chemotherapy

The Cost of Cancer Drugs

Source: www.cbsnew.com
Author: Lesley Stahl
 

The following is a script of “The Cost of Cancer Drugs” which aired on October 5, 2014, and was rebroadcast on June 21, 2015. Lesley Stahl is the correspondent. Richard Bonin, producer.

Cancer is so pervasive that it touches virtually every family in this country. More than one out of three Americans will be diagnosed with some form of it in their lifetime. And as anyone who’s been through it knows, the shock and anxiety of the diagnosis is followed by a second jolt: the high price of cancer drugs.

They are so astronomical that a growing number of patients can’t afford their co-pay, the percentage of their drug bill they have to pay out-of-pocket. As we first reported in October, this has led to a revolt against the drug companies led by some of the most prominent cancer doctors in the country.

Dr. Leonard Saltz: We’re in a situation where a cancer diagnosis is one of the leading causes of personal bankruptcy.

Dr. Leonard Saltz is chief of gastrointestinal oncology at Memorial Sloan Kettering, one of the nation’s premier cancer centers, and he’s a leading expert on colon cancer.

Lesley Stahl: So, are you saying in effect, that we have to start treating the cost of these drugs almost like a side effect from cancer?

Dr. Leonard Saltz: I think that’s a fair way of looking at it. We’re starting to see the term “financial toxicity” being used in the literature. Individual patients are going into bankruptcy trying to deal with these prices.

Lesley Stahl: The general price for a new drug is what?

Dr. Leonard Saltz: They’re priced at well over $100,000 a year.

Lesley Stahl: Wow.

Dr. Leonard Saltz: And remember that many of these drugs, most of them, don’t replace everything else. They get added to it. And if you figure one drug costs $120,000 and the next drug’s not going to cost less, you’re at a quarter-million dollars in drug costs just to get started.

Lesley Stahl: I mean, you’re dealing with people who are desperate.

Dr. Leonard Saltz: I do worry that people’s fear and anxiety are being taken advantage of. And yes, it costs money to develop these drugs, but I do think the price is too high.

The drug companies say it costs over a billion dollars to bring a new drug to market, so the prices reflect the cost of innovation.

The companies do provide financial assistance to some patients, but most people aren’t eligible. So many in the middle class struggle to meet the cost of their co-payments. Sometimes they take half-doses of the drug to save money. Or delay getting their prescriptions refilled.

Dr. Saltz’s battle against the cost of cancer drugs started in 2012 when the FDA approved Zaltrap for treating advanced colon cancer. Saltz compared the clinical trial results of Zaltrap to those of another drug already on the market, Avastin. He says both target the same patient population, work essentially in the same way. And, when given as part of chemotherapy, deliver the identical result: extending median survival by 1.4 months, or 42 days.

Dr. Leonard Saltz: They looked to be about the same. To me, it looked like a Coke and Pepsi sort of thing.

Then Saltz, as head of the hospital’s pharmacy committee, discovered how much it would cost: roughly $11,000 per month, more than twice that of Avastin.

Lesley Stahl: So $5,000 versus $11,000. That’s quite a jump. Did it have fewer side effects? Was it less toxic? Did it have…

Dr. Leonard Saltz: No…

Lesley Stahl: …Something that would have explained this double price?

Dr. Leonard Saltz: If anything, it looked like there might be a little more toxicity in the Zaltrap study.

He contacted Dr. Peter Bach, Sloan Kettering’s in-house expert on cancer drug prices.

Lesley Stahl: So Zaltrap. One day your phone rings and it’s Dr. Saltz. Do you remember what he said?

Dr. Peter Bach: He said, “Peter, I think we’re not going to include a new cancer drug because it costs too much.”

Lesley Stahl: Had you ever heard a line like that before?

Dr. Peter Bach: No. My response was, “I’ll be right down.”

Lesley Stahl: You ran down.

Dr. Peter Bach: I think I took the elevator. But yes, exactly.

Bach determined that since patients would have to take Zaltrap for several months, the price tag for 42 days of extra life would run to nearly $60,000. What they then decided to do was unprecedented: reject a drug just because of its price.

Dr. Peter Bach: We did it for one reason. Because we need to take into account the financial consequences of the decisions that we make for our patients. Patients in Medicare would pay more than $2,000 a month themselves, out-of-pocket, for Zaltrap. And that that was the same as the typical income every month for a patient in Medicare.

Lesley Stahl: The co-pay.

Dr. Peter Bach: Right. 20 percent. Taking money from their children’s inheritance, from the money they’ve saved. We couldn’t in good conscience say, “We’re going to prescribe this more expensive drug.”

And then they trumpeted their decision in the New York Times. Blasting what they called “runaway cancer drug prices,” it was a shot across the bow of the pharmaceutical industry and Congress for passing laws that Bach says allow the drug companies to charge whatever they want for cancer medications.

Dr. Peter Bach: Medicare has to pay exactly what the drug company charges. Whatever that number is.

Lesley Stahl: Wait a minute, this is a law?

Dr. Peter Bach: Yes.

Lesley Stahl: And there’s no negotiating whatsoever with Medicare?

Dr. Peter Bach: No.

