oral cancer

Don’t start, be smart: Local, Reno Rodeo competitor advocates being tobacco-free

Source: mynews4.com
Author: Kenzie Bales
Date: June 13th, 2017

RENO, Nev. (News 4 & Fox 11) — As a country phenomenon, Garth Brooks once said, “It’s bulls and blood, it’s dust and mud, it’s the roar of a Sunday crowd. It’s the white in his knuckles, the gold in the buckle, he’ll win the next go ’round. It’s boots and chaps, it’s cowboy hats, it’s spurs and latigo, it’s the ropes and the reins, and the joy and the pain and they call the thing rodeo.”

2017 Reno Rodeo competitor Cody Z Kiser has been riding and roping for as long as he can remember.

Born and raised to Carrie and P.D. Kiser in Carson City, Nevada, Cody started riding bulls as a Dayton High School student.

A horrific injury would set Kiser back, but by no means did it keep him from chasing his dreams.

Kiser says a bull stepped on his face and crushed all the bones in the left side of his face. After recovering, Kiser transitioned from bull riding to bareback bucking horses and hasn’t looked back since.

If traveling to rodeos all the time wasn’t enough to keep someone completely preoccupied, Cody competed while pursuing a Bachelor’s Degree in Civil Engineering at the University of Nevada, Reno.

After testing the waters in the engineering field for awhile, Kiser decided it was time to chase his lifelong dream and give rodeo his full attention.

During his endeavors as a cowboy, Cody was fortunate enough to establish a partnership with the Oral Cancer Foundation.

Everyone knows it is terrible for you, yet they still do it.

He says that being tobacco-free is something he advocates for because he understands the huge health risks that come along with it.

I have seen the impact it can have on a human’s health and it is something that I want no part of, and if I can help others from starting it, then I am happy.

Kiser says he is always willing to answer questions pre-existing tobacco users may have, but by no means is he trying to tell people how to live their life.

A big goal of his: to show people that you don’t have to smoke or chew to be a real cowboy or to be successful in the sport you love. Primarily focusing on kids, Kiser hopes to spread the movement to younger generations who haven’t picked up the bad habit yet.

The sport is hard enough on your body, no sense in making in harder on yourself.

Kiser says he strays away from just throwing facts and statistics at people, but rather making a positive, memorable impact and associating with people without the use of tobacco.

After partnering with the OCF three years ago, the cowboy says that he has had nothing but positive feedback and calls himself the “luckiest guy in the world.”

If you are interested in watching Cody Kiser compete in the 2017 Reno Rodeo, you can catch him on Father’s Day, Sunday, June 18 (making his dad, a former bucking horse rider proud) or Monday, June 19.

June, 2017|Oral Cancer News|

Study reveals high environmental cost of tobacco

Source: www.cnn.com
Date: May 31st, 2017
Author: Jacopo Prisco

Details of the environmental cost of tobacco are revealed in a study released Wednesday by the World Health Organization, adding to the well-known costs to global health, which translate to a yearly loss of $1.4 trillion in health-care expenses and lost productivity.

From crop to pack, tobacco commands an intensive use of resources and forces the release of harmful chemicals in the soil and waterways, as well as significant amounts of greenhouse gases. Its leftovers linger, as tobacco litter is the biggest component of litter worldwide.

“Tobacco not only produces lung cancer in people, but it is a cancer to the lungs of the Earth,” said Dr. Armando Peruga, who previously coordinated the WHO Tobacco Free Initiative and now works as a consultant. He reviewed the new report for the WHO.

Commercial tobacco farming is a worldwide industry that involves 124 countries and occupies 4.3 million hectares of agricultural land. About 90% of it takes place in low-income countries, with China, Brazil and India as the largest producers.

Because tobacco is often a monocrop — grown without being rotated with other crops — the plants and the soil are weak in natural defenses and require larger amounts of chemicals for growth and protection from pests.

“Tobacco also takes away a lot of nutrients from the soil and requires massive amounts of fertilizer, a process that leads to degradation of the land and desertification, with negative consequences for biodiversity and wildlife,” Peruga said.

The use of chemicals directly impacts the health of farmers, 60% to 70% of whom are women. This is especially prominent in low- and middle-income countries, where some compounds that are banned in high-income countries are still used.

300 cigarettes = one tree

Farming also uses a surprisingly large amount of wood, rendering tobacco a driver of deforestation, one of the leading causes of climate change.

About 11.4 million metric tonnes of wood are utilized annually for curing: the drying of the tobacco leaf, which is achieved through various methods, including wood fires. That’s the equivalent of one tree for every 300 cigarettes, or 1.5 cartons.

This adds to the impact of plantations on forest land, which the study describes as a significant cause for concern, citing “evidence of substantial, and largely irreversible, losses of trees and other plant species cause by tobacco farming.”

Deadly gases

In 2012, 967 million daily smokers consumed approximately 6.25 trillion cigarettes worldwide, the WHO estimates.”That means about 6,000 metric tones of formaldehyde and 47,000 metric tonnes of nicotine are released into the environment,” Peruga said.

