The synergistic effect of tobacco and alcohol consumption on oral squamous cell carcinoma: a systematic review and meta-analysis

Mello, Fernanda Weber; Melo, Gilberto; Pasetto, Júlia Jacoby; Silva, Carolina Amália Barcellos; Warnakulasuriya, Saman

doi:10.1007/s00784-019-02958-1

Cited by 117 publications

(93 citation statements)

References 52 publications

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“…It mostly arises from the mucosal epithelial lining of the oral cavity, which includes the anterior of the tongue, buccal cavity, lips, and lower alveolar ridges [ 3 , 4 ] Although the five-year survival rate is increased to 65%, diagnosis at advanced stages leads to a five-year survival of only 27%, necessitating the need for the development of early diagnosis and novel therapeutic approaches in combating this disease [ 5 , 6 , 7 ]. Tobacco chewing and alcohol consumption are the major risk factors associated with oral cancers [ 8 ]. Other factors include the chewing of areca nuts, poor oral health hygiene, betel leaf, and human papillomavirus (HPV) infection [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs as Modulators of Oral Tumorigenesis—A Focused Review

Rishabh

Khadilkar

Kumar

et al. 2021

IJMS

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Oral cancers constitute the majority of head and neck tumors, with a relatively high incidence and poor survival rate in developing countries. While the five-year survival rates of the oral cancer patients have increased to 65%, the overall survival for advanced stages has been at 27% for the past ten years, emphasizing the necessity for further understanding the etiology of the disease, diagnosis, and formulating possible novel treatment regimens. MicroRNAs (miRNAs), a family of small non-coding RNA, have emerged as master modulators of gene expression in various cellular and biological process. Aberrant expression of these dynamic molecules has been associated with many human diseases, including oral cancers. The deregulated miRNAs have been shown to control various oncogenic processes, including sustaining proliferative signaling, evading growth suppressors, resisting cell death activating invasion and metastasis, and inducing angiogenesis. Hence, the aberrant expression of miRNAs associated with oral cancers, makes them potential candidates for the investigation of functional markers, which will aid in the differential diagnosis, prognosis, and development of novel therapeutic regimens. This review presents a holistic insight into our understanding of the role of miRNAs in regulating various hallmarks of oral tumorigenesis.

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Section: Introductionmentioning

confidence: 99%

MicroRNAs as Modulators of Oral Tumorigenesis—A Focused Review

Rishabh

Khadilkar

Kumar

et al. 2021

IJMS

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“…Oral squamous cell carcinoma (OSCC) is a common malignancy of the head and neck, with more than 354,900 newly diagnosed cases each year worldwide, arising from the mucosal epithelium of the oral cavity and oropharynx. 1,2 The development of OSCC is a complex multistep process, and the main potential risk factors including smoking, 3 drinking, 3,4 and human papillomavirus. [5][6][7] Cancer therapy has improved rapidly over the past decade, in particular, advanced radiotherapy with or without chemotherapy, enhanced surgical procedures, and immunotherapy.…”

Section: Introductionmentioning

confidence: 99%

<p>Fisetin Modulates Human Oral Squamous Cell Carcinoma Proliferation by Blocking PAK4 Signaling Pathways</p>

Li¹,

Jia²,

Dai³

2020

DDDT

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Objective: Human oral squamous cell carcinoma (OSCC) is a major cause of mortality and morbidity worldwide. There is an urgent need to identify bioactive molecules and potential target genes that could inhibit carcinogenesis for OSCC therapy. Fisetin (3,7,3′,4′-tetrahydroxyflavone), a naturally occurring flavonoid, has been previously shown to have anti-proliferative activities in OSCC; however, its molecular mechanism is unknown. Methods: Colony formation, cell viability, Boyden chamber, wound healing, and tumor xenograft assays were used to detect the impact of fisetin on OSCC cells in vitro and in vivo. Western blot analysis was used to examine the corresponding protein expression. Results: Fisetin treatment significantly inhibited proliferation and promoted apoptosis by repressing PAK4 expression. Moreover, fisetin treatment attenuated cell migration by blocking PAK4 signaling pathways. In addition, the tumor xenograft showed anti-tumor growth effects of fisetin exposure in vivo. Conclusion: Fisetin may represent a potential therapeutic strategy for human OSCC by targeting PAK4 signaling pathways.