Another reason drug prices are so expensive is that according to an independent study, the single biggest source of income for private practice oncologists is the commission they make from cancer drugs. They’re the ones who buy them wholesale from the pharmaceutical companies, and sell them retail to their patients. The mark-up for Medicare patients is guaranteed by law: the average in the case of Zaltrap was six percent.

Dr. Leonard Saltz: What that does is create a very substantial incentive to use a more expensive drug, because if you’re getting six percent of $10, that’s nothing. If you’re getting six percent of $10,000 that starts to add up. So now you have a real conflict of interest.

But it all starts with the drug companies setting the price.

Dr. Peter Bach: We have a pricing system for drugs which is completely dictated by the people who are making the drugs.

Lesley Stahl: How do you think they’re deciding the price?

Dr. Peter Bach: It’s corporate chutzpah.

Lesley Stahl: We’ll just raise the price, period.

Dr. Peter Bach: Just a question of how brave they are and how little they want to end up in the New York Times or on 60 Minutes.

That’s because media exposure, he says, works. Right after their editorial was published, the drug’s manufacturer, Sanofi, cut the price of Zaltrap by more than half.

Dr. Peter Bach: It was a shocking event. Because it was irrefutable evidence that the price was a fiction. All of those arguments that we’ve heard for decades, “We have to charge the price we charge. We have to recoup our money. We’re good for society. Trust us. We’ll set the right price.” One op-ed in the New York Times from one hospital and they said, “Oh, okay, we’ll charge a different price.” It was like we were in a Turkish bazaar.

Lesley Stahl: What do you mean?

Dr. Peter Bach: They said, “This carpet is $500” and you say, “I’ll give you $100.” And the guy says, “Okay.” They set it up to make it highly profitable for doctors to go for Zaltrap instead of Avastin. It was crazy!

But he says it got even crazier when Sanofi explained the way they were changing the price.

Dr. Peter Bach: They lowered it in a way that doctors could get the drug for less. But patients were still paying as if it was high-priced.

Lesley Stahl: Oh, come on.

Dr. Peter Bach: They said to the doctor, “Buy Zaltrap from us for $11,000 and we’ll send you a check for $6,000.” Then you give it to your patient and you get to bill the patient’s insurance company as if it cost $11,000. So it made it extremely profitable for the doctors. They could basically double their money if they use Zaltrap.

“High cancer drug prices are harming patients because either you come up with the money, or you die.”

All this is accepted industry practice. After about six months, once Medicare and private insurers became aware of the doctor’s discount, the price was cut in half for everyone.

John Castellani: The drug companies have to put a price on a medicine that reflects the cost of developing them, which is very expensive and takes a long period of time, and the value that it can provide.

John Castellani is president and CEO of PhRMA, the drug industry’s trade and lobbying group in Washington.

Lesley Stahl: If you are taking a drug that’s no better than another drug already on the market and charging twice as much, and everybody thought the original drug was too much…

John Castellani: We don’t set the prices on what the patient pays. What a patient pays is determined by his or her insurance.

Lesley Stahl: Are you saying that the pharmaceutical company’s not to blame for how much the patient is paying? You’re saying it’s the insurance company?

John Castellani: I’m saying the insurance model makes the medicine seem artificially expensive for the patient.

He’s talking about the high co-pay for cancer drugs. If you’re on Medicare, you pay 20 percent.

Lesley Stahl: Twenty percent of $11,000 a month is a heck of a lot more than 20 percent of $5,000 a month.

John Castellani: But why should it be 20 percent instead of five percent?

Lesley Stahl: Why should it be $11,000 a month?

John Castellani: Because the cost of developing these therapies is so expensive.

Lesley Stahl: Then why did Sanofi cut it in half when they got some bad publicity?

John Castellani: I can’t respond to a specific company.

Sanofi declined our request for an interview, but said in this email that they lowered the price of Zaltrap after listening “to early feedback from the oncology community and … To ensure affordable choices for patients…”

Dr. Hagop Kantarjian: High cancer drug prices are harming patients because either you come up with the money, or you die.

Hagop Kantarjian chairs the department of leukemia at MD Anderson in Houston. Inspired by the doctors at Sloan Kettering, he enlisted 119 of the world’s leading leukemia specialists to co-sign this article about the high price of drugs that don’t just add a few weeks of life, but actually add years, like Gleevec.

It treats CML, one of the most common types of blood cancer that used to be a death sentence, but with Gleevec most patients survive for 10 years or more.

Dr. Hagop Kantarjian: This is probably the best drug we ever developed in cancer.

Lesley Stahl: In all cancers?

Dr. Hagop Kantarjian: So far. And that shows the dilemma, because here you have a drug that makes people live their normal life. But in order to live normally, they are enslaved by the cost of the drug. They have to pay every year.

Lesley Stahl: You have to stay on it. You have to keep taking it.

Dr. Hagop Kantarjian: You have to stay on it indefinitely.

Gleevec is the top selling drug for industry giant Novartis, bringing in more than $4 billion a year in sales. $35 billion since the drug came to market. There are now several other drugs like it. So, you’d think with the competition, the price of Gleevec would have come down.

Dr. Hagop Kantarjian: And yet, the price of the drug tripled from $28,000 a year in 2001 to $92,000 a year in 2012.

Lesley Stahl: Are you saying that the drug companies are raising the prices on their older drugs.

