Increase In Overall Cancer Risk Research Articles

Exploring the association between sleep duration and cancer risk in middle-aged and older Chinese adults: observations from a representative cohort study (2011–2020)

BackgroundThis prospective cohort study aimed to investigate the relationship between sleep duration and cancer incidence among 9996 participants over a median follow-up period of 9 years.MethodsParticipants without cancer at baseline were followed for over 88,790 person-years. The incidence of cancer and sleep duration was self-reported. The relationship between sleep duration and cancer incidence was analyzed using Cox proportional hazards models adjusted for various confounding factors, including age, gender, lifestyle factors, and comorbidities.ResultsDuring the follow-up, 325 participants were diagnosed with incident cancer, resulting in an incidence rate of 20.49 per 1000 person-years. After adjusting for confounders, a total sleep duration of less than 6 h was significantly associated with an increased risk of cancer (HR: 1.27; 95% CI: 1.01–1.61). This association was particularly strong for cancers in the digestive and respiratory systems (HR: 1.41; 95% CI: 1.03–1.93). Longer sleep durations (> 9 h) showed a potential increase in cancer risk, but results were not consistently significant. Age-stratified analyses revealed a similar significant increase in cancer incidence among individuals aged 60 years or younger with less than 6 h of sleep per day, showing a 35% increase in overall cancer risk and an 83% increase in digestive and respiratory system cancer. No significant association was found between nocturnal sleep durations or daytime naps and cancer incidence. However, a significant interaction was observed between daytime naps longer than 30 min and cancer incidence in women (p = 0.041).ConclusionsWe observed that short sleep duration may increase the risk of cancer, particularly cancers in the digestive and respiratory systems. Additionally, while longer sleep durations might also increase cancer risk, this finding requires validation with larger sample sizes.

Exploring the association between sleep duration and cancer risk in middle-aged and older Chinese adults: observations from a representative cohort study (2011-2020).

This prospective cohort study aimed to investigate the relationship between sleep duration and cancer incidence among 9996 participants over a median follow-up period of 9 years. Participants without cancer at baseline were followed for over 88,790 person-years. The incidence of cancer and sleep duration was self-reported. The relationship between sleep duration and cancer incidence was analyzed using Cox proportional hazards models adjusted for various confounding factors, including age, gender, lifestyle factors, and comorbidities. During the follow-up, 325 participants were diagnosed with incident cancer, resulting in an incidence rate of 20.49 per 1000 person-years. After adjusting for confounders, a total sleep duration of less than 6h was significantly associated with an increased risk of cancer (HR: 1.27; 95% CI: 1.01-1.61). This association was particularly strong for cancers in the digestive and respiratory systems (HR: 1.41; 95% CI: 1.03-1.93). Longer sleep durations (> 9h) showed a potential increase in cancer risk, but results were not consistently significant. Age-stratified analyses revealed a similar significant increase in cancer incidence among individuals aged 60 years or younger with less than 6h of sleep per day, showing a 35% increase in overall cancer risk and an 83% increase in digestive and respiratory system cancer. No significant association was found between nocturnal sleep durations or daytime naps and cancer incidence. However, a significant interaction was observed between daytime naps longer than 30min and cancer incidence in women (p = 0.041). We observed that short sleep duration may increase the risk of cancer, particularly cancers in the digestive and respiratory systems. Additionally, while longer sleep durations might also increase cancer risk, this finding requires validation with larger sample sizes.

Gut microbiota behavior, low carbohydrate dietary intake and cancer.

