Hookah smoke increases benzene exposure, risk for leukemia

Source: www.medicalnewstoday.com
Author: staff

Tobacco use is the leading preventable cause of mortality worldwide and is responsible for the deaths of 6 million people annually. Hookah smoking, a form of tobacco use that employs a partially filled water jar, has come under scrutiny in a new study, which suggests hookah smokers and non-smokers exposed to the smoke have increased uptake of benzene, a substance linked to increased risk of leukemia.
Hookah smokers

The study is published in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.

According to the researchers – led by Nada Kassem, associate director at the Center for Behavioral Epidemiology and Community Health at San Diego State University in California – the World Health Organization (WHO) and the US National Toxicology Program have classified benzene as a Group 1 carcinogen. WHO further report that benzene is carcinogenic to humans, recommending that there is no safe level of exposure. Hookah smoke, however, is a source of benzene exposure and is, therefore, a risk factor for leukemia.

The most popular kind of hookah tobacco is known as Moassel, which is sweetened and flavored tobacco that contains about 30% tobacco fermented with molasses and fruits mixed with glycerin and chemical flavors.

Kassem and her colleagues note that in the US in 2013, it was reported that 26.6% of male and 23.2% of female college students have used hookah at some point in time. Alarmingly, 8.1% of male and 6.6% of female middle and high school students have also used the substance.

Hookah tobacco smoking is not only linked to increased risks for leukemia, but also for lung and oral cancers, coronary heart disease and pulmonary disease.

Because hookah smoking is often practiced in social settings, the researchers examined uptake of benzene in both hookah smokers and non-smokers who attended hookah social events in “naturalistic settings” – where hookah tobacco alone was smoked.

Both smokers and non-smokers had increased SPMA uptake
The team analyzed levels of S-phenylmercapturic acid (SPMA) – which is a metabolite of benzene – in the urine of 105 hookah smokers and 103 non-smokers. The urine samples came from the morning of and the morning after study participants attended a hookah smoking event at either a lounge or a private home.

Results showed that for smokers, uptake of SPMA increased 4.2-fold after smoking hookah tobacco at a hookah lounge and 1.9-fold after smoking in a private home. Meanwhile, non-smokers’ uptake of SPMA increased 2.6-fold after attending an event at a hookah lounge.

Interestingly, non-smokers had similar levels of SPMA before and after attending a hookah event at a private residence. Kassem notes, however, that pre-house event benzene levels in non-smokers were as high as those found in post-hookah lounge event non-smokers – suggesting chronic benzene exposure in the former group.

“Hookah tobacco smoking involves the use of burning charcoal that is needed to heat the hookah tobacco to generate the smoke that the smoker inhales,” explains Kassem, adding:

“In addition to inhaling toxicants and carcinogens found in the hookah tobacco smoke, hookah smokers and non-smokers who socialize with hookah smokers also inhale large quantities of charcoal combustion-generated toxic and carcinogenic emissions.”

Hookah smoking ‘not a safe alternative’
Another finding from their sample of participants revealed that hookah smokers were younger than non-smokers, had more close friends who were current hookah smokers, were more likely to allow hookah smoking in their homes and were more likely to live with at least one hookah smoker.

Kassem says that since “there is no safe level of exposure to benzene, our results call for interventions to reduce or prevent hookah tobacco use, regulatory actions to limit hookah-related exposure to toxicants including benzene, and include hookah smoking in clean indoor air legislation.”

The researchers also note that health care professionals should raise public awareness that hookah tobacco smoke is a source of benzene exposure, a known risk factor for leukemia.

“In contrast to what is believed,” says Kassem, “hookah tobacco smoking is not a safe alternative to smoking other forms of tobacco.”

2014-11-25T09:36:27-07:00November, 2014|Oral Cancer News|

Study: smoking marijuana found non-carcinogenic

Source: americanlivewire.com
Author: staff

Smoking marijuana does not appear to increase the risk of lung cancer or head-and-neck malignancies, even among heavy users, researchers reported here.

“We expected that we would find that a history of heavy marijuana use, more than 500 to 1,000 uses, would increase the risk of cancer from several years to decades after exposure to marijuana, said Donald Tashkin, M.D., of the University of California in Los Angeles.