Dr. Hagop Kantarjian: That’s correct.

Lesley Stahl: Not just the new ones. So you have a new drug that might come out at a $100,000, but they are also saying the old drugs have to come up to that price, too?

Dr. Hagop Kantarjian: Exactly. They are making prices unreasonable, unsustainable and, in my opinion, immoral.

When we asked Novartis why they tripled the price of Gleevec, they told us, “Gleevec has been a life-changing medicine … When setting the prices of our medicines we consider … the benefits they bring to patients … The price of existing treatments and the investments needed to continue to innovate…”

[Dr. Hagop Kantarjian: This is quite an expensive medication.]

Dr. Kantarjian says one thing that has to change is the law that prevents Medicare from negotiating for lower prices.

Dr. Hagop Kantarjian: This is unique to the United States. If you look anywhere in the world, there are negotiations. Either by the government or by different regulatory bodies to regulate the price of the drug. And this is why the prices are 50 percent to 80 percent lower anywhere in the world compared to the United States.

Lesley Stahl: Fifty percent to 80 percent?

Dr. Hagop Kantarjian: Fifty percent to 80 percent.

Lesley Stahl: The same drug?

Dr. Hagop Kantarjian: Same drug. American patients end up paying two to three times more for the same drug compared to Canadians or Europeans or Australians and others.

Lesley Stahl: Now, Novartis, which makes Gleevec, says that the price is fair because this is a miracle drug. It really works.

Dr. Hagop Kantarjian: The only drug that works is a drug that a patient can afford.

The challenge, Dr. Saltz at Sloan Kettering says, is knowing where to draw the line between how long a drug extends life and how much it costs.

Lesley Stahl: Where is that line?

Dr. Leonard Saltz: I don’t know where that line is, but we as a society have been unwilling to discuss this topic and, as a result, the only people that are setting the line are the people that are selling the drugs.

Since we first broadcast our story, President Obama asked Congress to change the law and allow Medicare to negotiate prices with drug manufacturers. Few believe, however, that Congress will let that happen anytime soon.

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

 

Keytruda doubles efficacy of only targeted therapy for head and neck cancer

Source: www.curetoday.com
Author: Lauren M. Green

The immunotherapy Keytruda (pembrolizumab), in a recent study, proved twice as effective for the treatment of head and neck cancer as Erbitux (cetuximab), the only targeted therapy indicated as a therapy for the disease.

The multisite study offers the largest experience to date of how immunotherapy can be deployed in patients with head and neck cancer, and could change the way the disease is treated. The findings were announced May 29 during the annual meeting of the American Society of Clinical Oncology, a gathering of nearly 30,000 oncology professionals taking place in Chicago.

Keytruda is an antibody designed to disable the protein PD-1 so it cannot do its job of keeping the immune system in check; this allows T cells to become more active in recognizing and fighting cancer cells. In the study, investigators found that the drug produced broad and durable responses in patients with advanced head and neck cancer.

Fifty-six percent of patients in the study experienced some tumor shrinkage with Keytruda, and 86 percent of those patients continued to respond to treatment at data cutoff on March 23, 2015. Keytruda produced an overall response rate (ORR) of 25 percent, and it proved active in both HPV (human papillomavirus)-positive and HPV-negative patients.

“The efficacy was remarkable — pembrolizumab seems to be roughly twice as effective, when measured by response, as our only targeted therapy, cetuximab,” said Tanguy Seiwart, an assistant professor of medicine and associate leader of the head and neck cancer program at the University of Chicago, who presented the results in a press briefing during the ASCO meeting. “We have high hopes that immunotherapy will change the way we treat head and neck cancer.”

Recurrent/metastatic head and neck squamous cell carcinoma (HNSCC) has a poor prognosis with a median overall survival (OS) of 13 months in patients treated in the first-line setting, and six months in previously treated patients. Previously treated patients made up the majority of the population of the study, which built on earlier findings from the KEYNOTE-012 study (NCT01848834). In that study, Keytruda — administered at 10 mg/kg every two weeks — had a 20 percent response rate in patients with advanced HNSCC whose tumors were positive for the protein PD-L1.

The findings reported May 29 were based on results from an expansion of that first trial, which involved 132 patients with advanced HNSCC who were recruited regardless of their PD-L1 or HPV status. Importantly, said Seiwert, patients in this cohort received a fixed dose of Keytruda (200 mg every three weeks), representing “a very convenient dosing schedule.”

Eligible patients had measureable disease based on RECIST 1.1 response evaluation criteria and an ECOG performance status of 0 or 1. The majority of enrollees were male (83 percent), and 56.8 percent had received two or more lines of therapy for disease recurrence. Radiographic imaging was used to assess tumor response every eight weeks. Patients were treated as long as they didn’t show progression of disease or as long as they demonstrated clinical improvement, Seiwert explained.

Of 117 evaluable patients, 29 (24.8 percent; [95 percent confidence interval (CI), 17.3–33.6]) responded to treatment with Keytruda. For patients with HPV-positive HNSCC, the ORR was 20.6 percent, and in the HPV-negative cohort, ORR was 27.2 percent.

“In addition to the 25 percent response rate,” said Seiwert, “about 25 percent also had stable disease, so when we take these together, we have a disease control rate of about 50 percent, which is remarkable in this disease, especially in a heavily pretreated population.”

