Risk of oral cancer associated with tobacco smoking, alcohol consumption and oral hygiene: a case-control study in Madrid, Spain

Moreno-López, Luis-Alberto; Esparza-Gómez, Germán; González-Navarro, A; Cerero-Lapiedra, Rocío; González-Hernández, Milagros; Domínguez-Rojas, V.

doi:10.1016/s1368-8375(99)00084-6

Cited by 151 publications

(121 citation statements)

References 6 publications

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“…This study found that almost all of the smoking variables studied (smoking status, type of tobacco and pack-years of exposure of tobacco) conferred an increased oral cancer risk of at least two-fold. These findings are similar to global features of smoking worldwide (Moreno et al, 2000;Zavras et al, 2001;Lissowka et a., 2003;Subapriya et al, 2007;Muwonge et al, 2008;Javalekshmi et al, 2011). The only exception is for the number of sticks smoked per day, i.e.…”

Section: Discussionsupporting

confidence: 79%

Tobacco (Kretek) Smoking, Betel Quid Chewing and Risk of Oral Cancer in a Selected Jakarta Population

Amtha

Razak²,

Basuki³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Purpose: This study aimed to determine the association between tobacco consumption (kretek) and betel quid chewing with oral cancer risk. Materials and Methods: A total of 81 cases of oral cancers were matched with 162 controls in this hospital-based study. Information on sociodemographic characteristics and details of risk habits (duration, frequency and type of tobacco consumption and betel quid chewing) were collected. Association between smoking and betel quid chewing with oral cancer were analysed using conditional logistic regression. Results: Slightly more than half of the cases (55.6%) were smokers where 88.9% of them smoked kretek. After adjusting for confounders, smokers have two fold increased risk, while the risk for kretek consumers and those smoking for more than 10 years was increased to almost three-fold. Prevalence of betel quid chewing among cases and controls was low (7.4% and 1.9% respectively). Chewing of at least one quid per day, and quid combination of betel leaf, areca nut, lime and tobacco conferred a 5-6 fold increased risk. Conclusions: Smoking is positively associated with oral cancer risk. A similar direct association was also seen among betel quid chewers.

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Section: Discussionsupporting

confidence: 79%

Tobacco (Kretek) Smoking, Betel Quid Chewing and Risk of Oral Cancer in a Selected Jakarta Population

Amtha

Razak²,

Basuki³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Ying-Yao Zhang 1,2 , Zhi-Na Xu 2 , Jun-Xi Wang 1 , Dong-Min Wei 1 , Xin-Liang Pan 1 * carcinogenic components of tobacco smoke (van der Waal, 1996(van der Waal, , 1999La Vecchia et al, 1997;Moreno-López et al, 2000;Llewellyn et al, 2003;Dalla Vecchia et al, 2004). Another cause for the development of laryngeal squamous cell carcinoma in the Asian and African region, seems to be the consumption of betel nut Moreno-López et al, 2000;Jeng et al, 2001).…”

Section: G1/s-specific Cyclin-d1 Might Be a Prognostic Biomarker For mentioning

confidence: 99%

“…Another cause for the development of laryngeal squamous cell carcinoma in the Asian and African region, seems to be the consumption of betel nut Moreno-López et al, 2000;Jeng et al, 2001). The pathogenesis of squamous cell carcinoma, especially in the oral cavity, are persistent mechanical irritation, eg by poorly fitting dentures.…”

Section: G1/s-specific Cyclin-d1 Might Be a Prognostic Biomarker For mentioning

confidence: 99%

G1/S-specific Cyclin-D1 Might be a Prognostic Biomarker for Patients with Laryngeal Squamous Cell Carcinoma

Zhang¹,

Xu²,

Wang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Objective: To investigate the prognostic role of antigen KI-67 (Ki-67) and G1/S-specific cyclin-D1 (cyclin-D1) in patients with laryngeal squamous cell carcinoma (LSCC). Methods: Immunohistochemical staining (IHS) was used to determine the protein expression of Ki-67 and cyclin-D1 in LSCC tissues. Kaplan-Meier survival curves was calculated with reference to Ki-67 and cyclin-D1 levels. Results: Cyclin-D1 and Ki67 were expressed in the nuclei of cancer cells. Among the total of 92 cancer tissues examined by immunohistochemistry, 60 (65.22%) had cyclin-D1 overexpression and 56 (60.87%) had Ki67 overexpression. Cyclin-D1 overexpression is associated with the advanced stage of the cancer (P=0.029), but not with gender, age, stage of cancer, histological differentiation, anatomical site, smoking history and alcohol consumption history. Ki67 overexpression is not associated with the advanced stage, gender, age, histological differentiation, anatomical site, smoking history and alcohol consumption history. A statistically significant correlation was found between lymph node status and the expression of Ki67 (p = 0.025). Overexpression of cyclin-D1 was correlated to shorter relapse-free survival period (P<0.001). Conclusions: Overexpression of cyclin-D1 can be used as a marker to predict relapse in patients with LSCC after primary curative resection.

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“…Fresh tissue samples were consecutively obtained from 23 patients (14 males and nine females; age ranged from 29 to 67 years, mean 47 years; smoking status 27 Table 1. Normal oral mucosa was obtained from volunteers without leukoplakia during non-neoplastic or preprosthetic surgical procedures (control samples).…”

Section: Human Tissuementioning

confidence: 99%

Molecular alterations in the tumor suppressor gene WWOX in oral leukoplakias

et al. 2008

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SummaryOral leukoplakia is the most prevalent and potentially malignant disorder of the oral mucosa. Previous studies have demonstrated that molecular changes of the WWOX gene (WW-domain containing oxidoreductase), a candidate tumor suppressor gene located at 16q23.3-24.1 that spans FRA16D, the second most common fragile site, are present in several malignant neoplasias, including oral squamous cell carcinoma. In this report, the role of the WWOX gene was investigated in 23 cases of oral leukoplakias. Using nested RT-PCR and immunohistochemistry, altered mRNA transcription and/or reduced Wwox protein expression was observed in 35% of the lesions when compared with normal mucosa. The majority of lesions (4/6) with altered transcripts had a reduction in the expression of Wwox protein. Although normal WWOX expression was found in some lesions with dysplasia, all lesions with WWOX mRNA and/or protein expression showed histological evidence of dysplasia and none of the cases without dysplasia presented this alteration. These results show that the WWOX gene alteration is an early genetic alteration and may contribute to oral carcinogenesis.

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Risk of oral cancer associated with tobacco smoking, alcohol consumption and oral hygiene: a case-control study in Madrid, Spain

Cited by 151 publications

References 6 publications

Tobacco (Kretek) Smoking, Betel Quid Chewing and Risk of Oral Cancer in a Selected Jakarta Population

Tobacco (Kretek) Smoking, Betel Quid Chewing and Risk of Oral Cancer in a Selected Jakarta Population

G1/S-specific Cyclin-D1 Might be a Prognostic Biomarker for Patients with Laryngeal Squamous Cell Carcinoma

Molecular alterations in the tumor suppressor gene WWOX in oral leukoplakias

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