Tobacco smoke contains about 4,000 chemicals, at least 250 of which are known to be harmful. It also contains climate-warming carbon dioxide, methane and nitrous oxides. “The combination of greenhouse gases from combustion is equivalent to about 1.5 million vehicles driven annually,” Peruga said.

Secondhand smoke is particularly deadly: It contains twice as much nicotine and 147 times more ammonia than so-called mainstream smoke, leading to close to 1 million deaths annually, 28% of them children.

Some of these pollutants remain in the environment (and our homes) as “third-hand smoke,” accumulating in dust and surfaces indoors, and in landfills. Some, like nicotine, even resist treatment, polluting waterways and potentially contaminating water used for consumption, the study notes.

Non-biodegradable litter

Tobacco litter is the most common type of litter by count worldwide.

“We calculate that two-thirds of every cigarette ends up as litter,” Peruga said.

The litter is laced with chemicals including arsenic and heavy metals, which can end up in the water supply. Cigarette butts are not biodegradable, and tossing one on the ground is still considered a socially acceptable form of littering in many countries.

The WHO estimates that between 340 million and 680 million kilograms of tobacco waste are thrown away every year, and cigarette butts account for 30% to 40% of all items collected in coastal and urban clean-ups.

“In addition to that, there are 2 million tons of paper, foil, ink and glue used for the packaging,” Peruga said.

A way forward?

Even though smoking is declining globally, it is increasing in some regions, such as the eastern Mediterranean and Africa. China is a world leader both in production (44%) and consumption, with 10 times more cigarettes smoked than in any other nation.

Every stage of the production of a cigarette has negative effects on the environment and the people who are involved in manufacturing tobacco products, even before the health of smokers and non-smokers is affected.

Although governments worldwide already collect $270 billion in tobacco taxes a year, the WHO suggests that increasing tax and prices is an effective way of reducing consumption and help development priorities in each country, adding that by collecting 80 cents more per pack, the global tax revenue could be doubled.

“Tobacco threatens us all,” WHO Director-General Margaret Chan said in a note. “It exacerbates poverty, reduces economic productivity, contributes to poor household food choices, and pollutes indoor air.”

May, 2017|Oral Cancer News|

Padres Hall of Famer Randy Jones Battling Throat Cancer

Source: 10news.com
Author:
Mark Saunders
Posted: Jan 26, 2017

SAN DIEGO – Legendary San Diego Padres pitcher Randy Jones is battling throat cancer, the team’s website announced Thursday.

Jones was reportedly diagnosed in November 2016 and has been undergoing radiation and chemotherapy treatments since December at Sharp’s Hospital.

“I feel positive,” Jones said told the Padre’s Bill Center. “They caught it early. It’s all in the throat and not in the lymph nodes. I’m beating this thing.”

Jones said he used chewing tobacco as a player and has smoked cigars throughout his adult life.

“I’ve completed 90 percent of my treatment,” Jones told Center. He added that his physicians have said his cancer is linked to tobacco use. He also said his cancer is low-risk.

Since his playing days he has remained heavily involved with the team. He is a spokesperson for the team and a local radio and television personality.

The Friars drafted Jones in 1972, during the 5th round of the amateur draft.

Jones pitched for the Padres from 1973-1980. He recorded a 3.42 ERA and 735 strikeouts through his career. He was the first Padre to win the National League Cy Young Award and the first Padre to start an All-Star Game.

He was a National League all-star in 1975 and 1976, when he led the NL in ERA in 1975 and led in wins in 1976.

Jones’ number was retired by the team in 1997 and two years later, he was a member of the Padre’s first Hall of Fame class.

 

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

January, 2017|Oral Cancer News|

FDA Warns Against So-Called “Cancer Cure”

Source: http://www.curetoday.com/articles/fda-warns-against-socalled-cancer-cure

Published: 01/13/2017

Author: BRIELLE URCIUOLI

The US Food and Drug Administration (FDA) just added another agent, PNC-27, to the growing list of drugs that falsely claim to treat or cure cancer.

An FDA lab recently found the bacteria Variovorax paradoxus in PNC-27, a product that is claiming to treat and cure all cancers, claiming to affect lung cancer as affectively as head and neck cancer. Though no illness or serious adverse events were reported to the FDA, contact with contaminated samples can lead to life-threatening infections, especially in vulnerable populations, such as young children, elderly people, pregnant women and people who have weakened immune systems, according to a statement released by the FDA.

“In general, consumers should be cautious of products marketed and sold online claiming to treat, cure or prevent any disease. Products claiming to treat, cure or prevent disease, but are not proven safe and effective for those purposes not only defraud consumers of money, they can lead to delays in getting proper diagnosis and treatment of a potentially serious condition,” Kristofer Baumgartner, FDA spokesperson, said in an interview with CURE.

PNC-27 is being dosed in multiple ways, such as a nebulized solution, intravenous solution, vaginal suppository or rectal suppository.

The FDA is urging people not to purchase or use PNC-27, which is neither FDA evaluated or approved. Patients should consult with their licensed health care providers before deciding on a treatment plan, and if they have already taken PNC-27, they should see their doctor as soon as possible, and report any adverse events to the FDA’s MedWatch Adverse Event Reporting Program.

