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Defeating nicotine's double role in lung cancer
June 09, 2009A lung cancer treatment that inhibits nicotine receptors was shown to double survival time in mice, according to Italian researchers.
The results of the early phase animal model study were reported in the June 15 issue of the American Journal of Respiratory and Critical Care Medicine.
Changes in genes encoding nicotine receptors are strongly associated not only with the tendency to smoke, but with susceptibility to lung cancer. Nicotine exposure also heightens the expression of the nicotine receptors, which leads to increased cell proliferation and inhibition of apoptosis, further setting the stage for cancer.
Patrizia Russo, Ph.D. and Laura Paleari, Ph.D. of the Lung Cancer Unit of the National Cancer Research Institute in Genoa, Italy and colleagues from San Raffaele Pisana Scientific Institute for Research, Hospitalization and Health Care (IRCCS), Catholic University, Campus Biomedico University in Rome, Mario Negri Institute in Milan and CEA Gyf sur Yvette in France showed in past research that an antagonist of nicotine acetylcholine receptors (nAChRs), may serve as an anticancer agent. The antagonist, called d-tubocurarine/α-Cobratoxin (α-CbT), specifically targeted the α7 subunit of nAChRs, the area primarily associated with increased cell proliferation.
In this study, the authors took the research a step further and showed that α-CbT could inhibit non-small cell lung carcinoma (NSCLC) growth and prolong life in non-obese/severe combined immunodeficient (NOD/SCID) mice that had human NSCLC grafted to their lungs. This study attempted to mimic human cancer conditions more closely by delaying treatment until the tumors were well-established. In addition to control mice that were untreated, the researchers randomized one third of the mice to receive standard chemotherapy.
They found that NOD/SCID mice treated with the standard chemotherapy agent, cisplatin, had a 16 percent longer median survival time than untreated mice (p= 0.05). Mice treated with α-CbT, however, had an increased median survival time of 1.7-fold over the cisplatin-treated mice and 2.1-fold over the no-treatment controls (p=0.0005).
"The results of this study show that α-CbT, a powerful, high-affinity α-7-nAChR inhibitor, induces antitumor activity against NSCLC by triggering apoptosis," wrote Dr. Russo. "The prolonged survival of α-CbT-treated animals in our mouse model of NSCLC is most likely the result of several mechanisms, including various antiproliferative and antiangiogenic effects."
The research also found that unaffected (i.e., noncancerous) cells showed no inhibition of proliferation when treated with α-CbT, suggesting that the treatment would have limited if any toxic effects. Dr. Russo and colleagues postulated that this finding may be due to the reduced number of receptor binding sites on normal cells as opposed to cancerous cells. Conversely, they reported that cancer cells with the greatest number of receptor binding sites seemed to respond with the greatest sensitivity to the treatment.
"The goal of this research line is to explore the widest range of possibilities of intervention on the α7-nAChRs. We hope to move further on towards the clinical setting experimentation phase for the assessment of potentially new treatment strategies for NSCLC," said Dr. Russo.
An editorial in the same issue of the journal asked if nicotine may be to lung cancer what estrogen is to breast cancer. Eliot R. Spindel, M.D., Ph.D., of Oregon Health & Science University, stated that estrogen can stimulate the development of breast cancer and estrogen-receptor antagonists, such as tamoxifen, provide therapeutic benefit. In support of a carcinogenic role for estrogen, the incidence of breast cancer appears to be decreasing as estrogen hormone replacement therapy is being used less often. Likewise, nicotine may promote lung cancer yet nicotine receptor antagonists may offer treatment options for patients with lung cancer.
John Heffner, M.D., past president of the ATS stated that "this research clearly has profound clinical implications regarding the role of nicotine in stimulating lung cancer and nicotine receptor antagonists in treating the disease. The highly addictive nature of nicotine, however, complicates patients' ability to quit smoking and avoid ongoing nicotine exposure."
"This [addictive nature of nicotine] underscores the importance of potential FDA regulation of nicotine in tobacco products to limit exposure to this drug that promotes tumor growth," wrote Dr. Spindel.
American Thoracic Society
Patrizia Russo, Ph.D. and Laura Paleari, Ph.D. of the Lung Cancer Unit of the National Cancer Research Institute in Genoa, Italy and colleagues from San Raffaele Pisana Scientific Institute for Research, Hospitalization and Health Care (IRCCS), Catholic University, Campus Biomedico University in Rome, Mario Negri Institute in Milan and CEA Gyf sur Yvette in France showed in past research that an antagonist of nicotine acetylcholine receptors (nAChRs), may serve as an anticancer agent. The antagonist, called d-tubocurarine/α-Cobratoxin (α-CbT), specifically targeted the α7 subunit of nAChRs, the area primarily associated with increased cell proliferation.
In this study, the authors took the research a step further and showed that α-CbT could inhibit non-small cell lung carcinoma (NSCLC) growth and prolong life in non-obese/severe combined immunodeficient (NOD/SCID) mice that had human NSCLC grafted to their lungs. This study attempted to mimic human cancer conditions more closely by delaying treatment until the tumors were well-established. In addition to control mice that were untreated, the researchers randomized one third of the mice to receive standard chemotherapy.