Gut microbiota is a key intermediary between diet and host physiology, modulating several metabolic and neurological signaling pathways. Microbiota plays a key role in digestion, metabolism and behavior as well as microbial response to diet. Dysbiosis of gut microbiota has been strongly related to cancer. Ketogenic diet alters the gut microbiota and protects against multiple chronicle diseases and recent studies have linked ketogenic diet with cancer prevention. It is known that over 30 percent of all cancers can be prevented by lifestyle and dietary measures. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products impairs the glucose metabolism. The hypothesis that cytotoxicity induced by glucose deprivation in cancer cells is mediated by mitochondrial superoxide and H2O2 was confirmed by exposing glucose-deprived transformed human fibroblasts to electron transport chain blockers (ETCBs), known to increase mitochondrial superoxide and H2O2 production by a wide number of researchers. Therefore, glucose deprivation in the presence of ETCBs enhanced oxidative stress as well as cell death in several different human cancer cell lines (PC-3, DU145, MDA-MB231, and HT-29). Low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats contribute to an increase in overall cancer risk in both genders. Studies have show that when a diet is well balanced, it is likely that there would be at least a 60 percent decrease in breast, colorectal, and prostate cancers. Improving metabolites and immunological anticancer profile by k-PBD. There’s robust evidence that shows prolonged fasting, fastingmimicking diet (FMD) and ketogenic diet demonstrates a strong usefulness as adjuvants in cancer therapy.

Abstract P6-10-01: Consumption of sugar-containing beverages and cancer risk: Results from the NutriNet-Santé prospective cohort

Abstract OBJECTIVE To assess the associations between the consumption of sugar-containing and artificially sweetened beverages and cancer risk. DESIGN Population based prospective cohort study. SETTING AND PARTICIPANTS Overall, 101 257 participants aged ≥18y (mean age: 42.2±14.4y) from the French NutriNet-Santé cohort (2009-2017) were included. Consumptions of sugar-containing and artificially sweetened beverages were assessed using repeated 24h-dietary records, designed to register participants' usual consumption for 3300 different food and beverage items. MAIN OUTCOME MEASURES Associations between beverage consumption and overall, breast, prostate and colorectal cancer risk were assessed by multivariable Cox Proportional Hazard models adjusted for known risk factors. RESULTS A 100mL increase in the consumption of sugar-containing beverages was significantly associated with an increased risk of overall cancer (HR=1.08, 95% confidence interval 1.04 to 1.12, P<.0001) and breast cancer (HR=1.11, 95% confidence interval 1.04 to 1.19, P<0.002). The consumption of artificially sweetened beverages was not associated with cancer risk. In sub-analyses, a 100 mL increase in the consumption of 100% fruit juice was significantly associated with an increased risk of overall cancers (HR=1.08, 95% confidence interval 1.02 to 1.15, P=0.01). These associations were strongly mediated by the sugar contained in these beverages. In contrast, weight gain during follow-up did not appear as a strong mediator. Besides, results were similar in overweight and non-overweight participants. CONCLUSIONS In this large prospective study, a 100mL increase in the consumption of sugar-containing beverages in the diet was associated with an 8% significant increase in overall cancer risk and an 11% significant increase in breast cancer risk. 100% fruit juices were also associated with an 8% increased risk of overall cancers. Given the massive consumption of sugar-containing beverages in Western countries, these results suggest that they may represent a key modifiable risk factor for cancer prevention. Citation Format: Chazelas E, Srour B, Desmetz E, Kesse-Guyot E, Julia C, Druesne-Pecollo N, Galan P, Zelek L, Hercberg S, Latino-Martel P, Deschasaux M, Touvier M. Consumption of sugar-containing beverages and cancer risk: Results from the NutriNet-Santé prospective cohort [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P6-10-01.

Serum uric acid and cancer mortality and incidence: a systematic review and meta-analysis

Elevated serum uric acid (SUA) is a marker of chronic inflammation and has been suggested to be associated with increased risk of cancer, but its antioxidant capacity would justify an anticancer effect. Previous meta-analyses did not include all available results. We conducted a systematic review of prospective studies on SUA level and risk of all cancers and specific cancers, a conducted a meta-analysis based on random-effects models for high versus low SUA level as well as for an increase in 1 mg/dl SUA. The relative risk of all cancers for high versus low SUA level was 1.11 (95% confidence interval: 0.94-1.27; 11 risk estimates); that for a mg/dl increase in SUA level was 1.03 (95% confidence interval: 0.99-1.07). Similar results were obtained for lung cancer (six risk estimates) and colon cancer (four risk estimates). Results for other cancers were sparse. Elevated SUA levels appear to be associated with a modest increase in overall cancer risk, although the combined risk estimate did not reach the formal level of statistical significance. Results for specific cancers were limited and mainly negative.

