Familial risks of squamous cell carcinoma of the head and neck: retrospective case-control study

Foulkes, William D.; Brunet, Jean‐Sébastien; Sieh, Weiva; Black, Martin J.; Shenouda, George; Narod, Steven A.

doi:10.1136/bmj.313.7059.716

Cited by 136 publications

(99 citation statements)

References 32 publications

(39 reference statements)

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“…[3][4][5] An inherited component of susceptibility to oral and pharyngeal cancer has been suggested by case reports of families with multiple affected members, [14][15][16] by epidemiologic studies indicating familial tendency to oral and pharyngeal cancer or other cancers of upper aerodigestive tract, 1,[17][18][19][20][21][22][23] by segregation analysis in firstdegree relatives, 24 by elevated risks associated with polymorphic genes involved in the metabolism of tobacco and alcohol (i.e., ALDH2), [25][26][27][28][29] and by elevated risks associated with genes involved in DNA repair maintenance of genetic stability. 30,31 Familial aggregation of oral and pharyngeal cancers may also be due to shared environmental exposure to the main risk factors, i.e., alcohol and tobacco.…”

Section: Discussionmentioning

confidence: 99%

Family history and the risk of oral and pharyngeal cancer

Garavello

Foschi

Talamini

et al. 2007

Intl Journal of Cancer

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Scanty data are available on familial risk in oral and pharyngeal cancer. The relationship between oral and pharyngeal cancer and family history of cancer in first-degree relatives was investigated using data from a multicentric case-control study conducted in Italy and Switzerland between 1992 and 2005 on 956 cases aged less than 79 years, with histologically confirmed incident oral and pharyngeal cancer, and 2362 controls admitted to hospital for acute, nonneoplastic conditions. Logistic regression models conditioned on sex, age, study centre, and including terms for education, tobacco smoking, alcohol drinking, and number of siblings were used to estimate the odds ratios (OR) of oral and pharyngeal cancer. The multivariate ORs were similar for a family history of oral and pharyngeal cancer (2.6, 95% confidence interval, CI, 1.5-4.5) and laryngeal cancer (3.8, 95% CI, 2.0-7.2). The OR was 3.1 (95% CI, 2.0-4.8) for oral and pharyngeal cancer and laryngeal cancer combined. The OR was 7.1 (95% CI, 1.3-37.2) for subjects with 2 or more first-degree relatives with oral and pharyngeal/laryngeal cancers. Significant increases in risk were also observed for a family history of melanoma (OR 5 5.8; 95% CI, 1.3-26.4) and lung cancer (OR 5 1.4; 95% CI, 1.0-2.0). Compared to subjects without family history, nonsmokers, and non or moderate drinkers, the OR was 42.6 for current smokers, heavy drinkers with family history. History of oral and pharyngeal cancer and laryngeal cancer is a strong determinant of oral and pharyngeal cancer risk, independent from tobacco and alcohol. ' 2007 Wiley-Liss, Inc.Key words: oral neoplasms; familial risk; tobacco; alcohol drinking; risk factors Incidence and mortality from oral and pharyngeal cancer vary widely across the world. 1,2 This variation depends mostly on differences in exposure to tobacco and alcohol, the 2 major risk factors for oral and pharyngeal cancer. However, genetic factors may also contribute to explain the observed differences in rates. 2 Only a few epidemiologic studies have assessed familial risks in oral and pharyngeal cancer. A case-control study from the United States on 487 cases found odds ratios (OR) of 1.2 (95% confidence interval (CI), 0.7-2.3) in subjects with a family history of oral and pharyngeal cancer, and of 1.6 (95% CI, 0.7-3.8) for a family history of cancers of the esophagus and larynx. 3 Another case-control study from Puerto Rico on 342 oral and pharyngeal cancers showed ORs of 2.5 (95% CI, 0.8-8.0) in subjects reporting a first-degree relative with oral and pharyngeal cancer, and of 2.6 (95% CI, 1.4-4.8) in those reporting upper aerodigestive tract cancers. 4 A record-linkage study on the Utah Population Database, which includes 1 million individuals, found a standardized incidence ratio of oral and pharyngeal cancer of 1.8 (95%, 0.5-4.0) for subjects with a first-degree relative with cancer at the same site (8 observed versus 4.4 expected cases). 5 The familial aggregation of oral and pharyngeal cancers, however, may have different genetic and en...