Moreover, he said, about two-thirds of patients had received two or more prior lines of therapy, which generally is an indicator of a very poor prognosis.

For the 56 percent of patients whose tumors decreased in size, Seiwert said the responses often occurred early at eight or 16 weeks, although there were a few outliers with late responses.

“Importantly, those patients who did respond oftentimes continued to have responses — 86 percent of patients had durable responses in this cohort,” he continued, adding that not only are responders remaining on the therapy, but so are many patients who have stable disease, with a total of 40 patients staying on the drug.

“Overall, and in keeping with what we already know about pembrolizumab, this was a very well-tolerated agent,” said Seiwert, “certainly better tolerated than what we usually see in head and neck cancer with aggressive chemotherapy and radiotherapy.”

Serious side effects were reported in fewer than 10 percent of patients. The most common side effects were fatigue (15.2 percent of patients), hypothyroidism (9.1 percent), and decreased appetite and rash, each occurring in 7.6 percent of patients. Four patients discontinued treatment due to immune-related side effects: two due to grade 2 interstitial lung disease and grade 3 colitis, respectively, and two patients for grade 3 pneumonitis.

Analysis of the findings based on biomarker status is ongoing, and Seiwert is hopeful that with the emergence of new potential biomarkers, researchers will be able to pinpoint which patients with HNSCC are most likely to benefit from the immunotherapy.

For example, another related study that Seiwert and colleagues are reporting at ASCO (abstract 6017) has shown that the expression of the gene signature interferon-gamma in head and neck tumors had a very strong negative predictive value of response to Keytruda. “In the future, these results may help us, if validated, to determine which patients should or should not [be given] pembrolizumab,” Seiwert said.

Pembrolizumab versus standard treatment for HNSCC also is being evaluated in two phase 3 trials that are currently recruiting participants (NCT02252042 and NCT02358031).

Source:
Seiwert TY, Haddad RI, Gupta S, et al. Antitumor activity of the anti-PD-1 antibody pembrolizumab in biomarker-unselected patients with R/M head and neck cancer: preliminary results from the KEYNOTE-012 expansion cohort. J Clin Oncol. 2015;(suppl; abstr LBA6008) – See more at: http://www.curetoday.com/articles/keytruda-doubles-efficacy-of-only-targeted-therapy-for-head-and-neck-cancer/2#sthash.44VvpPH4.dpuf

Factors linked with better survival in oral cancer identified

Source: www.cancertherapyadvisor.com
Author: staff

Factors associated with improved survival in oral cavity squamous cell cancer (OCSCC) include neck dissection and treatment at academic or research institutions, according to a study published in JAMA Otolaryngology-Head & Neck Surgery.

Alexander L. Luryi, from the Yale University School of Medicine in New Haven, Conn., and colleagues analyzed correlations between treatment variables and survival in patients with stages I and II OCSCC. Data were included for 6,830 patients.

The researchers found that five-year survival was 69.7 percent. Treatment factors that correlated with improved survival on univariate analysis included treatment at academic or research institutions, no radiation therapy, no chemotherapy, and negative margins (all P < 0.001).

Improved survival was also seen in association with neck dissection (P = 0.001). Treatment at academic or research institutions correlated with increased likelihood of receiving neck dissection and decreased likelihood of receiving radiation therapy or having positive margins.

Neck dissection and treatment at academic or research institutions correlated with improved survival on multivariate analysis (hazard ratios, 0.85 and 0.88, respectively), while compromised survival was seen for positive margins, insurance through Medicare, and adjuvant radiation therapy or chemotherapy (hazard ratios, 1.27, 1.45, 1.31, and 1.34, respectively).

“Overall survival for early OCSCC varies with demographic and tumor characteristics but also varies with treatment and system factors, which may represent targets for improving outcomes in this disease,” the authors write.

Reference
Luryi, Alexander L., BS, et al. “Treatment Factors Associated With Survival in Early-Stage Oral Cavity Cancer: Analysis of 6830 Cases From the National Cancer Data Base.” JAMA Otolaryngology – Head & Neck Surgery. doi:10.1001/jamaoto.2015.0719. [epub ahead of print]. May 14, 2015.

Second-line afatinib shows promise

Source: www.nature.com
Author: David Killock

Patients with recurrent and/or metastatic head and neck squamous-cell carcinoma and disease progression after first-line platinum-based chemotherapy have a dismal prognosis. There is no standard second-line therapy; however, afatinib, an irreversible inhibitor of HER family kinases, has shown efficacy in this setting.

The LUX-Head & Neck 1 phase III trial randomly assigned patients to afatinib (n = 322) or methotrexate (n = 161) therapy. Median progression-free survival (PFS) was 2.6 months with afatinib versus 1.7 months (P = 0.03). “The study was also powered to detect a difference in overall survival, which was not significantly improved,” explains lead author Jean-Pascal Machiels, “however, patient-reported outcomes were better with afatinib.” Afatinib was associated with delayed deterioration of global health status, less pain, and improved swallowing, potentially related to the prolonged PFS, compared with methotrexate. Furthermore, afatinib toxicity was manageable and deemed favourable to that of methotrexate.