Menopausal hormone therapy and cancer risk: An overestimated risk?

AimWe aimed to assess the overall cancer risk among contemporary menopausal hormone therapy (MHT) users in Sweden and the risk for different cancer types. MethodsA nationwide Swedish population-based cohort study including all 290,186 women aged ≥ 40 years having used systemic MHT during the study period (July 2005 and December 2012), compared with the Swedish female background population. MHT ever-use (all MHT, oestrogen-only MHT [E-MHT] and oestrogen plus progestin MHT [EP-MHT]) was based on the nationwide Prescribed Drug Registry. Cancer diagnoses were grouped into 16 different anatomical locations, for which standardised incidence ratios (SIRs) and 95% confidence intervals (CIs) were calculated. ResultsThe SIR of any cancer was 1.09 (95% CI: 1.07–1.11) following ever MHT, 1.04 (95% CI: 1.01–1.06) for E-MHT and 1.14 (95% CI: 1.12–1.17) for EP-MHT. The highest SIR was found for EP-MHT among users aged ≥70 years (SIR = 1.33, 95% CI: 1.26–1.40). The risk for invasive breast, endometrial or ovarian cancer combined was increased for any MHT (SIR = 1.31, 95% CI: 1.28–1.34). The risk of invasive breast cancer was increased following MHT and increased with age for EP-MHT users. The risk of gastrointestinal cancers combined was decreased (SIR = 0.90, 95% CI: 0.86–0.94), particularly the oesophagus (SIR = 0.81, 95% CI: 0.64–1.00), liver (SIR = 0.81, 95% CI: 0.65–0.99) and colon (SIR = 0.90, 95% CI: 0.84–0.95). ConclusionsMHT, notably EP-MHT, was associated with a limited increase in overall cancer risk. The increased risk of female reproductive organ cancers was almost balanced by a decreased risk of gastrointestinal cancers.

The risk of malignancy among biologic-naïve pediatric psoriasis patients: A retrospective cohort study in a US claims database

Little published literature exists regarding malignancy risk in pediatric psoriasis patients. To compare malignancy risk in biologic-naïve pediatric psoriasis patients with a matched pediatric population without psoriasis. This retrospective cohort study used IMS LifeLink Health Plan Claims data covering 1998-2008. Cancer incidence was compared with the US Surveillance, Epidemiology, and End Results (SEER) data using standardized incidence ratios (SIR), and between cohorts using Cox models. Among 9045 pediatric psoriasis patients and 77,206 comparators, 18 probable or highly probable cancers were identified. Pediatric psoriasis patients had a nonsignificantly lower incidence than comparators (hazard ratio [HR] 0.43, 95% confidence interval [CI] 0.05-3.54). The HR increased to 1.67 (95% CI 0.54-5.18) when cancer diagnosed during the first 90days of follow-up was included. The pediatric psoriasis cohort had a significantly increased lymphoma rate compared with SEER (SIR 5.42, 95% CI 1.62-12.94), but no significant increase relative to the comparator cohort. Misclassification of disease and outcome might have occurred with patients in the claims database. Patients with pediatric psoriasis showed no significant increase in overall cancer risk compared with those without psoriasis. A potential increased risk for lymphoma was observed when compared with the general population.

Prospective association between cancer risk and an individual dietary index based on the British Food Standards Agency Nutrient Profiling System.