But in fact, they reported at the American Thoracic Society meeting here, marijuana use was associated with cancer risk ratios below 1.0, indicating that a history of pot smoking had no effect on the risk for respiratory cancers. Studies have shown that marijuana contains many compounds that when burned, produce about 50% higher concentrations of some carcinogenic chemicals than tobacco cigarettes.

In addition, heavy, habitual marijuana use can produce accelerated malignant change in lung explants, and evidence on bronchial biopsies of pre-malignant histopathologic and molecular changes, Dr. Tashkin said.

The investigators had also previously shown that smoking one marijuana cigarette leads to the deposition in the lungs of four times as much tar as smoking a tobacco cigarette containing the same amount of plant material. Marijuana cigarettes are not filtered and are more loosely packed than tobacco, so there’s less filtration of the tar. In addition, pot smokers hold the smoke in their lungs about four times longer than tobacco smokers do, Dr. Tashkin pointed out.

For the population-based case-control study, they identified cancer cases among people from the ages of 18 to 59, using the Los Angeles County Cancer Surveillance Program registry.

They identified 611 people with lung cancer, 601 with cancers of the head and neck, and 1,040 controls matched by age, gender and neighborhood (as a surrogate for socioeconomic status).

They conducted extensive personal interviews to determine lifetime marijuana use, measured in joint-years, with one joint-year equivalent to 365 marijuana cigarettes. The interviewers also asked participants about tobacco use, alcohol consumption, use of other drugs, socioeconomic status, diet, occupation, and family history of cancer.

The investigators also used logistic regression to estimate the effect of marijuana use on lung cancer risk, adjusting for age, gender, race/ethnicity, education, and cumulative tobacco smoking and alcohol use.

They found that the heaviest users in the study had smoked more than 60 joint years worth of marijuana, or more than 22,000 joints in their lifetime. Moderately heavy users smoked between 11,000 and 22,000 joints.

Despite the heavy use, “in no category was there any increased risk, nor was there any suggestion that smoking more led to a higher odds ratio,” he continued. “There was no dose-responsiveness,not even a suggestion of a dose response”and in all types of cancer except one, oral cancer, the odds ratios were less than one.”

In contrast, tobacco smoking was associated with increased risk for all cancers, and there was a “powerful” dose-response relationship. People who smoked more than two packs of cigarettes per day had a 21-fold risk for cancer, as opposed to a less than one-fold risk for marijuana, Dr. Tashkin said.

“When we restricted the analysis to those who didn’t smoke any tobacco we found the same results, and when we looked for interaction between tobacco and smoking ”would marijuana increase the risk, potentiate the carcinogenic effect of tobacco”we didn’t find that, nor did we find a protective effect against the effect of tobacco, which is very important, because the majority of marijuana smokers also smoke tobacco,” he commented.

It’s possible that tetrahydrocannabinol (THC) in marijuana smoke may encourage apoptosis, or programmed cell death, causing cells to die off before they have a chance to undergo malignant transformation, he said.

Note: Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco.

2014-11-25T09:01:35-07:00November, 2014|Oral Cancer News|

ctDNA ‘Liquid Biopsy’ could revolutionize cancer care

Source: www.medscape.com
Author: Janis C. Kelly

Bits of tumor cell somatic DNA shed into the circulation or released when cells die can now be detected and counted, thanks to advances in gene sequencing. This circulating tumor DNA (ctDNA) is derived from somatic mutations that occur in the tumor during an individual’s life, unlike hereditary mutations that are present in every cell in the body, so ctDNA is a specific cancer biomarker that can be detected, measured, and tracked.

Monitoring ctDNA is expected to provide clinicians with faster, cheaper, less invasive ways to assess cancer patients’ clinical status and response to therapy. ctDNA assay for multiple genes via next-generation sequencing (NGS) might become a “liquid biopsy” alternative to invasive tissue biopsy, experts told Medscape Medical News.

However, they also cautioned that rigorous testing of this concept is needed before the test can be used in practice, saying: “for now, we would counsel clinicians not to jump the gun on this.

Faster, Cheaper, More Accurate Tumor Tests
Paul B. Chapman, MD, a medical oncologist with the Melanoma and Sarcoma Service at Memorial Sloan Kettering Cancer Center in New York City and Chair of the Medical Advisory Panel at the Melanoma Research Alliance in Washington, DC, said that ctDNA assay is less invasive than biopsy, requires no radiation exposure, is relatively inexpensive, uses fresh DNA not exposed to preservatives, and allows near real-time monitoring of response to treatment.

