Tobacco.org

• Researchers find important 'target' playing role in tobacco-related lung cancers 

Researchers at Moffitt Cancer Center in Tampa, Fla., have discovered that the immune response regulator IKBKE (serine/threonine kinase) plays two roles in tobacco-related non-small cell lung cancers. Tobacco carcinogens induce IKBKE and, in turn, IKBKE induces chemotherapy resistance.

The study was published in a recent issue of Oconogene.

"IKBKE is a newly identified oconogene, a gene linked to cancer," said study lead author Jin Q. Cheng, Ph.D., M.D., who studies genetic alterations and their molecular mechanisms in cancer. "In our study, we demonstrated that IKBKE is a STAT 3 target gene and is induced by tobacco. STAT3 is a signaling and transcription gene that is activated in various types of cancer and is required for cell transformation."

As a "transcription factor" STAT3 plays a key role in many cellular processes, such as cell growth and programmed cell death, or "apoptosis."

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• Quitting Smoking May Halve Risk of Oral Health Problems 

Adult smokers are twice as likely to develop oral health problems as those who have kicked the habit, researchers from the U.S. Centers for Disease Control and Prevention have found.

Compared to people who never smoked, current smokers are four times more likely to develop oral conditions, such as mouth cancers, gum disease and cavities.

The CDC investigators also found that smokers between the ages of 18 and 64 are nearly 1.5 times as likely as former smokers and more than twice as likely as people who never smoked to have three or more oral health problems.

Although current smokers were more likely to acknowledge the importance of oral health issues, they were less likely than former or never smokers to visit a dentist for an existing problem, the findings showed. The researchers reported that people who smoke are about twice as likely to have not been to the dentist in more than five years or not at all.

The main reason smokers said they avoided the dentist, the CDC authors noted, was that they couldn't afford dental treatment.

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Smoking and Risk of Incident Psoriasis Among Women and Men in the United States: A Combined Analysis 

The authors observed a graded reduction of risk with an increase in time since smoking cessation (Ptrend <0.0001). In this study, smoking was found to be an independent risk factor for psoriasis in both women and men. Psoriasis risk was particularly augmented for heavy smokers and persons with longer durations of smoking.

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• Smoking tied to higher psoriasis risk  

But most have studied people at only one time-point, which makes it hard to be sure the smoking came before the psoriasis.

So for the new study, researchers used data from three large, long-running studies of U.S. health professionals.

Of nearly 186,000 men and women followed for 12 to 20 years, 2,410 developed psoriasis during that time. And the risk was greater among both current smokers and former smokers.

People who were current smokers at the study's start were almost twice as likely as lifelong non-smokers to develop psoriasis. And past smokers had a 39 percent higher risk than non-smokers.

The findings, reported in the American Journal of Epidemiology, do not prove that smoking, itself, causes psoriasis in some people.

But it is clear that the smoking came before the psoriasis, said senior researcher Dr. Abrar A. Qureshi, of Harvard Medical School and Brigham and Women's Hospital in Boston.

Past studies have found links between psoriasis and both obesity and heavy drinking. But after accounting for those factors, the smoking-psoriasis link remained, Qureshi told Reuters Health.

"I think if there's one message, it's that for now, smoking seems to be a risk factor for new-onset psoriasis," Qureshi said.

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"I've come here to have my teeth treated, not to quit smoking!" (PDF) ($$) 

"I have come here to have my teeth treated, and not to quit smoking! said – by way of a goodbye – a 40-year-old policewoman who I had tried to convince that without quitting smoking she could not possibly count on an improvement in the very bad condition of her oral cavity, the treatment she had consulted me about" − recalls a dental surgeon from one of the cities in Silesia.

Her task usually begins at the point when general dentists decide there is nothing more they can do. It turns out that during many years of practice she observed that cigarettes are one of the main causes of complications in the treatment of diseases affecting the oral cavity, and that without giving up smoking one cannot count on the efficiency of the treatment. . . .

Few people know that oral cavity comes 6th on the list of organs most frequently affected by cancer. Changes can appear on the tongue, the buccal mucosa, the floor of the mouth, the lips and the throat. That's why a visit to the dentist is often the beginning of a complex treatment of an oncological patient. . . .

Oral cancer, periodontitis, teeth loss, bad breath, inefficient teeth whitening, failure concerning dental implants, alveolar bone loss, gingival recession – this is just an indicative list of conditions of the oral cavity that can be caused by smoking. It should suffice as motivation for both dentists and their patients to mutually support each other in their fight against smoking.

Maybe reading this article will deter addictive smokers from pursuing their habit.