The Food Standards Agency Nutrient Profiling System (FSA-NPS) constitutes the basis for the Five-Colour Nutrition Label suggested in France to be put on the front-of-pack of food products. At the individual level, a dietary index (FSA-NPS DI) has been derived and validated and corresponds to a weighted mean of all FSA-NPS scores of foods usually consumed by the individual, reflecting the nutritional quality of his/her diet. Our aim was to investigate the association between the FSA-NPS DI and cancer risk in a large cohort. This prospective study included 6435 participants to the SUpplémentation en VItamines et Minéraux AntioXydants cohort (1994-2007) who completed at least six 24 h dietary records during the first 2 years of follow-up. FSA-NPS DI was computed for each subject (higher values representing lower nutritional quality of the diet). After a median follow-up of 12·6 years, 453 incident cancers were diagnosed. Associations were characterised by multivariate Cox proportional hazards models. The FSA-NPS DI was directly associated with overall cancer risk (hazard ratio (HR)for a 1-point increment=1·08 (95 % CI 1·01, 1·15), P trend=0·02; HRQ5 v. Q1=1·34 (95 % CI 1·00, 1·81), P trend=0·03). This association tended to be more specifically observed in subjects with moderate energy intake (≤median, HRfor a 1-point increment=1·10 (95 % CI 1·01-1·20), P trend=0·03). No association was observed in subjects with higher energy intake (P trend=0·3). Results were not statistically significant for breast and prostate cancer risks. For the first time, this study investigated the prospective association between the FSA-NPS individual score and cancer risk. The results suggest that unhealthy food choices may be associated with a 34 % increase in overall cancer risk, supporting the public health relevance of developing front-of-pack nutrition labels based on this score.

Second Solid Cancers after Allogeneic Hematopoietic Cell Transplantation Using Reduced-Intensity Conditioning

We examined risk of second solid cancers after allogeneic hematopoietic cell transplantation (AHCT) using reduced-intensity/nonmyeloablative conditioning (RIC/NMC). RIC/NMC recipients with leukemia/myelodysplastic syndrome (MDS) (n = 2833) and lymphoma (n = 1436) between 1995 and 2006 were included. In addition, RIC/NMC recipients 40 to 60 years of age (n = 2138) were compared with patients of the same age receiving myeloablative conditioning (MAC, n = 6428). The cumulative incidence of solid cancers was 3.35% at 10 years. There was no increase in overall cancer risk compared with the general population (leukemia/MDS: standardized incidence ratio [SIR] .99, P = 1.00; lymphoma: SIR .92, P = .75). However, risks were significantly increased in leukemia/MDS patients for cancers of lip (SIR 14.28), tonsil (SIR 8.66), oropharynx (SIR 46.70), bone (SIR 23.53), soft tissue (SIR 12.92), and vulva (SIR 18.55) and skin melanoma (SIR 3.04). Lymphoma patients had significantly higher risks of oropharyngeal cancer (SIR 67.35) and skin melanoma (SIR 3.52). Among RIC/NMC recipients, age >50 years was the only independent risk factor for solid cancers (hazard ratio [HR] 3.02, P < .001). Among patients ages 40 to 60 years, when adjusted for other factors, there was no difference in cancer risks between RIC/NMC and MAC in leukemia/MDS patients (HR .98, P = .905). In lymphoma patients, risks were lower after RIC/NMC (HR .51, P = .047). In conclusion, the overall risks of second solid cancers in RIC/NMC recipients are similar to the general population, although there is an increased risk of cancer at some sites. Studies with longer follow-up are needed to realize the complete risks of solid cancers after RIC/NMC AHCT.