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Section: Discussionmentioning

confidence: 99%

Family history and the risk of oral and pharyngeal cancer

Garavello

Foschi

Talamini

et al. 2007

Intl Journal of Cancer

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“…In an historical cohort study the relative risk (RR) for SSCHN was 7.89 (95% confidence interval -CI-1.50 to 41.6) in first degree relatives of patients with multiple primary head and neck cancer. 19 In a more recent pooled analysis with 8.967 SCCHN cases and 13.627 controls, having a family history of SCCHN in first-degree relative increased the risk of SCCHN 1.7, which was higher when the affected relative was a sibling (ORD 2.2, 95% CI 1.6-3.1) rather than a parent (OR D 1.5, 95% CI 1.1-1.8) and for more distal SCCHN anatomic sites (hypopharynx and larynx). 20 Genetic polymorphisms variants in tobacco carcinogen and alcohol metabolism genes may increase SCCHN risk.…”

Section: Genetic Susceptibilitymentioning

confidence: 99%

“…18 Moreover, T4 primary extension and more than 2 cm tumoral invasion of the base of the tongue were shown to be associated with increased salvage laryngectomy in the Veterans study. 19 …”

Section: Introductionmentioning

confidence: 99%

A genetic view of laryngeal cancer heterogeneity

2016

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During the recent decades significant improvements in the understanding of laryngeal molecular biology allowed a better characterization of the tumor. However, despite increased molecular knowledge and clinical efforts, survival of patients with laryngeal cancer remains the same as 30 years ago. Although this result may not make major conclusions as preservation approaches were not broadly used until the time of database collection, it seems to be clear that there is still window for improvement.

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“…In addition, second primary tumors, which are often a hallmark of inherited susceptibility to cancer, occur in up to 30% of patients with SCCHN (Day and Blot, 1992;Jones et al, 1995). A family history of SCCHN is more common for these cases than for single primary cases (Bongers et al, 1995;Foulkes et al, 1996) and it has been reported that non-smoking SCCHN patients are significantly more likely to be mutagen-sensitive than current smokers . It is, therefore, reasonable to suspect a role for inherited factors in determining predisposition to SCCHN.…”

mentioning

confidence: 99%

“…However, recent case-control studies indicate that SCCHN is also associated with a family history of this cancer (Copper et al, 1995;Foulkes et al, 1995Foulkes et al, , 1996. In addition, second primary tumors, which are often a hallmark of inherited susceptibility to cancer, occur in up to 30% of patients with SCCHN (Day and Blot, 1992;Jones et al, 1995).…”

mentioning

confidence: 99%

Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco

Hamel¹,

Karimi²,

Hébert‐Blouin³

et al. 2000

Int. J. Cancer

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Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco Tobacco and alcohol are important contributing factors to the development of squamous cell carcinoma of the head and neck (SCCHN) (Blot et al., 1988;Vokes et al., 1993). However, recent case-control studies indicate that SCCHN is also associated with a family history of this cancer (Copper et al., 1995;Foulkes et al., 1995Foulkes et al., , 1996. In addition, second primary tumors, which are often a hallmark of inherited susceptibility to cancer, occur in up to 30% of patients with SCCHN (Day and Blot, 1992;Jones et al., 1995). A family history of SCCHN is more common for these cases than for single primary cases (Bongers et al., 1995;Foulkes et al., 1996) and it has been reported that non-smoking SCCHN patients are significantly more likely to be mutagen-sensitive than current smokers . It is, therefore, reasonable to suspect a role for inherited factors in determining predisposition to SCCHN. Since large pedigrees with numerous cases of SCCHN are uncommon (Foulkes et al., 1996), genetic susceptibility to SCCHN is likely to be conferred by cancer genes of low penetrance.We and others (Vineis et al., 1994;Foulkes et al., 1996) All cases and controls were genotyped for presence or absence of both the GSTT1 and GSTM1 genes. Genotyping of GSTM1 was performed on genomic DNA by PCR amplification as previously described using three primers that amplify the GSTM1 sequence and a second internal control sequence simultaneously (Zhong et al.,1993). Absence of GSTM1-specific product indicated homozygosity for the null allele. The GSTT1 genotype was determined according to the method of Pemble et al. (1994) modified to incorporate the simultaneous amplification of partial ␤-globin sequences to serve as an internal control . As in the case of GSTM1, the absence of a GSTT1-specific product was indicative of homozygosity for the null allele.We observed 70 GSTT1 positives and 9 GSTT1 nulls in cases, compared with 81 positives and 20 nulls in controls (OR ϭ 2.57, p ϭ 0.04

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Familial risks of squamous cell carcinoma of the head and neck: retrospective case-control study

Cited by 136 publications

References 32 publications

Family history and the risk of oral and pharyngeal cancer

Family history and the risk of oral and pharyngeal cancer

A genetic view of laryngeal cancer heterogeneity

Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco

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