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“…Tobacco and alcohol have a synergistic effect on the risk for oropharyngeal cancer [22]. ACH of tobacco smoke dissolves into saliva during active smoking, resulting in a mean salivary ACH concentration of 260 µM [19].…”

Section: Major Factors Affecting Salivary Ach Levelsmentioning

confidence: 99%

Local Acetaldehyde: Its Key Role in Alcohol-Related Oropharyngeal Cancer

Salaspuro¹

2020

Visc Med

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Background: Alcohol consumption and ethanol in alcoholic beverages are group 1 carcinogens, that is, carcinogenic to humans. However, ethanol itself is neither genotoxic nor mutagenic. Based on unique gene-epidemiologic and gene-biochemical evidence, the first metabolite of ethanol oxidation – acetaldehyde (ACH) – acts as a local carcinogen in the oropharynx. This review is focused on those facts, which highlight the importance of the oropharynx and local ACH in the pathogenesis of alcohol-related oropharyngeal cancer. Summary: The strongest evidence for the local carcinogenicity of ACH in man provides a point mutation in the aldehyde dehydrogenase 2 (ALDH2) gene, which has randomized millions of alcohol consumers to markedly increased ACH exposure via saliva. This novel human cancer model is associated with manifold risk for oropharyngeal cancer and most importantly it is free from confounding factors markedly hampering epidemiological studies on alcohol-related cancer. The oropharynx is an ideal target organ for the cancer risk assessment of ACH. There is substantial epidemiological data on alcohol-related oropharyngeal cancer risk and also on salivary ACH concentrations among major risk groups for oropharyngeal cancer. Normal human saliva does not contain measurable levels of ACH. However, alcohol ingestion results within seconds in a concentration-dependent accumulation of ACH in saliva, which continues for up to 10–15 min after each sip of alcoholic beverage. This instant ACH exposure phase is followed by a long-term phase derived from ethanol diffused back to saliva from blood circulation. Microbes representing normal oral flora play a major role in local ACH formation from ethanol. In ALDH2-deficient subjects excess ACH during the long-term ACH exposure phase is most probably derived from salivary glands. Key Message: ALDH2 gene mutation proves the causal relationship between local ACH exposure via saliva and oropharyngeal cancer and provides new means for the quantitative assessment of local ACH exposure in relation to oropharyngeal cancer risk. Instant ACH formation from ethanol represents approximately 70–100% of total local ACH exposure. Ethanol present in “non-alcoholic” beverages and food forms an epidemiological bias in studies on alcohol-related upper digestive tract cancer. Responses: One should quit smoking, adopt sensible drinking habits, and maintain good oral hygiene. Genetic risk groups could be screened and educated. Consumption of beverages and foodstuffs containing low ethanol levels as well as alcoholic beverages containing high ACH levels should be minimized. To that aim, labelling of alcohol and ACH concentrations of all beverages and foodstuffs should be mandatory.

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The synergistic effect of tobacco and alcohol consumption on oral squamous cell carcinoma: a systematic review and meta-analysis

Cited by 117 publications

References 52 publications

MicroRNAs as Modulators of Oral Tumorigenesis—A Focused Review

MicroRNAs as Modulators of Oral Tumorigenesis—A Focused Review

<p>Fisetin Modulates Human Oral Squamous Cell Carcinoma Proliferation by Blocking PAK4 Signaling Pathways</p>

Local Acetaldehyde: Its Key Role in Alcohol-Related Oropharyngeal Cancer

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