As a matter of policy, the FDA cannot discuss any ongoing trials in detail, Baumgartner said. – See more at: http://www.curetoday.com/articles/fda-warns-against-socalled-cancer-cure#sthash.YgMC7JgV.dpuf

 

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

January, 2017|Oral Cancer News|

NCI-Designated Cancer Centers Issue Statement in Support of New CDC Recommendations on HPV Vaccination

Source: The ASCO Post
Posted: 1/11/2017

The 69 National Cancer Institute (NCI)-designated cancer centers have issued a joint statement in support of recently revised recommendations from the Centers for Disease Control and Prevention (CDC) to improve national vaccination rates for human papillomavirus (HPV).

According to the CDC, incidence rates of HPV-associated cancers have continued to rise, with approximately 39,000 new HPV-associated cancers now diagnosed each year in the United States. Although HPV vaccines can prevent the majority of cervical, anal, oropharyngeal, and other genital cancers, vaccination rates remain low across the United States, with just 41.9% of girls and 28.1% of boys completing the recommended vaccine series.

New Recommendations

The new guidelines from the CDC recommend that children under age 15 should receive 2 doses of the 9-valent HPV vaccine at least 6 months apart. Adolescents and young adults older than 14 should continue to complete the 3-dose series.

Research shows there are a number of barriers to overcome to improve vaccination rates, including a lack of strong recommendations from physicians and parents not understanding that this vaccine protects against several types of cancer. In an effort to overcome these barriers, NCI-designated cancer centers have organized a continuing series of national summits to share new research, discuss best practices, and identify collective action toward improving vaccination rates.

The original joint statement, published in January 2016, was the major recommendation from a summit hosted at The University of Texas MD Anderson Cancer in November 2015, which brought together experts from the NCI, CDC, American Cancer Society, and more than half of the NCI-designated cancer centers.

The updated statement is the result of discussions from the most recent summit, hosted this past summer by The Ohio State University Comprehensive Cancer Center. Nearly 150 experts from across the country gathered in Columbus to present research updates and plan future collaborative actions across NCI-designated cancer centers.

 

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

January, 2017|Oral Cancer News|

Immunotherapies Form New Frontier in Treating Head and Neck Cancers

Source: OncLive.com

Date: January 2nd, 2017

In August 2016, the FDA approved pembrolizumab (Keytruda) for patients with platinum-refractory squamous cell carcinoma of the head and neck (SCCHN).1 Not only was it the first immunotherapy approved for head and neck cancer (HNC), but it marked the first new drug approval for HNC in the United States in 20 years.

“Now we have an agent that really changes the paradigm—a new class of treatment—and we are seeing amazing benefit in some patients,” said Tanguy Seiwert, MD, during an OncLive Peer Exchange® panel held during the 2016 European Society for Medical Oncology (ESMO) Annual Meeting.

Less than a month later, the menu of immunotherapy options expanded as the FDA approved nivolumab (Opdivo) for the treatment of patients with recurrent or metastatic SCCHN with disease progression on or after a platinum-based therapy.

During the Peer Exchange, the panelists provided an overview of the immunotherapy terrain in HNC, a discussion that was filled with considerable hope and excitement. “When we try immunotherapies in the second-line setting, we see objective responses—sometimes deep, clinically meaningful, extremely durable responses—and we’re beginning to think that maybe, on some occasions, we may be able to cure patients with relapsed metastatic head and neck cancer,” said Kevin Harrington, MD, PhD. This is especially remarkable since such patients have generally had a survival of ≤1 year.

The panelists concurred that the care of patients with HNC will evolve significantly over the next 5 to 10 years, as the tip of the immunotherapy iceberg is just starting to be scratched. During the Peer Exchange, they provided a rationale for using immunotherapies in HNC, including human papillomavirus (HPV)-positive and HPV-negative disease; outlined key immunotherapy studies; and offered their thoughts on the future of immunotherapies in HNC, including use of biomarkers to guide therapy and the opportunity to improve response by using combination treatments.

“Next-generation sequencing efforts are beginning to shed light on the hidden complexities of these tumors, leading to the identification of multiple molecular subtypes,” said Ezra Cohen, MD, who served as moderator for the session. “As key differences between tumors, with and without HPV infection, are beginning to emerge, the challenge is to find ways to use this information to personalize treatment for individual patients.”

Rationale for Immunotherapy in HNC

In patients with locally advanced HNC, HPV status has generally determined outcomes, with HPV-positive patients having a good prognosis and higher likelihood of cure, and HPV-negative patients having a poorer prognosis and a lower likelihood of cure.

However, outcomes with conventional therapy in recurrent metastatic disease have been poor across the board, especially in the setting of platinum- refractory disease, indicating a tremendous unmet need. Before pembrolizumab was approved in this setting, the recommendation was to use a taxane, such as methotrexate or cetuximab (Erbitux), as a single agent, but the outcomes have been unsatisfactory. In contrast, immunotherapy studies have shown promising results in these patients, with HPV-negative patients also benefiting.