The patients were unselected for disease subtype, ~60% had received prior anti-EGFR antibody therapy, and 51% received further lines of treatment, possibly diluting the treatment effect of afatinib acheter levitra en ligne. Notably, patients with human papilloma virus (p16)-negative non-oropharyngeal cancer and local recurrence (rather than metastasis), who had not previously received an anti-EGFR antibody seemed to derive the most benefit in preplanned subgroup analyses.

Machiels concludes, “Afatinib has some activity in head and neck cancer, but we need to better understand which patients will benefit from this therapy.”

References
Machiels, J.-P. H. et al. Afatinib versus methotrexate as second-line treatment in patients with recurrent or metastatic squamous-cell carcinoma of the head and neck progressing on or after platinum-based therapy (LUX-Head & Neck 1): an open-label, randomised phase 3 trial. Lancet Oncol. doi:10.1016/S1470-2045(15)70124-5

Note: Nature Reviews Clinical Oncology (2015) doi:10.1038/nrclinonc.2015.86
Published online 05 May 2015

Laser Treatment Halts Oral Mucositis in Its Tracks

Source: www.medscape.com

Author: Fran Lowry

 

Spa-like treatment with a cool, low-level laser, similar to that use

for wrinkles, vanquishes oral mucositis, one of the most debilitating

toxicities of cancer therapy.

 

“I have been an oncology nurse for over 25 years, and in those 25

years, there has been nothing that helps prevent or is effective

against the treatment for oral mucositis, until now,” said Annette

Quinn, RN, MSN, from the University of Pittsburgh Cancer Institute.

 

“Patients say they rank it higher than nausea and vomiting when it

comes to adverse side effects, especially because we have good

medications to control nausea and vomiting. But the low-level laser

works better than we could have hoped,” Quinn told Medscape Medical

News.

 

She presented results from a pilot project at the Oncology Nursing

Society (ONS) 40th Annual Congress in Orlando, Florida.

 

Oral mucositis affects virtually all head and neck cancer patients

undergoing chemo and radiation therapy, and about 75% to 100% of

patients undergoing stem cell transplantation with whole-body

irradiation experience some degree of oral mucositis.

 

Low-level laser therapy (LLLT) has been used to treat oral mucositis

for a decade in Europe and South America, but it has not made its way

to the United States because there is no mechanism for reimbursement,

Quinn reported.

 

She hopes this study will change that.

 

“Reimbursement is the main obstacle to its use in the United States,

but for this study, I was able to secure the treatment through a

grant. Treating oral mucositis could easily add $20,000 to the cost of

patient care, but with the laser, we can decrease hospital

readmissions and the use of pain medication, IV antibiotics, and

feeding-tube placements. Even though we cannot receive reimbursement,

laser treatment is still cost-effective,” she said.

 

It is thought that LLLT works on the mitochondria to displace the

nitric oxide that is generated as a result of radiation or

chemotherapy, and helps to reoxygenate the cells, Quinn explained.

 

In the pilot project, 52 patients with head and neck cancer, all

deemed to be at high risk for oral mucositis, received LLLT 830 nm

wavelength three times a week, starting the first week of their

radiation treatment and continuing throughout the course of their

radiation therapy.

 

The initial intent was to see if the laser could control the oral

mucositis so patients would not be forced to have a break in their

treatment, Quinn explained.

 

“We know that patients who miss 5 days or more of radiation therapy

have poorer survival, so we wanted to focus on how to get these

patients through with no treatment breaks. We didn’t realize that we

would get them through with no mucositis. But we found that the very

first patient we treated made it all the way through,” she said.

 

None of the 52 patients treated with LLLT developed any oral mucositis.

 

When oncologists treating stem cell transplantation patients

discovered these results, they brought 23 of their stem cell

recipients for LLLT. These patients were treated until their absolute

neutrophil count was above 1000 cell/nm³.

 

Again, results were excellent, although two patients developed grade 3

oral mucositis.

 

“Normally, 100% of stem cell patients develop oral mucositis. It’s

unbelievable what the therapy has done for oral mucositis,” Quinn noted.

 

LLLT Simplicity Itself

 

“The treatment is administered immediately after the radiation

therapy. It takes only about 6 to 8 minutes to administer, and is all

done extraorally; none of the probes actually go into the mouth unless

the patient develops a lesion inside the mouth that we need to target

with the probe,” Quinn explained.

It is simplicity itself, and it works so incredibly well. We just have

to get the word out.

 

“We do five sites along their face, right along the jaw line, and then

we do their tongue. The patients love it. We call it their spa time.

It’s the same laser they use in cosmetics to prevent wrinkles. We have

not had one patient tell us they want to stop their treatment, and we

have had no adverse side effects,” she said.

 

The learning curve is very slight, Quinn added.

 

The training takes about half a day, and learning how to use the

equipment only takes about 30 minutes. “It’s just cold laser therapy,

there’s no heating, there’s no cutting. Nothing. It is simplicity

itself, and it works so incredibly well. We just have to get the word

out,” she said.

 

The poster generated a lot of buzz among the nurses attending the

Congress, noted Ruth C. Gholz, RN, MSN, from the Cincinnati Veterans

Administration Medical Center.

 

“There was a lot of excitement about the laser to treat oral

mucositis. So many people were talking about it,” Gholz told Medscape

Medical News.

