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Head and neck cancers are largely caused by smoking, alcohol and HPV virus (oral sex).Possible is there a (small) familial factor in this large (altough) retrospective trial, so not conclusive on this familial effect.Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE studyA large study in France confirms thisConclusion:To our knowledge, the ICARE study is the first population-based case–control study in France and one of the largest in the world which investigates the role of risk factors other than tobacco and alcohol consumption in the occurrence of oral cavity cancer. Strengths of this study include large sample size allowing us to perform analyses by subsite, and detailed data about family history of cancer and personal medical history.BackgroundThe aim of this study was to evaluate the role of family history of cancer and personal history of other medical conditions in the aetiology of the oral cavity cancer in FranceMethodsWe used data from 689 cases of cavity squamous cell carcinoma and 3481 controls included in a population-based case–control study, the ICARE study. Odds-ratios (ORs) associated with family history of cancer and personal medical conditions and their 95% confidence intervals (95% CI) were estimated by unconditional logistic regression and were adjusted for age, gender, area of residence, education, body mass index, tobacco smoking and alcohol drinking.ResultsPersonal history of oral candidiasis was related to a significantly increased risk of oral cavity cancer (OR 5.0, 95% CI 2.1-12.1). History of head and neck cancers among the first-degree relatives was associated with an OR of 1.9 (95% CI 1.2-2.8). The risk increased with the number of first-degree relatives with head and neck cancer.ConclusionA family history of head and neck cancer is a marker of an increased risk of oral cavity cancer and should be taken into account to target prevention efforts and screening. Further studies are needed to clarify the association between oral cavity cancer and personal history of candidiasis.Peer Review reportsBackgroundOral cavity cancer (International Classification of Diseases 10th revision (ICD-10) codes C00-C08 [1]) is an important public health burden with an annual worldwide incidence estimated at approximately 263,000 cases, and mortality at 127,000 [2]. Among developed countries, France has the highest age-standardized incidence rate for males (7.6/100,000) and one of the highest for females (1.5/100,000) [3]. As is the case for the other sites of upper aerodigestive tract (UADT), tobacco and alcohol consumption are the main risk factors for oral cavity cancer [4, 5].Besides the role of human papilloma viruses (HPV) 16 and 18 in the aetiology of UADT cancers, few other conditions such as herpetic infection [6–11], candidiasis [6, 10, 11], warts [6, 9–11], and gastro-oesophageal reflux [7] have been investigated. The results of the epidemiological studies on the role of these medical conditions in the occurrence of UADT cancers are contradictory and the underlying mechanisms are not complete elucidated.Other risk factors, such as genetic polymorphism in genes involved in the metabolism of tobacco and alcohol carcinogens and DNA repair seems to play a role in the development of UADT cancers [12–19]. Few epidemiological studies considered the risk of UADT cancers in relatives of subjects with cancer history [20–26]. Familial clustering of UADT cancers may indicate that genetic factors play a role in the process of carcinogenesis, but may also reflect a tendency of relatives to have similar behaviour towards tobacco and alcohol. Limited data are available on the combined effect of family history, and tobacco and alcohol consumption [20, 23, 26]. The literature is contrasted about whether the cancer risk varies according to UADT subsite, gender, type of affected relative (parents, siblings), and their cancer site.The present work aimed to investigate the role of family history of cancer and personal medical history in the aetiology of oral cavity cancer in France using data from a large case–control study, the ICARE study.MethodsICARE studyThe ICARE study (Investigation of occupational and environmental CAuses of REspiratory cancers) is a multicentre population-based case–control study on lung and upper aerodigestive tract cancers carried out from 2001 to 2007 in 10 French administrative areas (“départements”) covered by a general cancer registry. This study was set up to explore the role of lifestyle, environmental and occupational risk factors in lung and UADT cancers. The study design has been described in details elsewhere [27].Briefly, all newly diagnosed primary oral cavity, pharynx, larynx, sinusal cavities, trachea and lung cancers were selected. Only histologically confirmed cases aged 75 or younger at interview, identified between 2001 and 2007, and residing in one of the 10 départements, were eligible. Clinical and anatomo-pathology reports were reviewed to determine topography and histological type of the tumours according to the International Classification of Diseases for Oncology [28]. All histological types were included.Controls were selected from the general population by random digit dialling [29]. The controls were frequency-matched to the cases by age, gender and area of residence (“département”). Additional stratification ensured that controls were representative of the population of the “département” in terms of socio-economic status based on the last job held.Present analysisThe present analysis included all ICARE controls and only the cases with oral cavity cancer (ICD-10 codes C01-C06).Among the 1316 oral cavity cancer cases identified as eligible, 196 could not be reached, 81 were deceased and 71 were too sick to be interviewed. Of the 968 cases who were contacted, 176 refused to participate and 792 (81.8%) answered the questionnaire. We focused only on the cases with squamous cell carcinoma (772 subjects, 97.5% of all cases with oral cavity cancer).Of 4673 eligible controls, 4411 were contacted, and 3555 (80.6%) agreed to participate.Data collectionTrained interviewers administered a detailed standardised questionnaire during face-to-face interviews. If the subject was too sick to be interviewed, a shortened version of the questionnaire was used to interview him or a next-of-kin. Among the 772 subjects with squamous cell carcinoma of the oral cavity, 689 (89.2%) filled a complete questionnaire and 83 (10.8%) a shortened questionnaire. Among controls, 3481 (97.9%) filled a complete questionnaire and 74 a shortened questionnaire (2.1%). As the shortened version of the questionnaire did not contain information about family history of cancer and medical conditions, the present analysis was based on 689 cases with squamous cell carcinoma and 3481 controls, all with a complete questionnaire.The complete questionnaire consisted of the following items: socio-demographic characteristics (age, gender, birth country, education level, marital status), residential history, personal medical history, family history of