“The rationale for [using immunotherapies] for HPV-positive tumors may be the virus, as well as mutations, and for HPV-negative tumors, it’s likely the mutation load,” said Seiwert. He explained that HPV-negative tumors are often smoking-associated tumors and, therefore, have high mutation loads, a factor that has been associated with good response to immunotherapy, whereas HPV-positive tumors resemble melanoma, with significant inflammation, another factor associated with good response.

Although efficacy was found to be the same for HPV-positive and HPV-negative tumors in KEYNOTE-012, which was the study that led to pembrolizumab’s approval for HNC, some CheckMate-141 subanalyses suggest there might be slightly more activity in HPV-positive patients, noted Seiwert.

Despite such findings, he said, “HPV status should not actually dissuade us one way or the other from using immunotherapy—it’s clearly active in both HPV-negative and HPV-positive tumors.” And, as Harrington pointed out earlier in the discussion, since nothing else works well in the second-line setting, “why not try it?”

Key Pembrolizumab Studies

The panelists proceeded to provide an overview of several instrumental pembrolizumab studies, including the KEYNOTE-012 expansion study and KEYNOTE-055 studies, and of the phase III CheckMate-141 study, which paved the way for nivolumab’s approval.2-4 They also discussed a subanalysis of CheckMate-141 presented at ESMO that demonstrated good patient-reported outcomes following nivolumab therapy, lending further support to its use in SCCHN.5

KEYNOTE-012 Expansion Study

The phase Ib KEYNOTE-012 expansion study administered 200 mg of pembrolizumab intravenously once every 3 weeks to 132 patients with recurrent or metastatic SCCHN, irrespective of their programmed death-ligand 1 (PD-L1) or HPV status.2 Primary endpoints included overall response rate (ORR), and safety and secondary endpoints included progression-free survival (PFS), overall survival (OS), and PD-L1 expression’s impact on response.

Pembrolizumab was well tolerated, and yielded a clinically meaningful ORR with evidence of durable responses; median duration of response was not reached. The ORR was 18% by central imaging vendor review and 20% by investigator analysis. A statistically significant increase in ORR was observed for PD-L1–positive versus PD- L1–negative patients (22% vs 4%, respectively; P = .021).

At 6 months, PFS and OS rates were 23% and 59%, respectively. “And we have patients living far beyond what we usually expect for metastatic disease…we now have patients who have completed 2 years of treatment in a setting with a median life expectancy of about 6 months,” revealed Seiwert, who is involved with the study.

Pembrolizumab was also well tolerated. Grade ≥3 events occurred in 9% of patients. “[This is] within the range of toxicities that we have seen in other studies,” said Viktor Grünwald, MD. “Because we’re approaching a very sick and morbid patient population, we might expect different toxicity outcomes, so I think it’s very reassuring that we’re seeing the same amount of toxicity as in other studies,” he explained.

While checkpoint inhibitors are generally well tolerated and have favorable toxicity profiles, the panelists warned that severe side effects can occur and careful patient monitoring is required. A key concern they discussed is pneumonitis.

“Although it only occurs in about 1% to 2% of patients, you must screen for it because it’s life threatening,” said Seiwert. “If somebody says, ‘I am short of breath’ or ‘I have a little bit of a cough,’ I scan them right away to look for it,” he said, explaining that immediate treatment with high-dose steroids is warranted.

KEYNOTE-055 Preliminary Results

KEYNOTE-055 enrolled 172 patients with recurrent or metastatic SCCHN to receive pembrolizumab 200 mg every 3 weeks after progression on platinum plus cetuximab. The preliminary analysis, which reported on 92 evaluable patients, was initially presented at the 2016 American Society of Clinical Oncology (ASCO) Annual Meeting.3 Primary endpoints include ORR and safety.

As with KEYNOTE-012, pembrolizumab was found to be well tolerated and to have significant antitumor activity, with 17% to 18% response rates. Evaluation of the full study cohort will include analyses of HPV status and response by anatomic site. “I think that’s the story we’re seeing for pembrolizumab in head and neck cancer—patients are already being treated in single-arm clinical studies, which is somewhat unusual, but reflects the speed of knowledge that we’re gaining that is leading to approvals,” said Grünwald.

Nivolumab also had a lower incidence of treatment-related adverse events (TRAEs) than IC. Any grade TRAEs occurred in 59.3% and 77.5% of patients on nivolumab or IC, respectively. Grade 3/4 TRAEs occurred in 13.6% and 35.1% of patients, respectively, indicating the treatment is well tolerated, which also translated to improvements in quality of life in the patient-reported outcomes study.5

“A very detailed analysis of patient-reported outcomes using 3 well-validated questionnaires showed nivolumab was able to maintain good patient-re- ported outcomes in terms of their quality of life, their functioning, and their symptom scores, whereas IC showed serious detriment in those scores,” said Harrington.

In the study,5 patients treated with nivolumab had delayed worsening of functioning and symptoms compared with IC at approximately 4 months of follow-up, with patients receiving nivolumab reporting longer maintenance of function and less pain, fatigue, and dyspnea on treatment, as compared with those receiving IC.

“So not only do we have clear evidence that these drugs can work in terms of improving survival and delivering meaningful responses, but they do so with fewer episodes of treatment-related toxicity and disease-associated morbidity,” said Harrington.