 

Oral mucositis is a debilitating side effect that challenges us as we

move forward with patients and providers. Low-level laser therapy has

been a recognized treatment per guidelines, yet many have limited to

no experience in its use,” she said.

 

Gholz explained that these results challenge “all practices to

incorporate low-level laser therapy into their armamentarium.”

 

“The future is bright as we move forward in maximizing this therapy,”

she added.

 

Ms Quinn and Ms Gholz have disclosed no relevant financial relationships.

 

Oncology Nursing Society (ONS) 40th Annual Congress: Abstract 84.

 Presented April 24, 2015.

Medscape Medical News © 2015  WebMD, LLC Send comments and news tips to news@medscape.net.

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

May, 2015|Oral Cancer News|

Green tea polyphenol helps kill oral cancer cells by destroying mitochondria

Source: www.medicaldaily.com
Author: Chris Weller
First it targeted pancreatic cancer. Now it’s moved onto oral cancer. A new study from Penn State University shows the main antioxidant in green tea, epigallocatechin-3-gallate (EGCG), helps kill cancer cells through the destruction of the cells’ mitochondria.

 

green-tea

While highly effective at eradicating cancer cells, chemotherapy is quickly falling out of practice with doctors who seek targeted treatments. Instead of getting rid of just the harmful cells, chemo attacks healthy cells, which are often found in the hair and the intestines, resulting in the characteristic hair loss and frequent immune system-related illness.

“You don’t see these sorts of side effects with green tea consumption,” said Joshua Lambert, associate professor of food science at Penn State, in a press release. Lambert and his colleagues carried out their study by looking at cell cultures, which they injected with the same amount of EGCG a person would normally have in her saliva after chewing green tea-flavored gum. They saw a number of promising reactions.

“It looks like EGCG causes the formation of reactive oxygen species in cancer cells, which damages the mitochondria, and the mitochondria responds by making more reactive oxygen species,” Lambert explained. Over time, the mitochondria lose even more of its defenses with a breakdown in the expression of antioxidant genes. In their weakened state the cancer cells eventually succumb to EGCG in full, and they die.

This isn’t the first time EGCG revealed its cancer-killing power. In May of last year, scientists from the Los Angeles Biomedical Research Institute (LA BioMed) discovered the compound’s ability to prevent and slow the growth of pancreatic cancer. One of the key enzymes in pancreatic cancer cells is known as LDHA, and prior studies have shown the enzyme inhibitor oxamate is instrumental in destroying LDHA. In similar culture tests, LA BioMed researchers found EGCG rivaled oxamate in its destructive power.

The scientists on either coast share the same goal: getting rid of cancer. Many forms of the disease are rising in prevalence, particularly in developing nations where the Western diet wields a dangerous, processed influence. Lung cancer, for example, recently passed breast cancer as the most fatal form of cancer among women in the developed world. Pancreatic cancer is nearly just as bad. Of the 45,000 diagnoses each year in the U.S., 85 percent of cases are fatal.

For Lambert and his research team, the more immediate goal is to move out of cell cultures. The next step is animal models, so they can see what kind of side effects — if any — EGCG brings. If the mitochondria continue to wither in the compound’s presence, they’ll move a step closer to developing alternative therapies for oral cancer that don’t rely on the wide-scoped forces of chemo.

Source:
Tao L, Park J, Lambert J. Differential prooxidative effects of the green tea polyphenol, (–)-epigallocatechin-3-gallate, in normal and oral cancer cells are related to differences in sirtuin 3 signaling. Molecular Nutrition & Food Research. 2015.

March, 2015|Oral Cancer News|

Cure Possible for Some HPV-Positive Oropharyngeal Cancers

Source: www.medscape.com
Author: Fran Lowry

In a subset of patients with human papillomavirus (HPV)-related oropharyngeal cancer, the goal of achieving a “cure” is a realistic one, even in patients who have limited distant metastases, a prospective study has shown.

Of the patients with HPV-positive oropharyngeal cancer and distant metastases, 10% survived more than 2 years after intensive treatment, which the researchers defined as a cure.

The study was presented at the 5th International Conference on Innovative Approaches in Head and Neck Oncology (ICHNO) in Nice, France.

The research was praised by Jean Bourhis, MD, head of the Department of Radiation Oncology at Centre Hospitalier Université Vaudois in Lucerne, Switzerland, and cochair of the ICHNO conference scientific committee.

“This important piece of research adds substantially to what we know about the role and the importance of the human papillomavirus in oropharyngeal cancers and gives real hope of improvement in both diagnosis and treatment to those who are affected by the condition,” he said in a statement.

This study, from a world-leading group of head and neck cancer experts, is very interesting, and related to relevant clinical and interdisciplinary questions,” said Daniel Zips, MD, professor of radiation oncology at the University of Tübingen in Germany.

“HPV status is also important for the management of metastatic disease,” he told Medscape Medical News.

He agrees that for some patients with HPV-positive oropharyngeal cancer, using the researchers’ definition, a cure is possible.

“I also agree that the results from this study might begin to change the view of this disease and provide some hope for patients and their families,” Dr Zips explained.