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Smoking, Not HIV, Causes Higher Lung Cancer Risk In People With HIV  

Results from a recent Swiss study indicate that the higher risk of developing lung cancer in people with HIV compared to the general population arises from heavy smoking, not HIV infection.

Based on the results, the study authors recommended implementing strategies to reduce smoking, and therefore lung cancer risk, in HIV-positive adults.

The study authors also speculated that links between lung cancer and HIV or immune deficiency in previous studies were caused by overrepresentation of people with advanced HIV infections in lung cancer studies or accidental inclusion of cancers known to be caused by infectious diseases, such as Kaposi’s sarcoma of the lung.

According to the study authors, previous research has shown that people with HIV are at about a two- to seven-fold increased risk for lung cancer compared to people without HIV (see related AIDS Beacon news). However, scientists are uncertain whether this higher risk arises from HIV or from lifestyle factors, such as a greater rate of smoking in people with HIV.

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Effect of smoking on use of antibacterials: a 9-year follow-up study of 24 000 working-aged Finns. 

Background

Previous studies indicate an association between tobacco smoking and infectious diseases. However, large population-based follow-up studies including both accurate measurements of smoking behaviour and confounders and a reliable register-based follow-up of infections are lacking. . . .

Conclusions

Smoking is associated with increased use of antibacterials. Infectious periods experienced by patients should be used as an opportunity to encourage smoking cessation.

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Ear infections, living with smoker linked 

Here is more information on ear infections and smoking in children's living space.

Ear infections are common in children. They include acute otitis media, which is an infection in the middle ear space associated with pain and fever. There are an estimated 5 million ear infections each year in the United States.

There also is otitis media with effusion. Children with otitis media with effusion have extra fluid in the middle ear. Symptoms might include feeling like the ear is plugged or difficulty hearing.

Even if these infections are common, they can have consequences. Sometimes they require surgery and they might make the children at risk for hearing loss and delayed speech development.

A recent review in the Archives of Pediatrics and Adolescent Medicine showed having a family member who smoked raised the risk of ear infections in the children who shared their living space.

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New report tracks cancer trends 

A report released recently by the American Cancer Society indicates that while cancer death rates decreased in men and women between 2004 and 2008, the incidence of several cancers has increased in the past decade.

The report, titled Cancer Statistics 2012, indicates between 2004 and 2008, overall cancer incidence rates declined by 0.6 percent per year in men and were stable in women, while cancer death rates decreased by 1.8 percent per year in men and by 1.6 percent per year in women.

The cancers that are on the rise include cancers of the pancreas, liver, thyroid, and kidney and melanoma of the skin, as well as esophageal adenocarcinoma and certain subsites of oropharyngeal cancer associated with human papillomavirus (HPV) infection, according to the report.

Two of those types of cancers are also on the rise locally, according to Dr. Devaki Siva, a hematologist/oncologist with Marietta Memorial Hospital's Strecker Cancer Center. Cases of esophageal and oropharyngeal cancer-cancer of the head and neck- have increased, she said. The most recent data available indicates in Washington County, the incidence rate for oropharyngeal cancer in men is 16.1, while in women, it is 5.5. The rates are per 100,000, with adjustments having been made because of Washington County only having about 61,000 residents.

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The pathogenesis of COPD and IPF: distinct horns of the same devil? 

New paradigms have been recently proposed in the pathogenesis of both chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), evidencing surprising similarities between these deadly diseases, despite their obvious clinical, radiological and pathologic differences. There is growing evidence supporting a "double hit" pathogenic model where in both COPD and IPF the cumulative action of an accelerated senescence of pulmonary parenchyma (determined by either telomere dysfunction and/or a variety of genetic predisposing factors), and the noxious activity of cigarette smoke-induced oxidative damage are able to severely compromise the regenerative potential of two pulmonary precursor cell compartments (alveolar epithelial precursors in IPF, mesenchymal precursor cells in COPD/emphysema). The consequent divergent derangement of signalling pathways involved in lung tissue renewal (mainly Wnt and Notch), can eventually lead to the distinct abnormal tissue remodelling and functional impairment that characterise the alveolar parenchyma in these diseases (irreversible fibrosis and bronchiolar honeycombing in IPF, emphysema and airway chronic inflammation in COPD).

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Cancer Among Hispanics with HIV/AIDS 

The most common non-AIDS-defining cancers in patients with HIV are anal, lung, and liver cancers and Hodgkin lymphoma. These four cancers made up nearly half of all non-AIDS-defining cancers diagnosed in this population from 2001 through 2005. Higher risks for these cancers reflect co-infections such as human papillomavirus (HPV), hepatitis B and C viruses, and Epstein-Barr virus, as well as higher smoking rates in the HIV/AIDS population. Thus, although fewer people now die of AIDS, cancer is emerging as an important cause of death for the HIV-infected population.