“The beauty of ctDNA monitoring is the speed,” Dr Chapman said. “If you are looking for a change in a tumor, based on CT scan, you are talking about not only killing billions of tumor cells but also waiting for the resulting cell debris to be cleared by the body before the change shows up on imaging. That can take weeks. But cell death happens in minutes to hours, so you would expect the change in ctDNA to be a quick effect, and it is.”

Chetan Bettegowda, MD, Luis A. Diaz Jr, MD, and colleagues at Johns Hopkins Medical Institutions in Baltimore, Maryland, working in collaboration with 16 other institutions worldwide, recently reported that ctDNA levels differentiate early vs advanced tumors in a wide variety of cancers. In 640 patients, the researchers found that ctDNA was detectable in over 75% of advanced pancreatic, ovarian, colorectal, bladder, gastroesophageal, breast, melanoma, hepatocellular, and head and neck cancers but was found in less than 50% of primary brain, renal, prostate, and thyroid cancers. In 206 additional patients with metastatic colorectal cancers, ctDNA for KRAS gene mutations had 87.2% sensitivity and 99.2% specificity. The researchers also found that 96% of patients who relapsed after epidermal growth factor receptor (EGFR) blockade had ctDNA indicating one or more mutations in genes in the mitogen-activated protein kinase pathway.

Counting the methyl groups on ctDNA fragments might be even more precise. An assay for hypermethylation of one or more breast cancer genes was 95% accurate in detecting identifying patients with metastatic breast cancer.

However, Ben Ho Park, MD, PhD, from John Hopkins Sidney Kimmel Comprehensive Cancer Center and the department of chemical and biomolecular engineering at Johns Hopkins University in Baltimore, urged some caution in interpreting these data.

Dr Park told Medscape Oncology that key unanswered questions include: “Can we use ctDNA for identifying patients that have mutations that are susceptible to targeted therapies? Can we use ctDNA to follow response to therapies in metastatic disease that actually makes a positive difference for patient care? And can we use ctDNA as tumor biomarkers for assessing residual disease for early stage cancers, and to determine if we can tell patients that they are cured after surgery and do not need additional adjuvant therapies [including chemotherapy]?”

Advances in Gene Sequencing Led to Clinically Useful ctDNA Tests
A major factor in the surging interest in ctDNA has been the rapid drop in cost for analyzing genetic information. In a development that puts Moore’s Law to shame, costs for whole genome sequencing dropped from $1 billion for the first complete genome sequenced by the Human Genome Project to $350,000 per genome in 2008 and more recently to about $1,000 for a genome sequenced with Illumina’s commercially available HiSeq X Ten sequencing system.

Cancer researchers have been challenged by the problems of how to discriminate ctDNA from normal cell-free DNA, to detect extremely low levels of ctDNA, and to count accurately the number of mutant ctDNA fragments in a blood sample. The sensitivity of polymerase chain reaction (PCR)-based digital approaches improved with the addition of NGS, in which DNA is fragmented into small segments that can be quickly sequenced in millions of parallel reactions known as “reads” and then reassembled so that the set of reads shows the entire DNA sequence.

The half-life of ctDNA is about two hours, and changes in ctDNA levels can be apparent days to weeks before changes in imaging or in protein biomarkers. Because ctDNA is specific for the individual patient’s tumor, it is likely to avoid some of the false-positive problems associated with other cancer biomarkers.

Detecting Cancer and Monitoring Cancer Stages Without Biopsy
Most ctDNA strands contain between 180 and 200 base pairs, similar to the 180 base-pair multiples characteristic of apoptosis, and are thought to result mainly from passive release into the blood of ctDNA after cell death.

The presence of ctDNA after resection (but before adjuvant chemotherapy) indicates residual disease. Absence of ctDNA might identify a patient subgroup at low risk for recurrence who could be spared the risk, expense, and discomfort of adjuvant therapy. In 2008, a team of Johns Hopkins researchers reported that mutation-specific probes for 18 subjects undergoing multimodality therapy for colorectal cancer and monitored for two to five years showed that “ctDNA measurements could be used to reliably monitor the tumor dynamics in subjects with cancer who were undergoing surgery or chemotherapy.”