Distant Metastases Are Main Form of Failure
“The majority of patients with HPV-related oropharyngeal cancer can be cured, but distant metastasis can occur in about 15% of patients. In fact, distant metastasis has become the main form of failure for this patient population,” lead author Sophie Huang, a radiation therapist and assistant professor at the University of Toronto. Dr Huang was a physician in China but is an MRT(T) — a radiation therapist — in Canada.

“When distant metastasis occurs, it is generally viewed as incurable disease. However, long-term survival after distant metastasis has been observed in nasopharyngeal cancer patients, which is another viral-related head and neck cancer, associated with the Epstein–Barr virus. Also, long-term survival in HPV-related OPC patients with distant metastasis has also been reported, but anecdotally,” Dr Huang told Medscape Medical News. “Are these just miracles? And would more miracles be found if we were able to understand how they happen?”

Dr Huang and her colleagues established a prospective database in which they collected data on enough patients to allow them to study how distant metastasis is manifested, how the cancer behaves after distant metastasis, and whether there are any factors that influence survival after distant metastasis.

“We felt that the answers to these questions would help us tailor surveillance strategies for the early detection of distant metastasis and explore optimal management algorithms to improve outcomes,” she explained.

Prospective Follow-up of Patients
The team evaluated 1238 consecutive oropharyngeal cancer patients treated at the Princess Margaret Cancer Centre in Toronto from 2000 to 2011. They identified 88 patients with HPV-related cancer and 54 with smoking-related cancer who were HPV-negative, all with distant metastases.

They assessed the pace of the manifestation of the distant metastases, characteristics, and patient survival, and identified factors that might predict longer survival.

The proportion of patients with distant metastases was similar in the two groups. However, metastases associated with HPV-positive oropharyngeal cancer had a later onset, different characteristics, and longer survival than those associated with HPV-negative oropharyngeal cancer.

Specifically, more than 94% of metastases occurred in the first 2 years after treatment in HPV-negative patients, whereas only a quarter occurred in HPV-positive cancers. In the HPV-positive group, some occurred after 5 years.

“This observation indicates that HPV-related OPC patients who are disease-free for 2 years are not out of the woods. A longer surveillance period for HPV-related OPC patients is needed to detect, and hopefully cure, distant metastases,” Dr Huang said.

Additionally, the researchers found two phenotypes of distant metastases in HPV-positive patients.

The disseminating phenotype is aggressive and spreads to multiple organs in a short period of time. This phenotype was found in 55% of the HPV-positive group but in 0% of the HPV-negative group.

The indolent phenotype is characterized by a few lesions growing at a slow pace, and manifesting as oligometastasis, with five or fewer lesions. In patients with metastases in a single organ, this phenotype was found in 24% of the HPV-positive group and in 26% of the HPV-negative group.

The lung was the most common site for distant metastasis in both groups.

“This indolent phenotype has longer survival and might be curable,” Dr Huang reported.

More HPV-positive than HPV-negative patients were specifically treated for distant metastasis (60% vs 31%)

table1

More HPV-positive patients with distant metastases than HPV-negative patients survived to 3 years (25% vs 15%; P = .01).

“The survival advantage in HPV-positive patients is due to a number of factors. The cancer is more sensitive to radiotherapy and chemotherapy, patients tend to be younger by about 10 years, and they have fewer other health problems, including those caused by smoking. This allows them to receive the more aggressive treatment necessary to eradicate metastatic disease,” Dr Huang explained.

table2

“This research shows that metastatic HPV-positive patients who receive active treatment can survive considerably longer. One of the reasons patients with metastatic disease fail to receive aggressive treatment is due to the physician and patient perception that this is an incurable state. We hope these results will motivate researchers to optimize management strategies for these patients,” Dr Huang said.

“The first distant metastasis site is mostly in the chest region,” she noted. In fact, most of the cured patients had lung metastasis. “Computed tomography of the thorax for the early detection of distant metastases” might enhance the cure rate for this disease, she added.

Future studies should look for ways to identify patients at initial presentation who are at high risk for distant metastasis, and which type of distant metastasis will develop.

“We know there is a degree of correlation between the initial stage and the risk of distant metastasis, but we did not find a strong relationship between this stage and the type of metastasis,” Dr Huang reported. “The intensity of cigarette smoking in the years prior to the time of diagnosis is a possible factor. Being able to identify such relationships could be a huge help in deciding appropriate treatment at an early stage.”

Note:

1. Dr Bourhis, Dr Zips, Dr Huang, have disclosed no relevant financial relationships.
2. 5th International Conference on Innovative Approaches in Head and Neck Oncology (ICHNO): Abstract OC-044. Presented February 13, 2015.

March, 2015|Oral Cancer News|

Study finds how T cells cause inflammation with oral candidiasis

Source: www.drbicuspid.com
Author: Donna Domino, Features Editor

Ohio dental researchers have found a method to study how T cells cause inflammation during oral candidiasis infections, according to a new study in the Journal of Visualized Experiments (February 18, 2015). The discovery could lead to new therapies or drugs that may improve the functioning of weakened immune systems.

Pushpa Pandiyan, PhD, an assistant professor at Case Western Reserve School of Dental Medicine, and colleagues worked on mice to find a new way to model how T cells, the white blood cells critical for the body’s immune system, cause inflammation.