Preventing cancer

Preventing cancers that are increasing among the HIV-infected population is now a major focus of people who treat those with HIV. This effort includes trying to combat viral co-infections that cause cancer through prevention, screening, and treatment and avoiding exposure to other risk factors, such as smoking. Both men and women who are infected with HIV should discuss screening options for cancer with their medical providers. The risk of lung cancer can be reduced by quitting smoking. Because HIV-infected people have a higher risk of lung cancer, it is especially important that they do not smoke.

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Cancer Among African Americans with HIV/AIDS  

Racial and ethnic minorities in America have been hit harder than white Americans by the HIV/AIDS epidemic-they make up about one-third of the population but two-thirds of all cases. In 2009, African Americans made up 14 percent of the population but accounted for 44 percent of all new HIV infections. And Hispanics made up 16 percent of the population but 20 percent of new cases in 2009.

All patients infected with HIV, including racial and ethnic minorities, are benefiting from new, more effective therapies developed over the last 15 years. But as patients are living longer, the distribution of cancer has shifted dramatically. While the types of cancer that have been typically associated with AIDS progression are on the decline in the HIV/AIDS population, other types of cancer are now on the rise. . . .

The most common non-AIDS-defining cancers in patients with HIV are anal, lung, and liver cancers and Hodgkin lymphoma. These four cancers made up nearly half of all non-AIDS-defining cancers diagnosed in this population from 2001 through 2005. Higher risks for these cancers reflect co-infections such as human papillomavirus (HPV), hepatitis B and C viruses, and Epstein-Barr virus, as well as higher smoking rates in the HIV/AIDS population. Thus, although fewer people now die of AIDS, cancer is emerging as an important cause of death for the HIV-infected population.

Preventing cancer

Preventing cancers that are increasing among the HIV-infected population is now a major focus of people who treat those with HIV. This effort includes trying to combat viral co-infections that cause cancer through prevention, screening, and treatment and avoiding exposure to other risk factors, such as smoking. Both men and women who are infected with HIV should discuss screening options for cancer with their medical providers. The risk of lung cancer can be reduced by quitting smoking. Because HIV-infected people have a higher risk of lung cancer, it is especially important that they do not smoke.

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Cigarette Smoke Induction of Osteopontin (SPP1) Mediates TH17 Inflammation in Human and Experimental Emphysema 

We have shown that CD1a+ antigen-presenting cells (APCs) from lungs of patients with emphysema can induce autoreactive T helper 1 (TH1) and TH17 cells. Similarly, the canonical cytokines interferon-γ (IFN-γ) and interleukin-17A (IL-17A) are specifically linked to lung destruction in smokers, but how smoke activates APCs to mediate emphysema remains unknown. Here, we show that, in addition to increasing IFN-γ expression, cigarette smoke increased the expression of IL-17A in both CD4+ and γδ T cells from mouse lung. IL-17A deficiency resulted in attenuation of, whereas lack of γδ T cells exacerbated, smoke-induced emphysema in mice. Adoptive transfer of lung APCs isolated from mice with emphysema revealed that this cell population was capable of transferring disease even in the absence of active smoke exposure, a process that was dependent on IL-17A expression. Spp1 (the gene for osteopontin) was highly expressed in the pathogenic lung APCs of smoke-exposed mice and was required for the TH17 responses and emphysema in vivo, in part through its inhibition of the expression of the transcription factor Irf7. Thus, the Spp1-Irf7 axis is critical for induction of pathological TH17 responses, revealing a major mechanism by which smoke activates lung APCs to induce emphysema and identifying a pathway that could be targeted for therapeutic purposes.

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Study Maps Path From Smoking to Emphysema in Mice 

Smoking activates certain genes and portions of the immune system, which in turn causes inflammation that leads to emphysema.

So say researchers who mapped the destructive path from smoking to the debilitating lung disease in mice.

"Previously, emphysema was thought to be a nonspecific injurious response to long-term smoke exposure," study author Dr. Farrah Kheradmand, a professor of medicine and immunology at Baylor College of Medicine, said in a college news release. "These studies show for the first time that emphysema is caused by a specific immune response induced by smoke."

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Lung cancer in the Swiss HIV Cohort Study: role of smoking, immunodeficiency and pulmonary infection 

conclusion: Lung cancer in the SHCS does not seem to be clearly associated with immunodeficiency or AIDS-related pulmonary disease, but seems to be attributable to heavy smoking.

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