Future of Immunotherapy in HNC

The panelists noted that use of biomarkers and combination therapies are key areas of future development for HNC. Both areas are already being examined in clinical trials and have relevance across the vast HNC spectrum, from those with minimal disease to those with previously treated advanced disease, potentially offering a curative pathway to more patients.

“It’s fantastic to have drugs that work in second-line relapsed metastatic or first-line metastatic setting, but what I want and what patients want is to be cured at the time they first present with their disease so they never have treatment in relapsed metastatic setting,” said Harrington.

Biomarkers

Although biomarkers such as PD-L1 expression are already being used and can help identify patients who are more likely to respond, high PD-L1 expression does not guarantee response, nor does no or low PD-L1 expression ensure lack of response or lack of durable response.

Subsequently, use of pembrolizumab and nivolumab is without use of this biomarker for patient selection. “While [a PD-L1 assay] can help inform patients of their likelihood to respond, it is not an assay that can select patients,” said Seiwert, who is working to identify novel biomarkers.

“I’ve been involved in looking at a novel biomarker called interferon gamma signature, which can be assayed quite easily with a rapid turn-around, and seems to perform somewhat better than PD-L1 expression,” said Seiwert. “It seems to have a high negative predictive value, and it may eventually allow us to exclude some patients who have no chance of having benefit, but it needs further validation.” He said that other biomarkers are also under investigation, including mutational load, immunogenic mutations, and dynamic biomarkers, but all are still experimental.

“What we really need is a biomarker that would predict progressive disease,” said Grünwald. “To me, that would be much more usable than an assay that just allows us to say to patients ‘your chance of response is 30%.’ I see biomarkers as having the potential to guide development of treatment algorithms,” he said.

Combinations

Currently, PD-L1–targeted agents have seen the greatest development, and studies are starting to suggest that response with these agents can be enhanced when they are combined with other treatments, including chemotherapy, CTLA-4 blockade, and radiotherapy. “About 70% of HNCs have some level of PD-L1 expression—some level of inflammation—but we only see responses in 15% to 18% of patients, so the pool of patients who might benefit from combinations is huge,” said Seiwert.

He noted that the melanoma and lung cancer settings have already shown combining PD-1 inhibitors with chemotherapy or a second checkpoint inhibitor to be particularly promising in the front line, and he suspects one or both combinations will eventually receive approval in these settings and warrant serious investigation for patients with SCCHN.

“Some of our patients do not benefit from a checkpoint inhibitor, and we can’t identify these patients in advance, but giving them chemotherapy might buy us time,” he said. “It’s almost like a pharmacodynamic effect, where we have more time for the immunotherapy to work, and maybe, also make the immune system stronger and expose antigens.”

In the locally advanced setting, animal studies have shown promise combining chemoradiotherapy with immunotherapy, but results of a small study presented at ESMO revealed some dosing challenges in humans.6

In the study, 18 patients with various forms of intermediate- or high-risk SCCHN received ipilimumab, an anti–CTLA-4 antibody, in addition to standard intensity-modulated radiotherapy with cetuximab. Dermatologic immune-related adverse events limited dosing. “There are some safety hints that it may not be a piece of cake getting through radiotherapy, and maybe cetuximab might not be the optimal part now, but I think there is still a lot of promise combining radiochemotherapy with immunotherapy,” said Grünwald. “It could be a future way in how we successfully treat early forms of localized SCCHN.”

Combining checkpoint inhibition with radiation is another intriguing combination, and one that has the potential to act like an in situ vaccination that can lead to abscopal responses (ie, responses at distant sites), noted Harrington, something he has, thus far, only observed rarely with radiation.

“The idea behind combining checkpoint inhibition and radiation is that we could use the confluence of the two different mechanisms to make abscopal responses more predictable and more effective at a distant site, while engendering an immunologically relevant response that allows us to treat macroscopic metastatic disease while also getting rid of micrometastatic disease that could lead to metastatic failure,” he said.

Although immunotherapy combinations are showing promise in SCCHN and other cancers, the panelists warned that they should only be attempted as part of clinical trials. “There are still a lot of question marks about combinations, so they must be done as part of a clinical trial,” said Seiwert. Not only are toxicities and immunosuppressive effects best managed in clinical trials, but trials are essential in advancing these therapies and identifying the next breakthroughs in the field, he said.

 

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

January, 2017|Oral Cancer News|

We Now Know Exactly How Many DNA Mutations Smoking Causes

Every 50 cigarettes you smoke gives you one extra DNA mutation per lung cell.

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Source: The Verge
Author: James Vincent

A common tactic for people trying to give up smoking is to quantify exactly how much damage — financial or physical — each cigarette or pack of cigarette does. How much does smoking cost you per month, for example, or how much shorter is your life going to be for each drag you take? Well, a new study into the dangers of smoking now lets us measure this damage right down to the number of mutations in your DNA.

A research team led by scientists from Los Alamos National Laboratory compared tissue samples from 1,063 non-smokers and 2,490 smokers, examining each individual’s DNA to look for mutations. They found that for every 50 cigarettes smoked, there is one extra DNA mutation for each cell in the lungs. Over the course of a year, this means that someone who smokes a pack a day (20 cigarettes) has 150 extra mutations per cell in the lung, 97 per larynx cell, 23 per mouth cell, 18 per bladder cell, and six per liver cell.