Large Study Shows No Increase in Overall Cancer Risk in Children Born After Assisted Reproductive Technology

Children born after assisted reproductive technology (ART) are at slightly increased risk for prematurity, low birth weight, and congenital malformations, but information about long-term risks for rare but serious diseases is sparse. In a population-based study, investigators linked data on all children born after ART in Britain from 1992 through 2008 with national registry data on …

Cancer complicating systemic lupus erythematosus – a dichotomy emerging from a nested case-control study

ObjectivesWe determined whether any individual cancers are increased or decreased in a cohort of 595 patients with systemic lupus erythematosus (SLE) followed for up to 32 years at the University College London Hospitals Lupus Clinic, looking for any associated clinical or serological factors and the prognosis after cancer diagnosis.MethodsWe undertook a careful retrospective review of the medical records and identified all individuals diagnosed with cancer. For controls, we selected three other patients in the cohort who had not developed cancer, carefully matched for age, sex, ethnicity and disease duration, to determine if any obvious differences emerged in a nested case-control design.ResultsThirty-three patients developed cancer after being diagnosed with SLE. There was a statistically insignificant small increase in overall cancer risk, standardized incidence ratios (SIRs) 1.05 (95% CI 0.52–1.58) and increased SIRs for cervical, prostate, anal and pancreatic cancers and reduction in breast cancer SIRs.Haematological and musculoskeletal manifestations, anticardiolipin and antithyroid globulin antibodies were found to be positively associated with cancer risk in multivariate analysis. There was no drug, dose or duration was associated with cancer risk. There was a reduction in survival with a cancer fatality rate of 84.2% (p < 0.0001).ConclusionWe found a very small but statistically insignificant increased cancer risk with reduction in survival. Whereas some cancers appear to be more common in SLE, notably prostate and cervical cancer, others, particularly breast cancer, are less frequent. Multiple clinical and serological factors are involved in the increased risk of malignancy in SLE. No drug dose or duration effect was identified.

Use of benzodiazepines or benzodiazepine related drugs and the risk of cancer: a population‐based case‐control study

Studies of the carcinogenic potential of benzodiazepines and related drugs (BZRD) have been equivocal. A recent study reported a 35% excess cancer risk among users of hypnotics, including benzodiazepines. Using Danish nationwide registers, we conducted a matched case-control study of the association between BZRD and cancer risk. During 1 January 2002 and 31 December 2009, we identified 152 510 cases with a first time cancer who were matched (1:8) by age and gender to 1,220,317 cancer-free controls. A new-user design was applied by excluding all subjects who had used anxiolytics, hypnotics or sedatives during the first 2 years of available prescription data (1995-6). Odds ratios (ORs) with 95% confidence intervals (CI) were estimated using conditional logistic regression, adjusting for potential confounders. In the primary analysis, long term use of BZRD was defined by a cumulative amount of ≥500 defined daily doses of BZRD within a period of 1 to 5 years prior to the index date. The adjusted OR for cancer associated with BZRD use was 1.09 (95% CI 1.04, 1.14). ORs were close to unity for most cancer sites, except stomach 1.40 (95% CI 1.05, 1.88), oesophagus 1.43 (95% CI 1.01, 2.02), liver 1.81 (95% CI 1.18, 2.80), lung 1.38 (95% CI 1.23, 1.54), pancreas 1.35 (95% CI 1.02, 1.79) and kidney 1.39 (95% CI 1.01, 1.91). For tobacco-related cancers, the OR was 1.15 (95% CI 1.09, 1.22) and for the remaining cancer sites 1.01 (95% CI 0.94, 1.08). Sub-group analyses revealed only small differences between different levels of exposure or different patient subgroups. BZRD use was not associated with an overall increase in cancer risk, except for what is likely explained by minor lifestyle confounding, e.g. smoking.

Synchronous primary neoplasms of the bladder, skin and breast in a male patient: a case report

The incidence of multiple primary malignant neoplasms increases with age, reflecting an increase in overall cancer risk in older patients. Cases of two or more concurrent primary cancers are still rare, although its incidence is increasing. Here, we report the case of a 57-year-old man who was referred to our institution with synchronous squamous cell carcinoma of the skin on the forehead, infiltrating ductal carcinoma of the breast, and transitional cell carcinoma of the urinary bladder. To the best of our knowledge, this is the first reported case in literature of this combination of primary neoplasms.