The authors suggested that ctDNA levels reflect the total systemic tumor burden because they decreased after complete resection and increased as new radiologically-apparent lesions developed. The researchers also pointed out that micrometastatic lesions (smaller than a few millimeters) contribute to tumor burden and to ctDNA levels although they are not detectable by imaging.

“For a melanoma patient who is free of disease after surgery but at risk for recurrence, ctDNA could be a nice way to follow without having to do frequent CT scans,” Dr Chapman said. It is also expected to be useful in situations in which tissue biopsy is undesirable or cannot be done.

However, an important unanswered question is how often these tests should be done. “We need to know how meaningful small changes in the ctDNA level are — sensitivity, specificity, and lead-time bias,” he said.

Monitoring Tumor Burden, Response to Therapy, and Resistance
“Another key advantage is that ctDNA could overcome the issue of tumor heterogeneity,” commented Dr Park. “Different sites of disease often have different mutational profiles. Since blood, and therefore ctDNA, acts as a ‘reservoir’ for all sites of disease, ctDNA is representative for all sites of metastases.”

A research team from Dr Chapman’s lab led by Parisa Momtaz, MD, reported at this year’s American Society of Clinical Oncology (ASCO) Annual Meeting that in melanoma patients with BRAF-v600E mutations, ctDNA correlated well with tumor burden measured by radiographic imaging.

“The ASCO cohort of 11 patients was to convince ourselves that we could get the assay to work (proof-of-principle) and that it correlated with what was clinically going on,” Dr Chapman said. “We have now studied ctDNA in about 60 patients. We are focusing on patients treated with immunotherapy because radiographic evaluation of these responses are somewhat equivocal. We hope that ctDNA will add more clarity and tell us whether the immune system is attacking the tumor or not.”

Also at ASCO, Nicholas C. Turner, MD, consultant medical oncologist at the Institute of Cancer Research, London, United Kingdom, and colleagues reported that in primary breast cancer tumor-specific ctDNA levels can predict early relapse.

ctDNA might also provide early warning that the patient has developed treatment-resistant disease. Sarah B. Goldberg, MD, MPH, assistant professor of medicine at Yale University School of Medicine, New Haven, Connecticut, and colleagues reported that ctDNA could be used to detect both sensitizing and resistance EGFR mutations in patients with advanced lung cancer treated with EGFR tyrosine kinase inhibitors. The researchers suggested that using NGS to detect sensitizing and resistance mutations in plasma ctDNA might allow earlier identification of resistance in patients treated with targeted therapies.

Similarly, a team of researchers from nine cancer centers in Italy found that KRAS mutations in ctDNA could be detected in over 35% of patients with non–small-cell lung cancer who became resistant to tyrosine kinase inhibitors.

In discussing this research, Luis A. Diaz Jr, MD, from the Ludwig Center for Cancer Genetics and Therapeutics at Johns Hopkins University School of Medicine in Baltimore, and Alberto Bardelli, PhD, from the Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino, Italy, wrote, “This understanding of the mechanisms of acquired resistance to targeted agents at the molecular level can be used to plan combinatorial treatments with drugs that will suppress the expansion of the clones that are responsible for most of the current failures of medical treatment. This knowledge could result in the early adoption of alternate therapies before clinical resistance is detected.”

Dr Chapman said, “I have this fantasy that you might use this to screen chemotherapy drugs in a patient. You could give them one dose of drug, then measure their ctDNA response. If there is no tumor death, the ctDNA levels wouldn’t change.”

ctDNA: From Bench to Bedside
Currently, monitoring genetic changes in a tumor requires multiple biopsies. “In the future, it might just be a matter of drawing a tube of blood,” Dr Chapman said.

However, Dr Park warned that there has yet been little to no validation of ctDNA testing and that published studies show considerable variability due partly to lack of quality control and uniform standards.

“How the plasma is prepared makes a huge difference, which isn’t always appreciated. How the ctDNA is analyzed is also quite variable among studies, with some technologies being better suited for specific applications. So for now, we would counsel clinicians not to jump the gun on this. We have to be extremely thoughtful and careful when dealing with ctDNA and its applications,” Dr Park commented. He quoted another researcher (Dan Hayes, MD, from the University of Michigan), who says it best: “A bad test can be just as bad as a bad drug.”

“Therefore I believe we need to apply the same rigorous standards of testing drugs to the development of ctDNA as a liquid biopsy,” Dr Park said.