cancer, detailed tobacco and alcohol consumption (quantity, duration, type of product, age at starting, time since cessation), non-alcoholic beverage consumption (coffee, tea), anthropometric variables (height, weight at interview, two years before and at age 30), detailed lifelong job history and occupational exposures.To ascertain personal medical history, study participants were asked if, throughout their lives, they had ever had (“yes, no, or don’t know”) any of the following diseases: tuberculosis, chronic bronchitis, asthma, recurrent rhinitis, nasal polyps, recurrent nose bleeds, recurrent sinusitis, gastro-oesophageal reflux (heartburn or regurgitation), herpes, candidiasis, and warts. If the answer was “yes”, the subjects were asked to specify the age at first occurrence, the treatment and if the diagnosis was made by a doctor. Subjects reporting having ever had herpes, candidiasis or warts were asked to specify the location: lip and genitals for herpes, oral cavity and genitals for candidiasis, and hands, feet and head and neck for warts.To ascertain the family history of cancer, subjects were first asked to give the year of birth of their biological mother and father, and of their full brothers or sisters (“brother or sister having the same mother and the same father than you”). Then, they were asked for each of these relatives if she/he had ever had a cancer (“yes, no or don’t know”). If the answer was “yes”, the subjects were asked to specify the age at cancer diagnosis and if possible the type of cancer. No verification of the cancer diagnosis in the relatives was performed.Statistical analysisWe used unconditional logistic regression models to calculate odds ratios (OR) and their 95% confidence intervals (95% CI). All p-values were derived from two-sided statistical tests.All logistic regression models controlled for age (≤ 50, 51–59, 60–69, ≥ 70 years), gender, area of residence, education level (primary or less, vocational secondary, general secondary and university), BMI two years before the interview (categorical, according to the classification of the World Health Organization [30]: < 18.5, 18.5-24.9, 25.0-29.9, ≥ 30 kg/m2). Previous analyses of our data showed that the variables that best characterize the association between tobacco and alcohol consumption and oral cancer risk were smoking status, smoking duration, daily quantity of tobacco smoked and daily quantity of alcohol drinking [31]. To control for smoking, we used smoking status (never, current, former), average daily quantity of tobacco smoked (1–19, 20–39, ≥ 40 grams), and duration of smoking (1–30, 31–40, > 40 years) [32]. Average daily quantity of alcohol drinking in quartiles (never, < 0.6, 0.6-2.0, 2.1-4.5, > 4.5 standard glasses) was included in the models to adjust for alcohol drinking. The quantity of pure alcohol contained in a standard glass (15 cl of wine, 30 cl of beer, 5 cl of spirits, 10 cl of aperitif, and 30 cl of cider) is the same for each type of alcoholic beverage.We analysed the risk of oral cavity cancer related to the personal medical history using two variables: all medical conditions self-reported by the subjects and medical conditions reportedly diagnosed by a doctor. The date of interview was used as the date of reference for both cases and controls. This date was close to the date of diagnosis of the cases since cases were interviewed on average within three months of diagnosis.The family history of cancer was evaluated separately for mothers, fathers, brothers and sisters, and then among all first-degree relatives taken together. We analysed the risk of oral cavity cancer related to the cancer site among relatives: all sites together, head and neck (including oral cavity, pharynx, larynx, nasal cavity and sinuses) and non-head and neck cancers. Because a high number of cancers in family members were reported non-specifically as “cancer of the head and neck”, we chose to group the locations of head and neck cancers to reduce potential inaccurate reporting of cancer subsites. We nevertheless performed some analyses for family history of specific head and neck cancer sites among all first-degree relatives.We also conducted analyses stratified by tobacco and alcohol consumption. We also performed the same analyses using a more restricted definition of the oral cavity excluding base of tongue (C01), lingual tonsils (C02.4), soft palate (C05.1) and uvula (C05.2), since these subsites are often included in the oropharynx. In addition, seven subsites (base of the tongue, mobile tongue, floor of the mouth, gums, soft palate, hard palate, and other parts of the oral cavity) were compared for family history of cancer and personal history of other medical conditions using unconditional polytomous logistic regression.Statistical analyses were conducted using STATA software version 10.0 (StataCorp, Texas, USA).ResultsAmong the 689 cases, the most common tumour location was floor of the mouth (188 cases, 27.3%), followed by mobile tongue (162 cases, 23.5%) and base of the tongue (130 cases, 18.9%). Less frequent tumour locations were: other parts of the oral cavity (81 cases, 11.7%), soft palate (74 cases, 10.7%), gums (37 cases, 5.4%), and hard palate (17 cases, 2.5%). The analysis using the restricted definition of oral cavity involved 485 cases.The main characteristics of cases and controls are presented in Table 1.Table 1 Main characteristics of cases and controlsFull size tableMen represented more than two-thirds of subjects in both cases and controls. Cases were younger (mean age around 57 years) than controls (mean age around 59 years) (p < 0.001).Compared with controls, cases had a lower education level (p < 0.001), a higher consumption of tobacco (p < 0.001) and alcohol (p < 0.001), and a lower BMI two years before the interview (p < 0.001).Personal medical conditionsStatistical analysis showed significant positive associations between the risk of oral cavity cancer (C01-C06) and chronic bronchitis (OR 1.7, 95% CI 1.2-2.4) (Table 2). Histories of tuberculosis and candidiasis overall were associated with an increased risk of oral cavity cancer (ORs 1.6), but the results did not reach statistical significance. Among candidiasis locations, oral candidiasis was associated with an increased risk of oral cavity cancer (OR 5.0, 95% CI 2.1-12.1). Significant inverse relations were observed between the risk of oral cavity cancer and recurrent rhinitis (OR 0.6, 95% CI 0.4-0.9), nasal polyps (OR 0.3, 95% CI 0.1-0.9), and gastro-oesophageal reflux (OR 0.5, 95% CI 0.4-0.7). Herpetic lesions were not related to the risk of oral cavity cancer, regardless of the location of the herpes. The risks associated with a history of skin warts were reduced, but the results did not reach statistical significanceTable 2 Risks of oral cavity cancer associated with personal medical conditionsFull size tableBecause high prevalence of oropharyngeal candidiasis has been described in subjects with head and neck cancer undergoing radio/chemotherapy [33, 34], we also conducted analysis after excluding subjects declaring candidiasis at