Characteristics of cigarette smoking without alcohol consumption and laryngeal cancer: overall and time-risk relation. A meta-analysis of observational studies

Abstract

Tobacco smoking was one of the risk factors for upper aerodigestive tract cancer, but exclusive quantification of the impact of cigarette smoking on laryngeal cancer had not been investigated. A meta-analysis of researches that had reported quantitative estimates of cigarette smoking and risk of laryngeal cancer by March 2016 was performed. Pooled estimates of relative risks and their 95% confidence intervals were obtained and summarized. Sensitivity analysis and subgroup analysis were implemented to find out sources of research heterogeneity and the effect of potential confounders. Publication bias was investigated and corrected if found to be present through Egger's and Begg's test, and trim and fill algorithm. Thirty researches based on a total of 14,292 cases from three cohort and fifteen case-control studies were included and pooled estimate for the correlation between cigarette smoking and the risk of laryngeal cancer was 7.01 (95% confidence interval 5.56-8.85), with moderate heterogeneity across the researches (I = 56.7%, p = 0.002). The RRs were 5.04 (95% CI 3.09-8.22) for cohort studies (p = 0.121), 7.59 (95% CI 5.86-9.82) for case-control studies (p = 0.005). The risk kept elevated within the first fifteen years of quitting smoking(RR 3.62, 95% CI 1.88-7.00) but dropped in the 16 years and more after smoking cessation(RR 1.88, 95% CI 1.16-3.05). Individuals who smoked with 40 or more pack-years had nine times the risk of laryngeal cancer(RR 9.14; 95% CI 6.24-13.39). Subjects who smoked 30 or more cigarettes a day had sevenfolds the risk of laryngeal cancer (RR 7.02; 95% CI 4.47-11.02) and who smoked 40 or more years had five times the risk versus never smokers (RR 5.76; 95% CI 3.69-8.99). Evidence of publication bias was not detected for the correlation between current cigarette smoking and risk of laryngeal cancer (p = 0.225 with Begg's test, p = 0.317 with Egger's test). The results demonstrated strong correlation referring to dose-response and time-response between cigarette smoking and risk of laryngeal cancer for both men and women. The probability of developing laryngeal cancer was decreased by quitting smoking, particularly among former cigarette smokers who had stopped smoking for 15 or more years. The subgroup analysis demonstrated that study type influenced the RRs estimates of the studies.

The risk of recurrence within the first five years is very low in patients with papillary thyroid carcinoma treated with radioiodine

“…Risk factors (smoking and alcohol consumption), mean age of 60-65 years and higher prevalence in males were consistent with the latest studies 2,[5][6][7] . Recurrence or late metastasis was mainly due to lost of follow-up by the patient or advanced tumor at the surgical time.…”

Patterns of stress coping and depression among patients with head and neck cancer: A Japanese cross‐sectional study

“…In addition, smoking or drinking as well as seeking support can also be useful stress coping strategies for HNC patients. The history of smoking and drinking may be independent risk factors for the development of HNC . Indeed, almost all HNC patients in this study have had a history of smoking.…”

“…The history of smoking and drinking may be independent risk factors for the development of HNC. 29 Indeed, almost all HNC patients in this study have had a history of smoking. Therefore, being dependent on someone or something might be a coping skill that is easy to apply for patients with HNC.…”

The Evi5 oncogene promotes laryngeal cancer cells proliferation by stabilizing c-Myc protein

“…Laryngeal squamous cell carcinoma (LSCC) is the major type for laryngeal carcinoma (about 95%) [2]. Epidemiological investigations show that smoking is considered as the primary risk factor for laryngeal cancer and alcohol drinking is also an important pathogenic factor [3]. The mechanism of smoking may be due to a large amount of carcinogen in tobacco smoke, trigging cellular DNA damage and eventually leading to carcinogenesis [4].…”