Dr Chapman disclosed anticipated research funding from Trovagene. Dr Park reported no relevant financial interests.

Ann Transl Med. Published online January 2014. Abstract; Sci Transl Med. Published online February 2014. Abstract

2014-11-19T09:42:11-07:00November, 2014|Oral Cancer News|

Federal goal is set to increase the amount of boys and girls vaccinated against HPV by 2020

Source: www. wsj.com (Wall Street Journal.com)
Author: Caitlin McCabe

Public-health officials are pushing for higher HPV vaccination rates amid growing evidence that cancers linked to the virus are afflicting more men.

The National Cancer Institute announced recently it is pouring nearly $2.7 million into 18 U.S. cancer centers to boost HPV vaccinations among boys and girls. The cancer centers will work with local health clinics to set recommendations for vaccinating against the sexually transmitted infection, which in some cases can cause cancers in men and women later in life.

HPV, or human papillomavirus, was considered a women’s-only issue, after researchers discovered a link between it and cervical cancer in the 1980s. 

Now, as cervical-cancer rates are falling and oral-cancer rates in men steadily rise, “the burden of HPV cancer is shifting to men,” said Maura Gillison, a professor in the College of Medicine at Ohio State University Comprehensive Cancer Center.

Vaccination rates remain stifled, despite the availability of two vaccines that experts say provide effective coverage against cancer. 

The Department of Health and Human Services’ goal is to boost HPV-vaccination rates to 80% by 2020—which is far higher than the 38% of girls and 14% of boys who completed the three-dose HPV vaccine last year, according to data from the National Immunization Survey of teenagers.

Pediatricians say boosting those rates can be difficult. Pediatricians may feel uneasy talking to parents of young children about sexually transmitted infections, health experts say, while parents may resist the vaccine because they believe their child isn’t at risk.

“Discussing this vaccination is difficult because there’s an implication of sexual activity,” said Carrie Byington, a practicing pediatrician in Salt Lake City and chairwoman of the Committee on Infectious Diseases for the American Academy of Pediatrics. “It can make some pediatricians uncomfortable with the topic.”

A study conducted in 2011 by the Moffitt Cancer Center in Tampa, Fla., found fewer than 15% of physicians always recommended the vaccine to boys, and no more than 55% always recommended it to girls. Susan Vadaparampil, a professor in the department of oncologic services at Moffitt who helped lead the study, said she thinks recommendation rates have risen today but there’s a long way to go.

To ease difficult conversations, Dr. Vadaparampil said resources on the Centers for Disease Control and Prevention website suggests that pediatricians should emphasize the vaccine is ultimately a protection against cancer and explain why children should receive the shots at such a young age. 

Experts recommend the vaccine at age 11 or 12, but it can be given to girls up to age 26 and boys up to age 21. It is important for children to receive all three doses of the vaccine before they become sexually active.

“There’s science behind giving it at age 11—it’s not just about moral or family choices, or a child’s choice for sexual debut,” said Wendy Sue Swanson, a pediatrician and executive director of digital health at Seattle Children’s Hospital. “The immune response is better if you give it to an 11-year-old.”

Administering the vaccine at a young age doesn’t encourage sexual activity, Dr. Swanson said, citing a concern some parents have. A 2012 study comparing girls who had been vaccinated at ages 11 and 12 to nonvaccinated girls showed the vaccine made no difference in sexual behavior for at least three years after receiving the doses.

Not all cases of HPV are cancerous. Experts estimate nearly 79 million Americans are currently infected with one of the 100 different strains of HPV, which is passed via sex. 

Typically, a body’s immune system fights off HPV naturally within two years of exposure. Complications, such as genital warts or cancer, arise when the virus lingers. 

About 26,800 Americans are diagnosed with HPV-related cancers each year, about two-thirds of whom are women, according to 2010 data, the latest available, from the CDC.

The largest HPV-related threat to men is throat cancer, which has grown sharply in the past decade, Dr. Gillison said. 

Today, more than 90% of all oral cancers are HPV-related, according to trends Dr. Gillison has observed in clinical settings in developed countries. That is up from about 72% between 2000 and 2004 and 16% between 1984 and 1989, she said, referencing a study she conducted that analyzed throat tumors in the U.S.

Most of that growth has been in men: Each year, about 7,200 American men are diagnosed with HPV-related oral cancer, versus 1,800 cases in women, according to 2010 CDC data. 