the time of interview or at the time of diagnosis of another cancer; the association between oral cavity cancer risk and oral candidiasis remained practically unchanged (OR 6.0, 95% CI 2.2-16.4). Oral candidiasis may also constitute an early manifestation of the cancerous disease. When we excluded all subjects reporting a history of oral candidiasis near the current cancer (up to two years before the cancer diagnosis), the association between oral cavity cancer and oral candidiasis remained significant (OR 3.7, CI 95% 1.3-10.1).We calculated the ORs for oral candidiasis in strata of tobacco and alcohol consumption. The OR was slightly higher in ever smokers (OR 5.6, 95% CI 2.0-15.2) than in never smokers (OR 4.3, 95% CI 0.5-41.7), but the interaction between tobacco smoking and oral candidiasis was not significant (p-value for interaction = 0.14). Oral candidiasis was associated with an elevated risk of oral cavity cancer in drinkers of more than 2 glasses/day (OR 3.9, 95% CI 1.0-14.8) but not in drinkers of 2 glasses/day or less (OR 1.1, 95% CI 0.2-23.8), although the ORs were not statistically different (p-value for interaction = 0.50).When the analysis was restricted to medical conditions that the subjects reported as diagnosed by a doctor, similar results were observed, except for the association between bronchitis and oral cavity cancer which became weaker and non-significant (OR 1.2, 95% CI 0.9-1.6) (data not shown).Family history of cancerThe associations between family history of cancer and risk of oral cavity cancer are presented in Table 3.Table 3 Risks of oral cavity cancer associated with family history of cancer among first-degree relativesFull size tableHistory of cancer in general, and of head and neck cancer in particular, among fathers, were associated with a slightly elevated risk of oral cavity cancer, but the results were not statistically significant (OR 1.3, 95% CI 0.9-1.6, and 1.5, 95% CI 0.9-2.4, respectively).History of head and neck cancer among mothers was significantly associated with an elevated risk of oral cavity cancer (OR 5.2, 95% CI 1.2-23.9). This OR was higher than that observed for fathers. When cancer history among siblings was analysed, after adjustment for the number of sisters and brothers, we observed a significant association between the risk of oral cavity cancer and history of cancer of any type (OR 1.4, 95% CI 1.1-1.9). History of head and neck cancer among siblings was associated with an increased risk of oral cavity cancer (OR 2.3, 95% CI 1.2-4.2). Analysis by type of sibling showed a significantly increased risk only among subjects having brothers with a history of head and neck cancer (OR 2.6, 95% CI 1.2-5.8); history of head and neck cancer among sisters was not significantly associated with an increased risk of oral cavity cancer (OR 1.7, 95% CI 0.6-4.2).When we analysed the relationship between cancer history among all first-degree relatives and oral cavity cancer risk, we observed significant association for history of head and neck cancer (OR 1.9, 95% CI 1.2-2.8). A family history of any type of cancer slightly increased the risk of oral cavity cancer, but the results were not statistically significant (OR 1.2, 95% CI 0.9-1.5). The risk associated with first-degree relatives’ history of cancer (any type and head and neck) increased with the number of affected relatives.Analysis by type of head and neck cancer in first-degree relatives showed significantly increased risks of oral cavity cancer in subjects with family history of oral cavity cancer (OR 3.5, 95% CI 1.1-11.2) and of “head and neck cancer” (not specified) (OR 1.8, 95% CI 1.1-2.9). A family history of pharyngeal, laryngeal, and sinonasal cancer was associated with non-significantly elevated risks of oral cavity cancer (OR 4.6, 95% CI 0.5-44.8 for history of pharyngeal cancer; 1.6, 95% CI 0.6-4.4 for history of laryngeal cancer; and 1.7, 95% CI 0.3-8.8 for history of sinonasal cancer). However, few subjects reported a specific location of head and neck cancer in first degree relatives (26 oral cavity, 5 pharynx, 35 larynx, and 11 nasal cavity/sinuses cancer).Analysis stratified by gender of first-degree relatives showed that history of head and neck cancer among female relatives (mothers and sisters) was not significantly associated with the risk of oral cavity cancer (OR 2.3, 95% CI 0.9-5.4), although the result was borderline significant. Conversely, history of head and neck cancer in male relatives (fathers and brothers) was significantly associated with the risk of oral cavity cancer (OR 1.9, 95% CI 1.2-3.3). However, these ORs did not differ significantly (p-value of test of comparison of ORs = 0.91).We found a stronger association between the risk of oral cavity cancer and family history of head and neck cancer in subjects aged 45 or more (OR 2.3, 95% CI 1.5-3.4) compared to subjects aged less than 45 (OR 1.3, 95% CI 0.3-6.7), although the ORs were not statistically different (p-value for interaction = 0.46).Analysis by cancer site among first-degree relatives (Table 4) showed elevated ORs among subjects having a family history of lung, oesophagus, cervix and corpus uteri, brain and nervous system cancer, but the results were not statistically significant (OR 1.4, 95% CI 0.9-1.9; 1.5, 95% CI 0.7-3.3; 1.7, 95% CI 0.9-3.1; 2.0, 95% CI 0.9-4.8 respectively).Table 4 Odds ratios for oral cavity cancer risk related to family history of selected cancers in first-degree relativesFull size tableWhen we stratified by tobacco smoking and/or alcohol drinking (Table 5), significantly increased risks of oral cavity cancer related to family history of any type of cancer were observed only in smokers and/or moderate to heavy drinkers. Significantly elevated risks of oral cavity cancer associated with family history of head and neck cancer were seen for both never and ever smokers and for light and moderate to heavy drinkers. However, the increase in risk was small and not significant for never smokers who were also light drinkers.Table 5 Risks of oral cavity cancer related to family history of cancer in first-degree relatives stratified by tobacco smoking and alcohol drinkingFull size tableAnalyses restricted to intraoral cavityWhen the analyses were limited to intraoral cavity (C02.0-C02.3, C02.8, C02.9, C03, C04, C05.0, C05.8, C05.9, C06), the results were similar to that observed for oral cavity globally (C01-C06). Thus, family history of UADT cancer among first-degree relatives was associated with an OR of 1.7 (95% CI 1.1-2.7), personal history of oral candidiasis with an OR of 4.9 (95% CI 1.8-13.3), gastro-oesophageal reflux with an OR of 0.6 (95% CI 0.4-0.8), recurrent rhinitis with an OR of 0.6 (95% CI 0.4-0.9), and nasal polyps with an OR of 0.3 (95% CI 0.1-0.9).Analyses by subsiteWe assessed the risk of oral cavity cancer by anatomical site of the oral cavity (base of tongue, mobile tongue, gum, floor of mouth, hard and soft palate, and other parts of oral cavity) for personal medical conditions and for family history of cancer using a polytomous regression. We did not find any difference