These changes to the cells aren’t dangerous in themselves, but each one has the potential to turn into a cancerous growth. “Smoking is like playing Russian roulette: the more you play, the higher the chance the mutations will hit the right genes and you will develop cancer,” Ludmil Alexandrov, the co-lead author of the study, told the New Scientist. “However, there will always be people who smoke a lot but the mutations do not hit the right genes.”

The reason for all these extra mutations is found in tobacco smoke — a substance that contains some 7,000 different chemicals, over 70 of which are known to cause cancer. How exactly different types of cell mutations lead to cancer is less clear, and the team from Los Alamos are hoping next to drill down further into this line of research and find out the probabilities that any individual DNA mutation will turn into cancer.

The good news for smokers, though, is that it’s never too late to quit. Although smoking causes regular DNA mutations, as soon as people give up cigarettes, the mutations stop too. One UK study from 2004 found that those who quit smoking at age 30 nearly eliminate the risk of dying prematurely, while those who quit at 50 halve it. For people trying to give up, those are certainly some more comforting odds.

 

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

November, 2016|Oral Cancer News|

Smokeless Tobacco Use and the Risk of Head and Neck Cancer: Pooled Analysis of US Studies in the INHANCE Consortium.

Source: www.pubmed.gov
Author: Wyss AB, Gillison ML, Olshan AF

Abstract

Previous studies on smokeless tobacco use and head and neck cancer (HNC) have found inconsistent and often imprecise estimates, with limited control for cigarette smoking. Using pooled data from 11 US case-control studies (1981-2006) of oral, pharyngeal, and laryngeal cancers (6,772 cases and 8,375 controls) in the International Head and Neck Cancer Epidemiology (INHANCE) Consortium, we applied hierarchical logistic regression to estimate odds ratios and 95% confidence intervals for ever use, frequency of use, and duration of use of snuff and chewing tobacco separately for never and ever cigarette smokers. Ever use (versus never use) of snuff was strongly associated with HNC among never cigarette smokers (odds ratio (OR) = 1.71, 95% confidence interval (CI): 1.08, 2.70), particularly for oral cavity cancers (OR = 3.01, 95% CI: 1.63, 5.55). Although ever (versus never) tobacco chewing was weakly associated with HNC among never cigarette smokers (OR = 1.20, 95% CI: 0.81, 1.77), analyses restricted to cancers of the oral cavity showed a stronger association (OR = 1.81, 95% CI: 1.04, 3.17). Few or no associations between each type of smokeless tobacco and HNC were observed among ever cigarette smokers, possibly reflecting residual confounding by smoking. Smokeless tobacco use appears to be associated with HNC, especially oral cancers, with snuff being more strongly associated than chewing tobacco.

© The Author 2016. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved.

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

October, 2016|Oral Cancer News|

America’s Most Popular ‘Legal’ Drug is Responsible for 25% of ALL Cancer

Source: www.thefreethoughtproject.com
Author: John Vibes

There are many factors contributing to the massive rise in cancer cases in the US, but according to a new study from the American Cancer Society, cigarette smoke is by far the leading cause. The study found that roughly 25% of all cancer deaths could be attributed to cigarette smoking.

Although cigarette smoking has waned somewhat in recent years, nearly 40 million adults in the U.S. currently smoke cigarettes. The CDC says cigarette smoking is the leading cause of preventable disease and death in the U.S., responsible for more than 480,000 deaths annually.

According to the study:

We estimate that at least 167133 cancer deaths in the United States in 2014 (28.6% of all cancer deaths; 95% CI, 28.2%-28.8%) were attributable to cigarette smoking. Among men, the proportion of cancer deaths attributable to smoking ranged from a low of 21.8% in Utah (95% CI, 19.9%-23.5%) to a high of 39.5% in Arkansas (95% CI, 36.9%-41.7%), but was at least 30% in every state except Utah. Among women, the proportion ranged from 11.1% in Utah (95% CI, 9.6%-12.3%) to 29.0% in Kentucky (95% CI, 27.2%-30.7%) and was at least 20% in all states except Utah, California, and Hawaii. Nine of the top 10 ranked states for men and 6 of the top 10 ranked states for women were located in the South. In men, smoking explained nearly 40% of cancer deaths in the top 5 ranked states (Arkansas, Louisiana, Tennessee, West Virginia, and Kentucky). In women, smoking explained more than 26% of all cancer deaths in the top 5 ranked states, which included 3 Southern states (Kentucky, Arkansas, and Tennessee), and 2 Western states (Alaska and Nevada).

Smoking is one of the leading causes of illness and death in the world. The use of tobacco has become more widespread than ever and the substance itself is far more dangerous than it has ever been before.

Today, cigarettes are mass produced and treated with thousands of additives and chemicals. Carcinogenic, poisonous chemicals and toxic metals can all be found in modern tobacco products. These chemicals are present for many reasons ranging from taste and preservation to being purposely addictive. There are over 4000 of these chemicals in cigarettes and all of them are not revealed to the public. They are protected under law as “trade secrets” — meaning they can add anything they want in there without our knowledge.