Pandiyan’s previous work focused on isolating different types of oral T cells for study. In the latest study, the researchers injected T cells into genetically engineered immunodeficient mice to test how the cells function when fighting Candida albicans, a fungus found in about 60% of the population but controlled by a functioning immune system.

The infection becomes a particular health problem for people with the HIV/AIDS infection, cancer patients with immune systems weakened by chemotherapy, or those born with no immune defenses.

The researchers investigated how IL-17a (T helper 17, or Th17 cells, a type of T cells that secrete a cytokine) and T regulatory cells (Tregs) controlled the fungal infection and inflammation, respectively.

“Although Th17 cells are required for antifungal immunity, uncontrolled Th17 cells have been implicated with such illnesses as multiple sclerosis, lupus, psoriasis, cancers, and irritable bowel disease,” Pandiyan said in a statement.

The immunodeficient mice were infected with the fungus and injected with Th17 cells. One group of mice was also injected with Tregs.

The group of mice that received both Th17 and Tregs fared better in stopping the infection and thriving during inflammation, the researchers found. The other group of mice that did not receive Tregs lost weight and began to waste away.

The researchers also found the immune system doesn’t work well when the Th17 cells malfunction without appropriate control. “They can set into action a series of immune responses that develop into inflammation and greater health issues,” Pandiyan said.

While Pandiyan studied Th17’s role in fighting C. albicans, other researchers could use the method to study Th17 cell functions in other areas of the body, she noted.

Pandiyan believes the process could lead to identifying and testing new drugs to replace antifungal medicines that have become ineffective as the fungi develop a resistance to them.

March, 2015|Oral Cancer News|

Possibility of cure For HPV positive throat cancer patients—new research

Source: au.ibtimes.com
Author: Samantha Richardson

A new research conducted by Dr. Sophie Huang, assistant professor in the Department of Radiation Oncology, Princess Margaret Cancer Centre, University of Toronto, Canada revealed that throat cancer caused by the Human Papilloma virus (HPV+) can possibly be cured. The research is of utmost importance as it is the first to provide substantial evidence to prove that patients suffering from oropharynx cancer can be healed.

The disease also spreads to other parts of the body. The press release disclosed that the tumours remain passive and go undetected for over two years in most case, which makes it incurable. The research was presented at the 5th International Conference on Innovative Approaches in Head and Neck Oncology (ICHNO) on Friday. She states that cure is possible among patients suffering from oropharyngeal cancer is possible for the first time.

“Our research, the largest study to date to explore survival predictors for metastatic HPV+ and HPV- oropharyngeal cancer patients,” says Dr. Huang.

For the research, 934 patients suffering from HPV+ OPC were studied. All subjects were patients treated at the Princess Margaret Cancer Centre between 2000 and 2011. The researchers found two types of distinct metastases or tumours in other parts of the body away from the source in HPV+ patients: “explosive” and “indolent” metastases. The former grows and spreads quicker while the latter is slower and manifests itself as oligometastasis. However, they found the lung as the most common metastatic site in both HPV+ and HPV- patients. According to Dr. Huang, more aggressive treatments solely aimed at disease control resulted in a long term disease-free period, suggesting that some may be cured.

“In the HPV+ group with oligometases 25% were still alive after three years, whereas the percentage in the HPV- group was 15%,” the press release stated. The reason for higher survival rates among HPV+ patients is the younger age of the patients. In addition, the cancer is more sensitive to radiotherapy and chemotherapy. Those who receive treatment are at an advantage and can survive longer than those who do not undergo the process. Early detection of metastases and aggressive treatment can cure the patient.

Dr. Huang explained that they were aware of the correlation between the initial stages and the risk of a tumour on another site of the body. However, the degree by which they are related remains unknown. She highlights that identifying such relationships could help find an appropriate treatment at an early stage.

Professor Jean Bourhis, co-chair of the conference scientific committee, says that this is a very important research with respect to finding the cure of oropharynx cancer. He states that it provides hope in both the treatment and diagnosis of the patients.

February, 2015|Oral Cancer News|

Band Announces Iron Maiden Singer is Battling Tongue Cancer

Source: usatoday.com
Author: Maria Puente

 

Iron Maiden singer Bruce Dickinson is being treated for cancer of the tongue, the heavy metal band announced on its website Thursday. But it was caught early, seven weeks of chemotherapy and radiation have just been completed, and a full recovery is expected, the announcement said. “Bruce is doing very well considering the circumstances and the whole team are very positive,” it concluded.

The announcement said that before Christmas, Dickinson visited his doctor for a routine check-up. This led to tests and biopsies, which revealed a small cancerous tumor at the back of his tongue.

“As the tumor was caught in the early stages, the prognosis thankfully is extremely good,” the announcement said. “Bruce’s medical team fully expect him to make a complete recovery with the all-clear envisaged by late May.

“It will then take a further few months for Bruce to get back to full fitness. In the meantime we would ask for your patience, understanding and respect for Bruce and his family’s privacy until we update everyone by the end of May.”

Dickinson, 56, joined the British megastar band in the early 1980s, and is also a commercial airline pilot. Iron Maiden’s hits include Run to the Hills and The Number of the Beast.

Last year, the band announced that Clive Burr, former drummer with Iron Maiden, had died in his London home in March. He was 56 and had multiple sclerosis.

 

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.
February, 2015|Oral Cancer News|