between subsites for any variable of interest (tests of comparison of odds ratios non-significant) (data not shown).DiscussionTo our knowledge, the ICARE study is the first population-based case–control study in France and one of the largest in the world which investigates the role of risk factors other than tobacco and alcohol consumption in the occurrence of oral cavity cancer. Strengths of this study include large sample size allowing us to perform analyses by subsite, and detailed data about family history of cancer and personal medical history.The ICARE study was conducted in collaboration with the cancer registries, allowing us to recruit cancer cases in all healthcare establishments in the selected areas. The control group was population-based and common for both pathologies (lung and UADT cancers), which explains the significantly different distribution of age and area of residence between oral cavity cancer cases and controls. However, the large number of subjects in each category allowed for satisfactory adjustment for these variables.The results of the epidemiological studies are contrasted concerning the role of candidiasis in the occurrence of oral cavity cancer, Thus, history of oral candidiasis was associated with an increased risk of oral cavity and oropharyngeal cancer in one study [11], with a reduced risk of oral cavity cancer in another study [7], whereas other authors found no association [6]. Our results have shown that personal history of oral candidiasis was associated with an elevated risk of oral cavity cancer. The increase in cancer risk with oral candidiasis may be explained by the production of endogenous nitrosamines by Candida albicans[35]. These nitrosamines act on the normal epithelium leading to oral dysplasia and further development of oral carcinoma. Nevertheless, some authors suggested that Candida albicans have only an indirect role and that the possibility of their involvement exist in conjunction with other etiological factors such as tobacco smoking [36]. In our study, the risk of oral cavity cancer associated with history of candidiasis was slightly higher in smokers than in never smokers, but the ORs were not significantly different. Other studies showed that Candida albicans may metabolize ethanol into its carcinogenic metabolite, acetaldehyde and, accordingly, candidiasis may be associated with elevated acetaldehyde levels in the oral cavity [37, 38]. Consistent with this mechanism, we found a significantly elevated risk of oral cavity cancer associated with history of candidiasis in moderate to heavy drinkers but not in light drinkers. However, the interaction of oral candidiasis with alcohol drinking was not statistically significant. Also, chronic infections, specifically chronic hyperplastic candidiasis, may trigger cell proliferation, inhibit apoptosis, interfere with cellular signalling mechanisms and up-regulate tumour promoters [39, 40]. In our study only 14 cases and 80 controls reported prior candidiasis and the results should be confirmed by other studies, especially with medical conditions validated by a doctor.In agreement with previous studies [7, 8, 11], we did not find a significant association between the risk of oral cavity cancer and history of herpetic infection. Conversely, only one case–control study [10] found an increased risk of oral cavity and oropharynx cancer associated with this infection and two case–control studies [6, 9] found a decreased risk.Cutaneous warts are caused by different types of HPV, notably 2, 4, 7 and 57, whereas genital warts are caused mostly by HPV types 6 and 11 [41]. Three studies [6, 8, 11], like ours, did not find any association between history of warts (any location) and the risk of oral cavity cancer, whereas one study found a reduced risk of UADT cancer associated with feet, genital and head and neck warts [7].We found an inverse association between the oral cavity cancer risk and history of rhinitis and nasal polyps. These pathologies often have an allergic origin, and several studies found a decreased risk of head and neck cancer associated with a history of allergies [42–45]. The inverse association between allergies and cancer may be explained by an overactive immune function in allergic subjects that effectively detects and eradicates malignant cells, toxins or pathogens from the body [46, 47]. However, we did not find any association with the history of asthma, another allergies-related condition.We found also an inverse association between oral cavity cancer risk and history of gastro-oesophageal reflux but we cannot point to any specific mechanism. The possibility that this result is due to the chance may not be ruled out. Unlike our results, a recent case–control study [7] did not find any association between oral cavity cancer risk and gastro-oesophageal reflux.After controlling for main confounding factors, we observed a higher risk of oral cavity cancer among subjects having first-degree relatives with head and neck cancer history, compared to subjects without such a family history. The risk increased with the number of affected relatives. On the other hand we did not find a significant relationship between the risk of oral cavity cancer and family history of non-head and neck cancers. Several studies [20, 22, 23, 26] reported similar results.Early age of onset may be a feature of hereditary forms of cancer. Higher family risks for many cancers were found when the cancer subjects were diagnosed at an early age [48, 49]. Concerning the association between the risk of oral cancer and family history of head and neck cancer, no clear pattern emerges from epidemiological studies: some of them found a stronger association in younger subjects compared to older subjects [20, 21, 23], others found a contrary result [22, 26], but the differences in risk with age of onset were never significant. Similarly, in our study the interaction of family history of head and neck cancer with age was not significant, although the OR was somewhat higher in older subjects.Familial clustering of cancer cases could be explained by genetic polymorphism in genes involved in the metabolism of tobacco and alcohol carcinogens and DNA repair [12–19], but may also reflect a tendency of relatives to have similar behaviour concerning alcohol and tobacco.In our study, associations between oral cavity cancer risk and family history of cancer were observed among smokers and/or drinkers of >2 glasses/day only. Conversely, an increased risk of oral cavity cancer associated with a family history of head and neck cancer was also observed in non-smokers and light drinkers, but the risk increased with the exposure. Our results are similar to those of other studies on oral/pharyngeal or head and neck cancer [20, 23, 26].The differential ability of subjects to metabolize carcinogens when exposure to tobacco and/or alcohol occurs may explain the higher risk of oral cavity cancer observed in our study among smokers and drinkers having a family history of UADT cancer. Nevertheless, we did not observe an increased risk of oral cavity cancer