’Connor are trying to figure out why patients respond if they are pretreated with a drug that seems, at face value, to have nothing to do with the immune system. Perhaps azacitidine makes the cancer cells more recognizably foreign, or perhaps it forces immune cells to become more aggressive hunters.

Falchi and O’Connor are mixing and matching unexpected combinations of medicines based on previous responses — departing from the known world of chemotherapy. Even with the new combination, Falchi suspects, there will be resistant patients, and so he will divide these into subsets, and root through their previous responses, to determine what might make these patients resistant — grinding the data into finer and finer grains until he’s down to individualized therapy for every variant of lymphoma.

Suppose every cancer is, indeed, unique, with its own permutation of genes and vulnerabilities — a sole, idiosyncratic “mind.” It’s obviously absurd to imagine that we’ll find an individual medicine to treat each one: There are 14 million new cases of cancer in the world every year, and several million of those patients will present with advanced disease, requiring more than local or surgical treatment. Trying to individualize treatment for those cases would shatter every ceiling of cost.

15oncologist2-superJumbo-v2Cancer Development
Cancer works the same way all life works, through the process of cell division and mutation. All living things grow and heal through cell division, and all living things evolve and change through the occasional mutations that occur as the cells divide. But some mutations can be deadly, leading to the unchecked growth that defines cancer. More than 14 million Americans have a history of cancer; it is expected to kill 600,000 Americans this year.

 

But while the medical costs of personalized therapy are being debated in national forums in Washington, the patients in my modest waiting room in New York are focused on its personal costs. Insurance will not pay for “off-label” uses of medicines: It isn’t easy to convince an insurance company that you intend to use Lipitor to treat a woman with pre-leukemia — not because she has high cholesterol but because the cancer cells depend on cholesterol metabolism for their growth (in one study of a leukemia subtype, the increasing cells were highly dependent on cholesterol, suggesting that high doses of Lipitor-like drugs might be an effective treatment).

In exceptional cases, doctors can requisition pharmaceutical companies to provide the medicines free — for “compassionate use,” to use the language of the pharma world — but this process is unpredictable and time-consuming. I used to fill out such requests once every few months. Now it seems I ask for such exceptions on a weekly basis. Some are approved. A majority, unfortunately, are denied.

So doctors like Falchi and O’Connor do what they can — using their wiles not just against cancer but against a system that can resist innovation. They create minuscule, original clinical trials involving just 10 or 20 patients, a far cry from the hundred-thousand-patient trials of the ’80s and ’90s. They study these patients with monastic concentration, drawing out a cosmos of precious data from just that small group. Occasionally, a patient may choose to pay for the drugs out of his or her own pockets — but it’s a rare patient who can afford the tens of thousands of dollars that the drugs cost.

But could there be some minimal number of treatments that could be deployed to treat a majority of these cancers effectively and less expensively? More than any other scientist, perhaps, Bert Vogelstein, a cancer geneticist at Johns Hopkins University, has tackled that conundrum. The combination of genetic mutations in any individual cancer is singular, Vogelstein acknowledges. But these genetic mutations can still act through common pathways. Targeting pathways, rather than individual genes, might reorganize the way we perceive and treat cancer.

15oncologists7-master675Deep freezers containing bone marrow, bone-marrow plasma and blood serum in Siddhartha Mukherjee’s research lab. Credit Kirsten Luce for The New York Times

 

Imagine, again, the cell as a complex machine, with thousands of wheels, levers and pulleys organized into systems. The machine malfunctions in the cancer: Some set of levers and pulleys gets jammed or broken, resulting in a cell that continues to divide without control. If we focus on the individual parts that are jammed and snapped, the permutations are seemingly infinite: Every instance of a broken machine seems to have a distinct fingerprint of broken cogs. But if we focus, instead, on systems that malfunction, then the seeming diversity begins to collapse into patterns of unity. Ten components function, say, in an interconnected loop to keep the machine from tipping over on its side. Snap any part of this loop, and the end result is the same: a tipped-over machine. Another 20 components control the machine’s internal thermostat. Break any of these 20 components, and the system overheats. The number of components — 10 and 20 — are deceptive in their complexity, and can have endless permutations. But viewed from afar, only two systems in this machine are affected: stability and temperature.

Cancer, Vogelstein argues, is analogous. Most of the genes that are mutated in cancer also function in loops and circuits — pathways. Superficially, the permutations of genetic flaws might be boundless, but lumped into pathways, the complexity can be organized along the archetypal, core flaws. Perhaps these cancer pathways are like Hollywood movies; at first glance, there seems to be an infinite array of plot lines in an infinite array of settings — gold-rush California, the Upper West Side, a galaxy far, far away. But closer examination yields only a handful of archetypal narratives: boy meets girl, stranger comes to town, son searches for father.

How many such pathways, or systems, operate across a subtype of cancer? Looking at one cancer, pancreatic, and mapping the variations in mutated genes across hundreds of specimens, Vogelstein’s team proposed a staggeringly simple answer: 12. (One such “core pathway,” for instance, involves genes that enable cells to invade other tissues. These genes normally allow cells to migrate through parts of the body — but in cancer, migration becomes distorted into invasion.) If we could find medicines that could target these 12 core pathways, we might be able to attack most pancreatic cancers, despite their genetic diversity. But that means inventing 12 potential ways to block these core paths — an immense creative challenge for scientists, considering that they haven’t yet figured out how to target more than, at best, one or two.