Dr. Gillison said researchers estimate that around 2020, HPV-related oral cancers in men will eclipse cervical cancer, which afflicts some 12,000 new women each year, according to 2014 data from the American Cancer Society.

It’s unclear why men are more at risk for oral cancer than women, though some researchers suggest a person’s number of sexual partners may be related. The rise is problematic, Dr. Gillison said, because no preventive screening against throat cancer exists. 

“The problem with HPV-positive oral cancer is that premalignant lesions are not clinically detectable. They’re deep within the tonsils that are in the base of the tongue,” Dr. Gillison said. “By the time HPV-infection is detected, they usually already have Stage 3 or 4 cancer.”

That is why doctors and experts are relying so heavily on vaccination as prevention.

Two vaccines—Cervarix, manufactured by GlaxoSmithKline Inc., and Gardasil, manufactured by Merck & Co.—are currently available, though only Gardasil is usually recommended for boys.

Cervarix offers protection against two strains of HPV; Gardasil against four. A third vaccination from Merck currently awaiting approval from the Food and Drug Administration would offer protection against an additional five strains of HPV—nine in total. Doctors expect approval within in the next several months.


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

2014-11-12T11:39:19-07:00November, 2014|Oral Cancer News|

UK researchers improve comfort levels for cancer patients by 3D printing radiotherapy body molds

Source: 3dprint.com
Author: Bridget Butler Millsaps

Cancer patients undergoing brain or head and neck radiotherapy are required to be immobilized, which is certainly not always popular with those undergoing the procedure, who may already be suffering from anxiety. To make things worse, in order to be immobilized completely during the procedure, it is crucial that they are wearing a fitted mold to prevent motion. Having the mold made is a whole process in itself before the procedure can begin.


In a recent study produced by the Journal of Radiotherapy in Practice, over half of the patients describe the process of having a mold made as ‘horrific.’ Many of them also described the process as ‘uncomfortable.’

Topping that off with molded shells that quite often do not fit appropriately, the anxiety levels are heightened for patients — enough so that researchers centered their study around the creation of molded shells through 3D printing that could be created from data conveniently already existing in the form of a CT scan. The process would increase the comfort level for the patient and save a great deal of time in preparing a molding.

Radiotherapy is a type of cancer treatment which uses high-energy rays to zap cancer cells. The procedure has to be precisely aimed directly at specific areas to have effect, and it’s not a procedure anyone wants immediately repeated; therefore, It’s important to have the head shell or molding during radiotherapy because the patient must lie still. The mold or shell holds the head and neck in the correct position, and is fixed to the radiotherapy treatment table.


The shell is made in what is usually a 30-minute process, and there are a number of factors involved in the process which make it even more inconvenient, such as hairstyle, dental issues, facial hair, and more. The current method for using molds during radiotherapy in the UK is in using the Orfit mask, which is made through soft draping, in a process where soft plastic is draped over the head and shoulders of the patient and it is molded to their body. Another method for making mask3the mask or mold is completed through use of high-temperature thermoplastics which are molded onto a plaster of the patient’s face.

In the study, the multiple researchers confronted the issue of patient discomfort and anxiety over the radiotherapy molds and evaluated whether it would be possible to 3D print them and if the time, expense, and product outcome would make it a feasible idea. Their focus was on 3D printing the front of a test shell, and measuring whether it would interfere with the dose being given to the patient in radiotherapy. The actual material used in 3D printing was of obvious concern as well.

The researchers reconstructed the head and neck of a whole body scan at a slice thickness of 3.75 mm and processed Digital Communications in Medicine (DICOM) data from MRI or CT scans with data relating to items such as masking, segmenting, conversion of the data from black to white, conversion to a hollowed out positive head, creation of a negative shell, and then conversion to an .stl file format for 3D printing. Visijet clear and EOS PA 3200 were the materials used, and researchers point out that any materials used for 3D printing of the shells should be the same or of even better quality to reach the same standard or better.

Using a Z-Corps 650 printer from 3D Systems, researchers 3D printed their shells and set out to measure how they would affect the dosage being sent through the radiotherapy. Their findings were quite positive. Using three different types of materials, they found that the dosimetric properties of the 3D printing were promising in that all materials produced a small decrease in the dose of radiotherapy of up to one percent. All of the materials also produced an increase in skin dose between 54 and 80 percent, which could be minimized in using thinner materials, or creating holes in the masks, as having it increased too much is obviously not a good idea.