in subjects having a family history of other cancers related to smoking and/or alcohol drinking (e.g. lung, oesophagus, liver, pancreas), suggesting that other genetic factors might explain these findings.When the analyses were limited to intraoral cavity (C02.0-C02.3, C02.8, C02.9, C03, C04, C05.0, C05.8, C05.9, C06), excluding the sites usually attached to oropharynx (C01, C02.4, C05.1, C05.2), the results were similar to that observed for oral cavity C01-C06. We did not find any difference between subsites base of the tongue, mobile tongue, gums, floor of the mouth, soft palate, hard palate, and other parts of the mouth for any variable of interest.Some limitations of our study can be discussed. The subjects self-reported their own medical history and family history of cancer. Thereby, recall bias could not be ruled out and it is possible that the cases had a higher motivation to recall their personal and family medical history than the controls. Nevertheless, two studies have shown that subjects in case–control studies are able to report accurately family history of common types of cancer among first-degree relatives, with little observable recall bias [50, 51]. In addition, family history of cancer sites other than head and neck was not associated with an increased risk of oral cavity cancer in this study, suggesting that no major recall bias concerning cancer in general has affected our results.With regards to oral candidiasis, a possible explanation would be that cases with oral cancer are more prone to recall previous oral lesions than controls. However, no association was found with labial herpes, another oral condition, suggesting that differential recall between cases and controls is unlikely to explain our results. Moreover, when we limited the medical conditions to those reportedly diagnosed by a doctor, the results were similar. Medical treatments were also collected and those reported for candidiasis were consistent with this pathology. So, we think that misclassification of candidiasis is unlikely to explain our results.Information about other known risk factors for oral cavity cancer such as diet, human papilloma virus (HPV) or dental health was not collected, and residual confounding cannot be excluded. Nevertheless, no association between diet, HPV infection or dental health and family history of cancer has ever been shown in the literature. Also, the possibility of residual confounding for the main risk factors may not be ruled out.We have no way to assess whether cases included in our study differed according to past medical conditions and family history of cancer from cases that could not be included. Nevertheless, the distribution of included cases by age, gender and cancer subsite was very similar to that of all oral cancer cases diagnosed in France [52], suggesting that no major selection bias occurred. We excluded from analysis all subjects with shortened questionnaires because information on medical conditions and family history of cancer was not available. However, these subjects were comparable in age, gender, and tobacco and alcohol consumption to subjects with complete questionnaires.ConclusionThis study showed that family history of head and neck cancer is related to an increased risk of oral cavity cancer, and suggested an association with personal history of oral candidiasis. From a public health point of view, these factors should be taken into account to target prevention efforts and screening.References1.World Health Organization: International Classification of Diseases 10th Revision. 2007, Geneva: World Health OrganizationGoogle Scholar2.Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM: Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. 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J Natl Cancer Inst. 1994, 86: 1600-1608. 10.1093/jnci/86.21.1600.CASArticlePubMedGoogle Scholar50.Kerber RA, Slattery ML: Comparison of self-reported and database-linked family history of cancer data in a case–control study. Am J Epidemiol. 1997, 146: 244-248. 10.1093/oxfordjournals.aje.a009259.CASArticlePubMedGoogle Scholar51.Love RR, Evans AM, Josten DM: The accuracy of patient reports of a family history of cancer. J Chronic Dis. 1985, 38: 289-293. 10.1016/0021-9681(85)90074-8.CASArticlePubMedGoogle Scholar52.Ligier K, Belot A, Launoy G, Velten M, Bossard N, Iwaz J, Righini CA, Delafosse P, Guizard AV: Descriptive epidemiology of upper aerodigestive tract cancers in France: incidence over 1980–2005 and projection to 2010. Oral Oncol. 2011, 47: 302-307. 10.1016/j.oraloncology.2011.02.013.ArticlePubMedGoogle ScholarPre-publication historyThe pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2407/13/560/prepubDownload referencesAcknowledgementsICARE study was supported by the French National Research Agency (ANR), the French Agency for Food, Environmental and Occupational Health and Safety (ANSES), the French Institute for Public Health Surveillance (InVS), the Foundation for Medical Research (FRM), the Foundation of France, the Agency for Research on Cancer (ARC), the French Ministry of Work, Solidarity and Public Function (Direction Générale du Travail), and the Ministry of Health (Direction Générale de la Santé). L. Radoï was supported by the French National Cancer Institute (InCA), grant n° 2009–349 for this work.Author informationAffiliationsCentre for Research in Epidemiology and Population Health (CESP), Inserm U1018, Epidemiology of Occupational and Social Determinants of Health Team, F-94807, Villejuif, FranceLoredana Radoï, Sophie Paget-Bailly, Diane Cyr, Gwenn Menvielle, Annie Schmaus, Matthieu Carton & Danièle LuceUniversity Versailles St-Quentin, F-78035, Versailles, FranceLoredana Radoï, Sophie Paget-Bailly, Diane Cyr, Gwenn Menvielle, Annie Schmaus, Matthieu Carton & Danièle LuceCentre for research in Epidemiology and Population Health (CESP), Inserm U1018, Environmental Epidemiology of Cancer Team, F-94807, Villejuif, FranceFlorence Guida, Sylvie Cénée, Marie Sanchez & Isabelle StückerUniversity Paris-Sud, UMRS 1018, F-94807, Villejuif, FranceFlorence Guida, Sylvie Cénée, Marie Sanchez & Isabelle StückerCalvados Cancer Registry, F-1400, Caen, FranceAnne-Valérie GuizardHérault Cancer Registry, F-34298, Montpellier, FranceBrigitte TrétarreInserm U1085, Irset, Faculté de Médecine, Campus de Fouillole, BP 145, 97154, Pointe-à-Pitre, Guadeloupe French West IndiesDanièle LuceCorresponding authorCorrespondence to Danièle Luce.Additional informationCompeting interestThe authors declare that they have no conflict of interest.Authors’ contributionsDL and LR conceived and designed the current study and drafted the manuscript; LR and DC analyzed the data; DL and IS are the principal investigators of ICARE, conceived the study, designed the questionnaire, and coordinated the original collection of the data. AS, DC, SC, MS, AVG and BT contributed to data collection and quality control; SPB, FG, GM, MC contributed to the statistical analysis. All authors participated to data interpretation and critical revision of the manuscript. All authors read and approved the final manuscript.Rights and permissionsReprints and PermissionsAbout this articleCite this articleRadoï, L., Paget-Bailly, S., Guida, F. et al. Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE study. BMC Cancer 13, 560 (2013). Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE studyDownload citationReceived18 January 2013Accepted03 November 2013Published28 November 2013http://DOIhttps://doi.org/10.1186/1471-2407-13-560Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkKeywordsFamily historyMedical conditionsOral cavity cancerRisk factorsCase–control studyDownload PDFBMC CancerISSN: 1471-2407Contact usSubmission enquiries: Access here and click Contact UsGeneral enquiries: [email protected] more on our blogsReceive BMC newslettersManage article alertsLanguage editing for authorsScientific editing for authorsPoliciesAccessibilityPress centerSupport and ContactLeave feedbackCareersFollow BMCBMC Twitter pageBMC Facebook pageBMC Weibo pageBy using this website, you agree to our Terms and Conditions, Privacy statement and Cookies policy. 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★★★★NOTE: This is a review of the 2015-2016 23andMe kit and website available to US customers. From 2013 to late 2015, 23andMe offered a somewhat different product (wiki), so when reading any 23andMe reviews be sure to take note of the review date.In this review I will be coveringThe kit (ease of use, processing, time frame)The product (what you get, reports overview, accuracy, website layout)The Privacy Policy (you should read it)Overall thoughts and suggestionsThe KitI received the 23andMe kit as a Christmas gift. The box is small and light, and comes with return postage so that you can send it back at no cost. Instructions in the kit are very straightforward, and all the tools you need are there. Just add spit :)First, I registered the kit at 23andMe and also set up my user account. This included agreeing to 23andMe's Terms of Service and Privacy Policy, and filling out a questionnaire that resembled a medical history form. Then I spat into the tube and sealed it as directed. I took it to a post office the same day, 1/7/16. The post office gave me a tracking number, so I was able to see when the box was picked up (around 1/12). On 1/19 I received an email from 23andMe informing me that my DNA was being extracted. I was encouraged to visit the website and view a short video on 23andMe's DNA extraction process.How long does it take? 23andMe provides a tracking bar at the top of your main account page that shows which process your sample is going through currently, and its progress toward the end reports. My reports were ready by 2/2, so from start to finish, the entire process took about a month. I thought that this was very reasonable considering the 6-8 week estimate given by 23andMe.The ProductI was excited to see my reports and logged in right away to view them. Upon logging in I was presented with the Reports Overview page. This page had six clickable boxes: All Reports, Carrier Status Reports, Ancestry Reports, Wellness Reports, Traits Reports, and Tutorials.I chose to view All Reports, and was brought to a page with clickable links to each report. Here is a list of the reports you'll receive with the current 23andMe, in the order that they appeared on my page:Ancestry CompositionFacial FeaturesHairPhysical CharacteristicsPhysical ResponsesSkinTaste and SmellHaplogroupsNeanderthal AncestryAlcohol Flush ReactionCaffeine ConsumptionLactose IntoleranceMuscle CompositionCarrier Status for the following genetic disorders: ARSACS, ACCPN, ARPKD, Beta Thalassemia, Bloom Syndrome, PMM2-CDG, Cystic Fibrosis, DBPD, DLD, Familial Dysautonomia, Fanconi Anemia Group C, GRACILE Syndrome, GSDIa, GSDIb, Hereditary Fructose Intolerance, LSFC, LGMD2D, LGMD2E, LGMD2I, MCAD Deficiency, MSUD 1B, CLN5-related NCL, PPT1-related NCL, Niemann-Pick Disease Type A, Nijmegen Breakage Syndrome, DFNB1, DFNB4, PH2, RCDP1, Sickle Cell Anemia, Sjögren-Larsson Syndrome, Tay-Sachs Disease, Tyrosinemia Type I, Usher 1F, Usher 3A, and ZSS.Let's get Carrier Status reports out of the way first. Most of these disorders you won't have heard of (I sure hadn't). There are gene variants that can determine whether or not you carry these disorders, and 23andMe looks for SOME of these variants. If you are thinking of having children and have a family history of genetic disorder(s), these tests may be relevant to you. Personally they are less relevant to me, but I found the information to be interesting nonetheless.As an example, here is my Cystic Fibrosis test result.According to the report explanation, I still have up to a 1 in 210 chance of carrying a Cystic Fibrosis variant. Basically, these tests are not meant to diagnose, and with current technology it's still impossible (or at least wildly time consuming and expensive) to test for ALL variants of these diseases.There is a tab at the top of this page (and almost every other 23andMe report page) that says Scientific Details. Clicking on this will take you to a very descriptive analysis of your DNA "markers" that were tested, and an interpretation of the results (based on not only your own testing but also on disorder prevalence in certain ethnic groups).In addition to all of this information, you can download your raw DNA data from 23andMe and have it analyzed by other companies to discover statistics for more common health concerns. I'll try that out in the future and add the results to this review.Next, the main reason you're probably interested in DNA testing: Ancestry, Haplogroup, and Neanderthal Ancestry reports.Going back to the main Reports page, you can click on Ancestry Composition. The summary page gives us a colorful map that shows where your ancestors came from on BOTH sides of your family.Clicking on "See all 31 tested populations" will give you a more detailed percentage page. My grandmother was Japanese, and she married someone of European descent. My father is also of European/Irish descent. It was nice to see evidence of my 1/4 Japanese lineage in these reports :)Further down the page, 23andMe gives you the option to link parents and other relatives to your biological profile. Doing this will give you more accurate results based on either their DNA tests or their answers to survey questions. Relatives do NOT need to take the DNA test to create an account.Check out this quote from the ancestry page:"This report CANNOT tell you the precise origins of all of your ancestors. The results presented here are estimates, which may change over time as our algorithm improves. This report cannot tell you ancestry estimates for populations for which we do not have sufficient data."When analyzing your DNA, algorithms are used to determine which population segments match your genetic profile with a high degree of certainty. You should not assume that the information presented here is completely accurate, and you should not be surprised if your ethnicity percentages change a bit over time. 23andMe is gathering data, and new data means changes to existing data. Capeesh?Again, the Scientific Details tab