Immunological therapies provide a second solution to the impasse of unlimited diversity. One advantage of deploying a patient’s own immune system against cancer is that immunological cells are generally agnostic to the mutations that cause a particular cancer’s growth. The immune system was designed to spot differences in the superficial features of a diseased or foreign cell, thereby identifying and killing it. It cares as little about genes as an intercontinental ballistic missile cares about the email addresses, or dietary preferences, of the population that it has been sent to destroy.

A few years ago, in writing a history of cancer, I interviewed Emil Freireich. Freireich, working with Emil Frei at the National Cancer Institute in the 1960s and ’70s, stumbled on the idea of deploying multiple toxic drugs simultaneously to treat cancer — combination chemotherapy. They devised one of the first standard protocols — vincristine, Adriamycin, methotrexate and prednisone, known as VAMP — to treat pediatric leukemias. Virtually nothing about the VAMP protocol was individualized (although doses could be reduced if needed). In fact, doctors were discouraged from trying alternatives to the formula.

Yet as Freireich recalled, long before they came up with the idea for a protocol, there were small, brave experiments; before trials, there was trial and error. VAMP was brought into existence through grit, instinct and inspired lunges into the unknown. Vincent T. DeVita Jr., who worked with Freireich in the 1960s, wrote a book, “The Death of Cancer,” with his daughter, Elizabeth DeVita-Raeburn. In it, he recalled a time when the leukemic children in Freireich’s trial were dying of bacterial meningitis during treatment. The deaths threatened the entire trial: If Freireich couldn’t keep the children alive during the therapy, there would be no possibility of remission. They had an antibiotic that could kill the microbe, but the medicine wouldn’t penetrate the blood-brain barrier. So Freireich decided to try something that pushed the bounds of standard practice. He ordered DeVita, his junior, to inject it directly into the spinal cords of his patients. It was an extreme example of off-label use of the drug: The medicine was not meant for use in the cord. DeVita writes:

“The first time Freireich told me to do it, I held up the vial and showed him the label, thinking that he’d possibly missed something. ‘It says right on there, “Do not use intrathecally,” ’ I said. Freireich glowered at me and pointed a long, bony finger in my face. ‘Do it!’ he barked. I did it, though I was terrified. But it worked every time.”

When I asked Freireich about that episode and about what he would change in the current landscape of cancer therapy, he pointed to its extreme cautiousness. “We would never have achieved anything in this atmosphere,” he said. The pioneer of protocols pined for a time before there were any protocols.

Medicine needs standards, of course, otherwise it can ramble into dangerous realms, compromising safety and reliability. But cancer medicine also needs a healthy dose of Freireich: the desire to read between the (guide)lines, to reimagine the outer boundaries, to perform the experiments that become the standards of the future. In January, President Obama introduced an enormous campaign for precision medicine. Cancer is its molten centerpiece: Using huge troves of data, including gene sequences of hundreds of thousands of specimens and experiments performed in laboratories nationwide, the project’s goal is to find individualized medicines for every patient’s cancer. But as we wait for that decades-long project to be completed, oncologists still have to treat patients now. To understand the minds of individual cancers, we are learning to mix and match these two kinds of learning — the standard and the idiosyncratic — in unusual and creative ways. It’s the kind of medicine that so many of us went to medical school to learn, the kind that we’d almost forgotten how to practice.

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

May, 2016|Oral Cancer News|

California Raises Smoking Age To 21

Source: www.huffingtonpost.com
Author: Huffington Post Staff
 

The law makes it the second state to raise the minimum age to 21, following Hawaii.

 

SAN FRANCISCO, CA - MAY 31:  Isaiah Atkinson smokes a cigarette in front of the San Francisco Centre on May 31, 2011 in San Francisco, California.  Since 1987, the World Health Organization has celebrated "World No Tobacco Day" to raise awareness to the health risks associated with smoking tobacco. Smoking is the second biggest cause of death globally and is responsible for the death of one in ten adults worldwide.  (Photo by Justin Sullivan/Getty Images)

SACRAMENTO, Calif. (Reuters) – California will raise the legal age for purchasing tobacco products to 21 from 18 under a bill signed on Wednesday by Democratic Governor Jerry Brown, part of a package of anti-smoking measures that also regulates electronic cigarettes.

Under five bills signed into law on Wednesday, California will ban the sale of vaping products or tobacco to anyone under the age of 21, imposing a fine of up to $5,000 against companies that violate the law.

“It is long past due for California to update our approach to tobacco,” said Steven Larson, president of the California Medical Association. “There has been an alarming rise in the use of e-cigarettes by teens, putting them at risk for lifelong addiction.”

Under the measures, electronic cigarettes will be regulated like traditional ones. That means that wherever cigarettes are banned, such as in restaurants, workplaces and public areas, use of e-cigarettes will also be prohibited.

The state will also expand its funding for anti-smoking programs under the bills.

Brown stopped short of allowing local counties to impose their own tobacco taxes, noting in his veto message that several proposed new taxes would be placed before voters on the November ballot.

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

May, 2016|Oral Cancer News|