They found that NOD/SCID mice treated with the standard chemotherapy agent, cisplatin, had a 16 percent longer median survival time than untreated mice (p= 0.05). Mice treated with α-CbT, however, had an increased median survival time of 1.7-fold over the cisplatin-treated mice and 2.1-fold over the no-treatment controls (p=0.0005).
"The results of this study show that α-CbT, a powerful, high-affinity α-7-nAChR inhibitor, induces antitumor activity against NSCLC by triggering apoptosis," wrote Dr. Russo. "The prolonged survival of α-CbT-treated animals in our mouse model of NSCLC is most likely the result of several mechanisms, including various antiproliferative and antiangiogenic effects."
The research also found that unaffected (i.e., noncancerous) cells showed no inhibition of proliferation when treated with α-CbT, suggesting that the treatment would have limited if any toxic effects. Dr. Russo and colleagues postulated that this finding may be due to the reduced number of receptor binding sites on normal cells as opposed to cancerous cells. Conversely, they reported that cancer cells with the greatest number of receptor binding sites seemed to respond with the greatest sensitivity to the treatment.
"The goal of this research line is to explore the widest range of possibilities of intervention on the α7-nAChRs. We hope to move further on towards the clinical setting experimentation phase for the assessment of potentially new treatment strategies for NSCLC," said Dr. Russo.
An editorial in the same issue of the journal asked if nicotine may be to lung cancer what estrogen is to breast cancer. Eliot R. Spindel, M.D., Ph.D., of Oregon Health & Science University, stated that estrogen can stimulate the development of breast cancer and estrogen-receptor antagonists, such as tamoxifen, provide therapeutic benefit. In support of a carcinogenic role for estrogen, the incidence of breast cancer appears to be decreasing as estrogen hormone replacement therapy is being used less often. Likewise, nicotine may promote lung cancer yet nicotine receptor antagonists may offer treatment options for patients with lung cancer.
John Heffner, M.D., past president of the ATS stated that "this research clearly has profound clinical implications regarding the role of nicotine in stimulating lung cancer and nicotine receptor antagonists in treating the disease. The highly addictive nature of nicotine, however, complicates patients' ability to quit smoking and avoid ongoing nicotine exposure."
"This [addictive nature of nicotine] underscores the importance of potential FDA regulation of nicotine in tobacco products to limit exposure to this drug that promotes tumor growth," wrote Dr. Spindel.
American Thoracic Society
Nicotine Current Events and Nicotine News RSSCrushing cigarettes in a virtual reality environment reduces tobacco addiction
Smokers who crushed computer-simulated cigarettes as part of a psychosocial treatment program in a virtual reality environment had significantly reduced nicotine dependence and higher rates of tobacco abstinence than smokers participating in the same program who grasped a computer-simulated ball.
Smoking gun: just 1 cigarette has harmful effect on the arteries of young healthy adults
Even one cigarette has serious adverse effects on young adults, according to research presented by Dr. Stella Daskalopoulou at the Canadian Cardiovascular Congress 2009, co-hosted by the Heart and Stroke Foundation and the Canadian Cardiovascular Society.
Cancer survivors may not be getting the help they need to stop smoking
More than a quarter of cancer survivors who still smoke have not been advised to quit smoking by their health care providers in the last year, according to a study published by researchers at Fox Chase Cancer Center in the current issue of the Journal of General Internal Medicine.
Nation's leading experts on substance abuse outline new research agenda
With substance abuse now accounting for one in 14 hospital admissions and generating billions in health care costs, leading scientists held a briefing on Capitol Hill today to present the evidence that we already have and the evidence we need in treating and preventing the use and abuse of alcohol, drugs and tobacco.
Curcumin may inhibit nicotine-induced activation of head and neck cancers
Curcumin, the compound that gives curry powder its yellow/orange color, may inhibit the adverse effects of nicotine in patients with head and neck cancer who continue to smoke.
Lung cancer risk increases with expression of specific genes
A recent study published in the October 2009 issue of the Journal of Thoracic Oncology determined that variations of specific genetic markers identified in previous research, or SNPs, may indicate a greater lung cancer risk in African Americans than in whites.
Anti-smoking law helps waiters to quit smoking
Researchers from the Catalan Institute of Oncology have studied the impact of the law banning smoking in public places such as bars and restaurants on those working in these places.
Poor money saving linked to general impulsiveness
Financial imprudence is linked to other impulsive behaviour such as overeating, smoking and infidelity, according to a new study led by UCL researchers, published in the journal Personality and Individual Differences.
It pays to quit smoking before surgery
People who start nicotine replacement therapy at least four weeks before surgery can halve their risk of poor wound healing. This is what the German Institute for Quality and Efficiency in Health Care (IQWiG) concludes in information published on informedhealthonline.org today.
New study expands the list of hazardous chemicals in smokeless tobacco
Attention all smokeless tobacco users! It's time to banish the comforting notion that snuff and chewing tobacco are safe because they don't burn and produce inhalable smoke like cigarettes.
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