explains this concept further by allowing you to see exactly which parts of your DNA are assigned to your ancestries. You can use the "confidence level" scroll bar above your DNA data to see how 23andMe provides a combination of accurate ancestry data and speculative algorithm analysis.I admit that this is still a little confusing for me. Fortunately 23andMe offers an extremely detailed explanation as to how they come up with these results. I haven't read it yet but you can bet I will.Further down on the Scientific Details page is a Change Log. This is where 23andMe will update you on changes made to your data over time. I'm interested and curious to see what new information will be added as more people participate in DNA testing.Ok, on to Haplogroup. Haplogroups are basically a single line of descent that can be traced back thousands of years to a small group of ancestors using a portion of your DNA.An important note: if you are a woman, you have two X chromosomes (as opposed to men who have an X and a Y). Because of this you can ONLY see your maternal haplogroup unless your father or other male relative on your father's side takes the 23andMe test as well to give you your paternal haplogroup. It's a bummer, but that's genetics.For me, this was the part of DNA testing that I was really looking forward to. For years my aunts have suspected that their mother (my grandmother) was of Ainu descent. My maternal haplogroup test results show that this is very likely true.It's hard to see on my map, but Japan is highlighted in yellow. As you can see on this Ancestry Composition explanation page, others may have a more colorful map with a larger haplogroup depending on where their ancestors are from. The Scientific Details page for your haplogroup will give you a tree displaying the migration pattern/lineage of your inherited DNA. Interesting stuff!Now let's take a look at Neanderthal Ancestry. According to 23andMe, "Neanderthals were ancient humans who interbred with modern humans before becoming extinct 40,000 years ago. This report tells you how much of your ancestry can be traced back to Neanderthals."According to my results, I have more neanderthal variants than 78% of 23andMe customers...yet neanderthal ancestry accounts for less than 4% of my DNA. I have no idea what this means. Scrolling down a bit, the Neanderthal Background section somewhat explains:"Non-African populations have Neanderthal ancestry amounting to about 1-2% of their genomes. With few exceptions, Sub-Saharan African populations have virtually no Neanderthal ancestry. Average numbers from the 23andMe database are shown to illustrate this difference."That statement is accompanied by a little graph that shows that the average number of neanderthal variants among non-Africans tends to be high, while for Sub-Saharan African populations it is low.Still confused, I clicked on the Scientific Details tab. Here is a wealth of information and explanation that I'll probably spend a month poring over. This page provides a graph detailing the genetic markers tested for neanderthal ancestry and three other subcategories (these are the four clickable boxes across the top of the graph).Scrolling down gives you a list of your own neanderthal traits (I didn't have any). There is also a "white paper" link that takes you to a brief dissertation on Neanderthal Ancestry Inference. Obviously there is a lot of information here. If it turns out that you have neanderthal traits (such as a hairier back or a different posture) I suppose this might be pretty interesting stuff!A brief look at the other reports provided by 23andMe, most of which focus on physical traits, characteristics, and other fun stuff. At first glance these reports may seem a bit silly because you already know what your eye color is, how long your fingers are, whether you are lactose intolerant, etc. But the science behind the reports is pretty fascinating, and this also gives you a chance to find out if you have recessive or rare traits for your genetic makeup.Let's look at my Facial Features report for example. Clicking on "Facial Features" will give you subcategory reports for Face, Eyes, and Ears. The category Face currently contains four reports, which are Cleft Chin, Dimples, Unibrow, and Widow's Peak. 23andMe compares your DNA to that of its other customers with similar DNA profiles, and determines your likelihood of having these traits. Sometimes the algorithm is wrong, and sometimes it's right. In my case, about 90% of the reports were accurate compared to my actual traits. Here is one that was wrong:I definitely have a widow's peak. Notice the paragraph at the bottom...it's telling you that the report "best applies to customers of European descent". Maybe my widow's peak is inherited from the Japanese side!Basically this is a bell curve. No matter how good the algorithm is, everyone is different and no one can predict with 100% accuracy what traits you have based on a group model. So don't be upset when 23andMe gets something "wrong". This is the data-gathering part of 23andMe, and you are participating in the research.Below each result graph is a little box with more information about the trait you're viewing: the biology and genetics behind the traits, and other factual tidbits. I thought these were interesting and fun. Again, the Scientific Details tab gives you a more in-depth look at your reports and the process of calculating your results.Similar data is available for the other remaining reports. Another report that was "wrong" for me was the lactose intolerance report. I am definitely lactose intolerant, but my report said that I was "likely tolerant" based on the analysis of a particular gene marker. 23andMe explains how there are many other determining factors for this particular trait, and even takes time to describe some of these variants.That about sums it up for the 23andMe reports. But wait! There's MORE.When you are done perusing your reports, click on the Tools tab. Here you have the opportunity to use your newfound data in a variety of ways: Share & Compare, DNA Relatives, Family Tree, Find Genetic Counseling, Forums, and Raw Data.Share & Compare allows you to invite family members to create accounts on 23andMe. Again, they don't need to take the DNA test to do this. 23andMe will ask them medical history and physical trait questions, and use the answers to supplement your reports and build your genetic model. With your permission, your relatives (and friends if you choose) will also be able to view your test results.DNA Relatives is a great tool for those who are searching for close relatives. I've heard several awesome stories about adopted or orphaned kids who were able to find relatives this way. It does involve the sharing of your genetic information, so look the page over carefully before agreeing to anything. Again, you can also take your raw DNA data to other sites and search for relatives there if you don't find anything in 23andMe's pool. Knowing most of my close relatives already, I decided it couldn't hurt to opt into this. The result for me was a long list of 