Drs Kao and Liang Reply

Article AbstractBecause this piece does not have an abstract, we have provided for your benefit the first 3 sentences of the full text.To the Editor: We appreciate the comments of Selaman and colleagues.Our population-based retrospective cohort study unexpectedly found a significant increase in overall cancer risk, as well as some individual cancers. Our findings contradict the previous thinking and lack of theoretical rationale.

A population-based study of DNA repair gene variants in relation to non-melanoma skin cancer as a marker of a cancer-prone phenotype.

For unknown reasons, non-melanoma skin cancer (NMSC) is associated with increased risk of other malignancies. Focusing solely on DNA repair or DNA repair-related genes, this study tested the hypothesis that DNA repair gene variants contribute to the increased cancer risk associated with a personal history of NMSC. From the parent CLUE II cohort study, established in 1989 in Washington County, MD, the study consisted of a cancer-free control group (n 5 2296) compared with three mutually exclusive groups of cancer cases ascertained through 2007: (i) Other (non-NMSC) cancer only (n 5 2349); (ii) NMSC only (n 5 694) and (iii) NMSC plus other cancer (n 5 577). The frequency of minor alleles in 759 DNA repair gene single nucleotide polymorphisms (SNPs) was compared in these four groups. Comparing those with both NMSC and other cancer versus those with no cancer, 10 SNPs had allelic trend P-values <0.01. The two top-ranked SNPs were both within the thymine DNA glycosylase gene (TDG). One was a non-synonymous coding SNP (rs2888805) [per allele odds ratio (OR) 1.40, 95% confidence interval (CI) 1.16-1.70; P-value 5 0.0006] and the other was an intronic SNP in high linkage disequilibrium with rs2888805 (rs4135150). None of the associations had a P-value <6.6310(-5), the threshold for statistical significance after correcting for multiple comparisons. The results pinpoint DNA repair genes most likely to contribute to the NMSC cancer-prone phenotype. A promising lead is genetic variants in TDG, important not only in base excision repair but also in regulating the epigenome and gene expression, which may contribute to the NMSC-associated increase in overall cancer risk.

Abstract 2636: Nonmelanoma skin cancer as a marker of a cancer-prone phenotype: Potential role of DNA repair gene variants

Abstract Purpose: For unknown reasons, nonmelanoma skin cancer (NMSC) is associated with increased risk of other malignancies. This study tested the hypothesis that DNA repair gene variants contribute to the increased cancer risk associated with a personal history of NMSC. Methods: From the parent CLUE II cohort study, established in 1989 in Washington County MD, the study consisted of a cancer-free control group (n=2,296) compared to three mutually exclusive groups of cancer cases ascertained through 2007: 1) Other (non-NMSC) cancer only (n=2,349); 2) NMSC only (n=694); and 3) NMSC plus other cancer (n=577). The frequency of minor alleles in 759 DNA repair single nucleotide polymorphisms (SNPs) was compared in these four groups. Results: Comparing those with both NMSC and other cancer versus those with no cancer, 10 SNPs had additive model p-values&amp;lt;0.01. The two top-ranked SNPs were both within the thymine DNA glycosylase gene (TDG). One was a nonsynonymous coding SNP (rs2888805) (per allele odds ratio (OR) 1.40, 95% confidence interval (CI) 1.16-1.70; p-value=0.0006) and the other was an intronic SNP in high linkage disequilibrium with rs2888805 (rs4135150). Conclusion: The results pinpoint DNA repair genes most likely to contribute to the NMSC cancer-prone phenotype. A promising lead is genetic variants in TDG, important not only in base excision repair but also in regulating the epigenome and gene expression, which may contribute to the NMSC-associated increase in overall cancer risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2636. doi:1538-7445.AM2012-2636