The financial advantage alone should be enough of an argument to quit smoking. In most states, cigarettes are now over 6 dollars a pack, more than half of which is taxes. So people are literally paying the government and rich multinational corporations an average of 10 dollars every day, for a product that destroys their bodies. It is true that there are addictive chemicals in cigarettes but their strength and power has been blown way out of proportion.

The psychological addiction is always much stronger than the physical addiction even with harsh narcotics like heroin and especially with nicotine. All you have to do is stop and get through a few days without it. Soon enough the smell and taste will no longer be desirable to you and you will be happy to have that extra 6 dollars a pack in your pocket. It will be easier to breathe, you won’t get sick as often and you will overall be in better spirits. Quitting cigarettes is one decision that you can make that will drastically improve your life in a number of ways and it will give the elite less control of your money and your health.

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

October, 2016|Oral Cancer News|

Can your own immune system kill cancer?

Source: www.cnn.com
Author: Jacqueline Howard

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There was another big win in the advancement of immunotherapy treatments for cancer this week.

The Food and Drug Administration approved an immunotherapy drug called Keytruda, which stimulates the body’s immune system, for the first-line treatment of patients with metastatic non-small-cell lung cancer.

In other words, the drug could be the very first treatment a patient receives for the disease, instead of chemotherapy. Keytruda is the only immunotherapy drug approved for first-line treatment for these patients.

So it seems, the future of cancer care may be in our own immune systems, but how exactly does it work, and what are its pros and cons?

“It’s certainly going to become an independent way of treating cancers,” said Dr. Philip Greenberg, head of immunology at the Fred Hutchinson Cancer Research Center in Seattle, during a Q&A session at the International Cancer Immunotherapy Conference in New York in September.

“We always talk about the three pillars of cancer therapy — radiation therapy, chemotherapy and surgery — and it’s become quite clear now that there’s going to be a fourth pillar, which is immunotherapy,” he said. “There are times where it will be used alone, and there will be times that it will be used in conjunction with the other therapies, but there’s very little to question that this is going to be a major part of the way cancers are treated from now on, going forward.”

Here’s a look at the past, present and future of cancer immunotherapy.

It began with Bessie

In the summer of 1890, 17-year-old Elizabeth Dashiell, affectionately called “Bessie,” caught her hand between two seats on a passenger train and later noticed a painful lump in the area that got caught, according to the Cancer Research Institute.

She met with a 28-year-old physician named Dr. William Coley in New York to address the injury. He performed a biopsy, expecting to find pus in the lump, probably from an infection. But what he found was more disturbing: a small gray mass on the bone. It was a malignant tumor from a type of cancer called sarcoma.

Dashiell had her arm amputated to treat the cancer, but the disease quickly spread to the rest of her body. She died in January 1891. A devastated Coley went on to devote his medical career to cancer research.

Coley is sometimes referred to as the “father of cancer immunotherapy,” according to the Memorial Sloan Kettering Cancer Center.

During his career, he noticed that infections in cancer patients were sometimes associated with the disease regressing. The surprising discovery prompted him to speculate that intentionally producing an infection in a patient could help treat cancer.

To test the idea, Coley created a mixture of bacteria and used that cocktail to create infections in cancer patients in 1893. The bacteria would sometimes spur a patient’s immune system to attack not only the infection but also anything else in the body that appeared “foreign,” including a tumor. In one case, when Coley injected streptococcal bacteria into a cancer patient to cause erysipelas, a bacterial infection in the skin, the patient’s tumor vanished — presumably because it was attacked by the immune system.

Coley’s idea was occasionally studied by various researchers in the 1900s but was not widely accepted as a cancer treatment approach until more recently.

“Immunotherapy has essentially undergone a sort of revolution in the last decade in the sense that something that was experimental — and there were still questions about what role it would have in the way cancer is treated — is completely turned around, and now it’s clear it’s effective,” Greenberg said.

German physician Dr. Paul Ehrlich, who won the Nobel Prize in physiology or medicine in 1908, proposed using the immune system to suppress tumor formation in the “immune surveillance” hypothesis — an idea that seems to follow Coley’s.

Yet it wasn’t until the early 2000s that the hypothesis became more widely accepted, according to the Cancer Research Institute. A landmark review published in the journal Nature Immunology in 2002 supported the validity of cancer immunosurveillance.

“Cancer immunotherapy really refers to treatments that use your own immune system to recognize, control and hopefully ultimately cure cancers,” said Jill O’Donnell-Tormey, CEO of the Cancer Research Institute, during the conference in New York last month.

“Many people for many years didn’t think the immune system was really going to have a role in any treatment for cancer,” she said, “but I think the entire medical community (and) oncologists now agree that immunotherapy’s here to stay.”

‘Turning oncology on its head’

One of the most famous cancer patients to have received a form of immunotherapy is former President Jimmy Carter, who had a deadly form of skin cancer called melanoma. Last year, he announced that he was cancer-free after undergoing a combination of surgery, radiation and immunotherapy.

Carter was taking Keytruda. It’s approved to treat melanoma, non-small-cell lung cancer, and head and neck cancer. However, it’s not the only approved immunotherapy option out there.