2nd-through-7th cousins. *shrug*Family Tree uses myheritage.com to help you build a family tree, if you're into that.Genetic Counseling is for people who receive results from their DNA testing that require further assistance or analysis. Carriers who want to have children, folks with a strong history of genetic disease or cancer, or people interested in alternate testing would find this feature useful.Forums is exactly what you'd expect: a forum for 23andMe members to discuss the product, get help, complain, etc.Raw Data is where you can download your DNA data to use however you see fit. I plan to take mine to a company like Promethease to gather additional health information. If you are REALLY into genetics, this page is also where you can click on individual chromosomes and get a long, long, long, long, LONG list of genetic information. Here is like 1/4 page of my chromosome #1:Yeah.You can also continue to participate in 23andMe's genetic research by answering survey questions about your health, environment, etc. (To do this you must read and agree to the Research Consent Document available on the site). Survey questions pop up randomly across the site, or you can access them intentionally at the bottom of almost any report page. An example question:I should mention that so far, I have not been spammed at all by 23andMe by phone or email. Once in a while I get a little "digest" sort of email, that's all. Opting into the survey questions doesn't equal spam, thankfully.Privacy and TermsNOTE: Again, please check the date of any review you read. The "new" 23andMe released in late 2015 is under a privacy policy currently dated 12/2015. Any reviews dated earlier than that should be checked for relevance and accuracy.If you are into medical privacy, you need to know that 23andMe will share your information under certain circumstances. There is no question, it's very clear in their privacy policy. If you do not want the results of your 23andMe's analysis to be available to 3rd parties EVER, don't take the test. It's as simple as that.Here are just a few relevant bullet points that I gathered from the privacy policy:With a court order, 23andMe can disclose your information.23andMe stores your information in the US and other countries (other countries = different laws).In the event of a merger/acquisition, your information will be transferred to the new company."If you do not complete a Consent Document or any additional consent agreement with 23andMe, your information will not be used for 23andMe Research. However, your Genetic Information and Self-Reported Information may still be used by us and shared with our third-party service providers to provide and improve our Services (as described in Section 4.a), and shared as Aggregate or Anonymous Information that does not reasonably identify you as an individual (as described in Section 4.d)."23andMe "will use your information and share it with third parties for scientific research purposes ONLY if you sign a Consent Document. Note that we will disclose your individual-level information only if we obtain additional explicit consent from you.""You may withdraw your consent to participate in Research at any time by changing your consent status on your 23andMe Account Settings page, or by sending a request to the Human Protections Administrator. 23andMe will not include your Genetic Information or Self-Reported Information in new research occurring after 30 days from the receipt of your request."Here are some terms bullet points as well. These are all things you should consider before having your DNA tested:"You should not assume that any information we may be able to provide to you, whether now or as genetic research advances, will be welcome or positive.""You may discover things about yourself that trouble you and that you may not have the ability to control or change (e.g., your father is not genetically your father)."Here's a biggie: "The laboratory may not be able to process your sample...if your saliva does not contain a sufficient volume of DNA, you do not provide enough saliva, or the results from processing do not meet our standards for accuracy." The Terms go on to describe what you should do if your sample cannot be processed. I have seen SO many reviews complaining about this. If it happens, don't freak out. Follow the instructions and you'll be just fine."Genetic research is not comprehensive. While we measure many hundreds of thousands of data points from your DNA, only a small percentage of them are known to be related to human traits or health conditions...an important mission of 23andMe is to conduct and contribute to this research. Many ethnic groups are not included in genetic studies...some interpretations may not apply to you. Future scientific research may change the interpretation of your DNA.""You should be careful about sharing your Genetic Information with others. Currently, very few businesses or insurance companies request genetic information, but this could change in the future.""Genetic Information that you choose to share with your physician or other health care provider may become part of your medical record and through that route be accessible to other health care providers and/or insurance companies in the future."23andMe does NOT provide medical advice or diagnosis.To Sum It Up:I found 23andMe's service to be informative, interesting, and fun. I enjoyed learning about my ancestry, and am fascinated by the information in the traits reports. There is some information that I still don't understand and probably never will, but I'm ok with that. I'm glad to have this data available, and am excited to be a part of 23andMe's research project. I think that DNA will become a bigger part of our lives in the future, and by having my DNA analyzed I hope to contribute information that will be helpful to others as this technology improves.I found the process of submitting the sample to be easy. I thought the website was easy to navigate and the information was accessible and displayed clearly. I was satisfied with the data I received, and although there are more things I'd like to know I did my research and went into the testing knowing what 23andMe could and could not provide. As of now I haven't used Customer Service so can't review it.I would recommend 23andMe to people whoWant to find relativesWant to look into their carrier status and other medical information that can be uncovered through DNA testingWant to learn about their genetic traits and ancestryWant a copy of their own DNA dataAre interested in participating in DNA researchI would NOT recommend 23andMe to people whoDon't want to wait up to 3 months to receive their reportsDo not want their DNA data to be available to companies or individuals with either good or bad intentionsDo not want to contact/be contacted by relatives they do not knowHave no interest in reading through detailed reports on their genetic traits and ancestryAre not tech-savy enough to set up a user account or navigate a basic websiteThanks for reading and sorry it was so long...I wanted to cover all the bases :)