The risk of cancer in people with diabetes and chronic kidney disease

Diabetes and chronic kidney disease (CKD) are both associated with an increased risk of cancer but it is unclear whether diabetes complicated by CKD further augments an individual's cancer risk. The aim of our study was to determine the association of CKD [defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min] with the overall and site-specific risks of incident cancers among individuals with Type 2 diabetes. Cox proportional hazard regression models and competing risk analyses were used to examine the univariate and multivariate adjusted associations between reduced kidney function and the overall and site-specific risks of cancer in participants enrolled in the Action in Diabetes and Vascular disease: Preterax and Diamicron MR controlled evaluation (ADVANCE) trial. Over a median follow-up of 5.0 years, 700 malignant neoplasms occurred in the 11 140 (6.4%) participants. There was no increase in overall cancer risk [adjusted hazard ratio: 1.07 (95% confidence interval: 0.89-1.29, P = 0.50)] or site-specific cancer risk for individuals with CKD (defined as eGFR < 60 mL/min) compared to those without CKD at baseline. These results were robust to multiple methods and thresholds used to estimate CKD. Mild to moderate CKD does not increase the risk of cancer in people with Type 2 diabetes. ADVANCE is registered with ClincalTrial.gov (number NCT00145925).

A cohort study of cancer among sarcoidosis patients

Sarcoidosis is a chronic inflammatory condition that may increase the risk of cancer, but limited information is available on occurrence of cancer in these patients. We compared the incidence of cancer among 2,013 White and 3,755 Black male patients admitted to Veterans hospitals in the United States during 1969-1996 with a diagnosis of sarcoidosis, with that of 2,792,503 White and 662,204 Black nonsarcoidosis patients admitted to the same hospitals. Patients suffering from pulmonary and autoimmune diseases were excluded from the study, as was the first year of follow-up after first admission for sarcoidosis. A total of 241 malignant neoplasms were diagnosed in sarcoidosis patients [relative risk 0.99, 95% confidence interval (CI) 0.87-1.13]. The risks of rectal cancer (relative risk 2.12; 95% CI 1.27-3.52), colon cancer (relative risk 1.55; 95% CI 0.99-2.43) and kidney cancer (relative risk 1.84; 95% CI 1.02-3.33) were increased in sarcoidosis patients when compared with other Veterans hospital patients, whereas the risk of lung cancer was decreased (relative risk 0.60; 95% CI 0.42-0.85). The risk of kidney cancer remained elevated 10 years after first admission. Results were generally consistent among ethnic groups, although the increased risk of colon and kidney cancer was observed only in White patients. These results provide further evidence for an increased risk of specific cancers in patients with sarcoidosis, but do not support any additional increase in overall cancer risk.

Incidence of cancer in children perinatally exposed to nucleoside reverse transcriptase inhibitors

Long-term studies of tolerance to perinatal exposure to antiretroviral nucleoside reverse transcriptase inhibitors are required, in view of the potential genotoxicity of some of these molecules. To evaluate the incidence of cancers in uninfected children born to HIV-infected mothers. Cancers were detected in a nationwide prospective cohort of children born to HIV-infected mothers by standardized questionnaire during the prospective follow-up period of 2 years; thereafter, they were detected by spontaneous pharmacovigilance declaration and by crosschecking data with the national registries of childhood cancer. Standardized incidence ratio for incidence comparisons with general population. Ten cases of cancer were detected among the 9127 exposed HIV-uninfected children (median age: 5.4 years, 53 052 person-years of follow-up). The overall incidence did not differ significantly from that expected for the general population: 10 cases observed versus 8.9 and 9.6 expected depending on whether 1990-1999 or 2000-2004 national rates were used as reference [standardized incidence ratio of 1.1 (0.3-1.5) and 1.0 (0.5-1.9)]. Five cases of central nervous system cancer were observed (standardized incidence ratio of 3.1 [1.0-7.2] P = 0.05 and 2.4 [0.8-5.6], P = 0.12). The relative risk of cancer for children exposed to didanosine-lamivudine combination was higher than that for zidovudine monotherapy [hazard ratio: 13.6 (2.5-73.9)]. This study did not evidence an overall increase in cancer risk in nucleoside reverse transcriptase inhibitor exposed children until 5 years of age. Results suggesting associations with specific nucleoside reverse transcriptase inhibitor combinations need further investigations. A longer surveillance, including differential analysis of the different cancer sites and various nucleoside reverse transcriptase inhibitors administered is warranted.