“The advances and the results we’ve seen with using the immune system to treat cancer in the last five years or so are turning the practice of oncology on its head,” said Dr. Crystal Mackall, a professor at the Stanford University School of Medicine and expert on cancer immunotherapy.

You don’t want to overstate it. As an immunotherapist, I see things from my vantage point, which is biased, but my clinical colleagues use words like ‘revolution,’ ” she said. “When I hear them say that, I think, ‘Wow, this really is a paradigm shifting for how we think about treating cancer.’ ”

Immunotherapy comes in many forms — treatment vaccines, antibody therapies and drugs — and can be received through an injection, a pill or capsule, a topical ointment or cream, or a catheter.

The FDA approved the first treatment vaccine for cancer, called sipuleucel-T or Provenge, in 2010. It stimulates an immune system response to prostate cancer cells and was found in clinical trials to increase the survival of men with a certain type of prostate cancer by about four months.

Another treatment vaccine, called T-VEC or Imlygic, was approved by the FDA in 2015 to treat some patients with metastatic melanoma.

Some antibody therapies have been approved, as well. Antibodies, a blood protein, play a key role in the immune system and can be produced in a lab to help the immune system attack cancer cells.

The FDA has approved several antibody-drug conjugates, including Kadcyla for the treatment of some breast cancers, Adcetris for Hodgkin lymphoma and a type of non-Hodgkin T-cell lymphoma, and Zevalin for a type of non-Hodgkin B-cell lymphoma.

The FDA also has approved some immunotherapy drugs known as immune checkpoint inhibitors. They block some of the harm that cancer cells can cause to weaken the immune system.

Keytruda, which Carter took, is a checkpoint inhibitor drug. Other such drugs include Opdivo to treat Hodgkin lymphoma, advanced melanoma, a form of kidney cancer and advanced lung cancer. Tecentriq is used to treat bladder cancer, and Yervoy is used for late-stage melanoma.

Additionally, there are many immunotherapy treatments in clinical trials, such as CAR T-cell therapy. The cutting-edge therapy involves removing T-cells from a patient’s immune system, engineering those cells in a lab to target specific cancer cells and then infusing the engineered cells back into the patient. The treatment is being tested to treat leukemia and lymphoma.

“The real excitement now in cellular therapy, in T-cell therapies, is it reflects the developments in an area that we call synthetic biology, which is that you can add genes to cells and you can change what they do, how they behave, how they function, what they recognize,” Greenberg said.

The high price of new immunotherapy drugs has also garnered attention in the field, according to the Fred Hutchinson Cancer Research Center. For instance, some estimates suggest that checkpoint inhibitor treatments could cost as much as $1 million per patient.

As approvals continue, many scientists caution that doctors and patients alike should prepare for potential severe side effects and downsides.

Boosting the immune system with such therapies may cause skin reactions, flu-like symptoms, heart palpitations, diarrhea and a risk of infection. New cancer immunotherapy drugs have even been linked to arthritis in some patients.

A clinical trial conducted by Juno Therapeutics to test the effectiveness of an experimental immunotherapy treatment for lymphoblastic leukemia was halted after three patients died. They suffered cerebral edema or brain swelling.

Greenberg is a scientific co-founder of Juno Therapeutics.

However, “one of the best attributes of immunotherapy and the future of medicine is that it’s very precise in the way that it kills tissue and spares normal tissue, so in some way, immunotherapy is less toxic (than other therapies). There are patients who are treated with checkpoint inhibitors who have essentially no side effects,” Mackall said. “That would never happen with chemotherapy. They would always have side effects.

“Still, you know, the fact remains that probably nothing is perfect, and there are likely to be some side effects, but as far as we know now, they are less likely to be as severe or prevalent.”

As immunotherapy continues to develop as an option for cancer treatment, experts plan to be realistic about forthcoming challenges.

The challenges of immunotherapy

Experts say they hope to better understand why some patients may have different responses to immunotherapy treatments than others — and why some treatments may result in remissions instead of relapses, or vice versa.

“There’s this whole problem of, you give people an immunotherapy, it looks like it’s working, and then it stops working. We get recurrences or progression after some period, and the question is, why did that happen? How can you change it?” Greenberg said.

“This is where the science has come to play an important part: Is it because the immune response was working and somehow the tumor turned it off? And if that’s the case, then we have to look at ways in which we can reactivate the immune system,” he said. “Or is it not that, is it just that the immune system did what it’s supposed to do, but now a variant grew out, now a tumor grew out that’s no longer recognized by the immune response you are enforcing? If that’s the case, then we need ways to build subsequent immune responses to tackle that.”

Therefore, researchers have to better understand the behavior of not only the immune system but also cancerous tumors — and it’s no simple task.

“If there’s a perception that it’s easy, that’s a mistake. I think our lab has spent decades trying to figure out how to manipulate the immune response,” Greenberg said.

“Some patients are anticipating things to change overnight and be immediately available as a therapy. It takes quite a while,” he said, “but I’m quite certain immunotherapy is going to be enormously useful. It’s just, right now, we are limited in what can be done.”

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

October, 2016|Oral Cancer News|