Z-Corps 650 printer

While 3D printing of the shells proved to be a bit more expensive than the more conventional methods, the researchers point out that this can be reduced if multiple masks are created in the same build chamber. It’s also possible that multiple hospitals could coordinate to purchase 3D printers together, thus reducing upfront cost.

The bottom line was that the items can be feasibly 3D printed without reducing the dose, saving patients the anxiety of having the molds created through direct contact with their bodies, and affordability should be not be an issue in the near future as prices have been coming down consistently.

2014-11-12T06:54:21-07:00November, 2014|Oral Cancer News|

Smoking associated with elevated risk of developing a second smoking-related cancer

Source: medicalxpress.com
Author: staff

Results of a federally-funded pooled analysis of five prospective cohort studies indicate that cigarette smoking prior to the first diagnosis of lung (stage I), bladder, kidney or head and neck cancer increases risk of developing a second smoking-associated cancer. This is the largest study to date exploring risk of second cancers among current smokers.

An analysis of five large, prospective cohort studies indicates that lung (stage I), bladder, kidney and head and neck cancer survivors who smoked 20 or more cigarettes a day prior to their cancer diagnoses have an up to five-fold higher risk of developing a second smoking-associated cancer compared to survivors of the same cancers who never smoked. The association between smoking and developing a second primary smoking-associated cancer was similar to the association between smoking and developing a first primary smoking-associated cancer (patients who smoked more than 20 cigarettes per day had a 5.41-fold higher risk of developing cancer than individuals who have never smoked). Notably, current smoking at any level increased the risk of overall mortality across all cancer disease sites. The study, published on November 10 in the Journal of Clinical Oncology, affirms the 2014 Surgeon General report’s conclusion that patients and survivors who smoke are at a higher risk of developing a second cancer.

Clinicians term an individual’s initial diagnosis a first primary cancer. A second primary cancer is one diagnosed at some point after the first diagnosis. Second primary cancers are not metastases of the first cancer but instead are distinct, new malignancies. This study focused on patients with a history of cancer who developed a second primary cancer.

“As survival improves for a number of smoking-related cancers, patients are living longer; however, smoking may increase the risk of developing a second smoking-related cancer among these survivors,” said lead study author Meredith S. Shiels, PhD, MHs, a research fellow with the National Cancer Institute’s Division of Cancer Epidemiology and Genetics. “Our study demonstrates that health care providers should emphasize the importance of smoking cessation to all their patients, including cancer survivors.”

Tobacco use constitutes the largest preventable cause of death and disability in developed countries and is a rapidly growing health problem in developing nations. It is responsible for 30% of all cancer deaths and is associated with increased risk for at least 17 types of cancer , . However, few studies have explored the association between smoking and second cancer risk. According to the authors, this is the largest study of its kind.

Researchers examined data from five prospective epidemiologic cohorts, which included 2,552 patients with stage I lung, 6,386 with bladder, 3,179 with kidney and 2,967 with head and neck cancer from the following studies:

  • National Institutes of Health-AARP Diet and Health Study
  • Agricultural Health Study
  • Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study
  • Iowa Women’s Health Study
  • Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial

A total of 866 second primary smoking-associated cancers were diagnosed among the survivors. The association between smoking status prior to primary cancer diagnosis and second smoking-associated cancer risk was assessed. Across all four cancer types, survivors who smoked 20 or more cigarettes per day at prior to their first primary diagnoses were more likely to develop a second smoking-associated cancer when compared to those who never smoked. Specifically, the risk increases were as follows:

  • Stage I Lung Cancer: 3.3 times more likely to develop a second cancer
  • Bladder Cancer: 3.7 times more likely to develop a second cancer
  • Head and Neck Cancers: 4.5 times more likely to develop a second cancer
  • Kidney Cancer: 5.3 times more likely to develop a second cancer

Current smokers who smoked fewer than 20 cigarettes per day and former smokers who had quit before their first cancer diagnosis also had an elevated risk of developing a second primary smoking-associated cancer compared to survivors who never smoked (although risks decreased with the number of years since smoking cessation).

Dr. Shiels stated that further research should directly assess the association between smoking after a first cancer diagnosis and second cancer risk.

2014-11-12T06:41:24-07:00November, 2014|Oral Cancer News|
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