Periodontal diseases and cancer

Chronic periodontitis and aggressive periodontitis are inflammatory forms of periodontal disease (figure) caused by microorganisms from plaque biofilm that forms around the teeth. Chronic inflammation of the periodontium results in continuous release of cytokines, prostaglandins, bacterial toxins, and many other destructive enzymes from cells in the area. This chronic process leads to formation of periodontal pockets and progressive destruction of connective tissue and alveolar bone. 1 Pihlstrom B Michalowicz B Johnson N Periodontal diseases. Lancet. 2005; 366: 1809-1820 Summary Full Text Full Text PDF PubMed Scopus (2535) Google Scholar Chronic periodontitis and aggressive periodontitis are the most common causes of tooth loss in adults. Many studies have shown an association between periodontal diseases and systemic manifestations of cardiovascular disease, diabetes, and premature low-weight birth. 1 Pihlstrom B Michalowicz B Johnson N Periodontal diseases. Lancet. 2005; 366: 1809-1820 Summary Full Text Full Text PDF PubMed Scopus (2535) Google Scholar However, there is no evidence for a causal effect. A recent study assessed periodontitis and premature death in young adults in urban regions of Sweden. 2 Söder B Jin L Klinge B Söder P Periodontitis and premature death: a 16-year longitudinal study in a Swedish urban population. J Periodontal Res. 2007; 42: 361-366 Crossref PubMed Scopus (49) Google Scholar The findings showed that young individuals with periodontitis and missing molar teeth, compared with those with no periodontitis, had increased risk of premature death because of cancer, circulatory, and digestive diseases. In this issue of The Lancet Oncology, Michaud and colleagues 3 Michaud DS Liu Y Meyer M Giovannucci E Joshipura K Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study. Lancet Oncol. 2008; 9: 550-558 Summary Full Text Full Text PDF PubMed Scopus (261) Google Scholar present important data from a prospective study that shows an increase in cancer risk in a large population of well-characterised US male health professionals who self-reported having periodontal disease with alveolar bone loss. Their findings showed a significant association between periodontal disease and haematological, kidney, and pancreatic cancer. The cancer risk persisted in individuals who never smoked. In a previous study, 4 Michaud D Joshipura K Giovannucci E Fuchs C A prospective study of periodontal disease and pancreatic cancer in US male health professionals. J Natl Cancer Inst. 2007; 99: 171-175 Crossref PubMed Scopus (205) Google Scholar Michaud and co-workers suggested an association between periodontal disease and pancreatic cancer in the same population of health professionals. They concluded that plausible biological mechanisms, such as systemic inflammation or increased concentrations of carcinogenic compounds (or both) as a result of bacteria in the oral cavity of those with periodontal disease, could be involved in the development of cancer. Furthermore, a recent case–control study suggested that chronic periodontitis is associated with increased risk of developing tongue cancer. 5 Tezal M Sullivan M Reid M et al. Chronic periodontitis and the risk of tongue cancer. Arch Otolaryngol Head Neck Surg. 2007; 133: 450-454 Crossref PubMed Scopus (130) Google Scholar However, other researchers believe that the association between periodontal disease and cancer might be spurious. 6 Hujoel P Drangsholt M Spiekerman C Weiss N An exploration of the periodontitis-cancer association. Ann Epidemiol. 2003; 13: 312-316 Summary Full Text Full Text PDF PubMed Scopus (192) Google Scholar Therefore, future studies that assess in more detail potential mechanisms for the association between periodontal diseases and cancer are warranted. (A) Diagnosis should include clinical presentation, periodontal pocket probings, and radiographical assessment of bone levels. Note that the gingival tissues are red and swollen, and the level of the gingival margins is irregular. (B) Radiograph of top teeth shows only the tips of the roots inserted in alveolar bone (arrow). Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort studyPeriodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk. Full-Text PDF