食管癌、贲门癌易感性与白细胞介素10基因启动子区多态性

目的研究白细胞介素10(IL-10)基因启动子区G-1082A和C-592A单核苷酸多态性(SNP)与高发区涉县人群食管鳞状细胞癌(ESCC)和贲门腺癌(GCA)易感性的关系。方法采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测了涉县203例ESCC、152例GCA患者和443例健康对照个体IL-10G-1082A和C-592A SNP的基因型,比较各组间等位基因及基因型频率的分布。结果吸烟与ESCC和GCA的风险性经年龄和性别校正OR(95%CI)值分别为1.88(1.29~2.74)和2.89(1.86~4.48),上消化道肿瘤家族史与ESCC和GCA的风险性经年龄和性别校正OR(95%CI)值分别为1.84(1.28~2.66)和2.92(1.89~4.53),二者均显著增加患ESCC和GCA的风险性。ESCC、GCA患者IL-10G-1082A和C-592ASNP的基因型及等位基因频率分布与健康对照组相比无显著性差异(均P>0.05)。在IL-10-1082位点中,相对于A/A基因型,A/G和G/G基因型相加并没有增加ESCC和GCA的发病风险,经年龄和性别校正OR(95%CI)值分别为1.05(0.53~1.73)和1.22(0.44~2.01)。在IL-10-592位点中,相对于A/A基因型,A/C和C/C基因型相加也没有增加ESCC和GCA的发病风险,经年龄和性别校正OR(95%CI)值分别为1.13(0.95~1.35)和1.04(0.71~1.54)。两多态性位点联合分析显示,ESCC、GCA患者与健康对照组的单体型分布也无显著性差异(均P>0.05)。结论本研究未发现IL-10基因启动子区G-1082A及C-592A多态性与涉县人群ESCC和GCA的易感性有关。     

Nucleotide variation in IL‐10 and IL‐12 and their receptors and cervical and vulvar cancer risk: A hybrid case–parent triad and case–control study

Given the important role of cell mediated immunity in viral clearance and control of premalignant lesions, we hypothesize that variation in the IL‐12/IL‐10 cytokine and cytokine receptor genes may influence cervical and vulvar cancer risk. We evaluated 76 tagSNPs from seven candidate genes (IL-10, IL-12A, IL-12B, IL-10RA, IL-10RB, IL-12RB1, and IL12RB2) in case–parent sets (n=43 cervical squamous cell carcinoma (SCC), n=96 cervical adenocarcinoma, n=53 vulvar SCC), additional cases (n=356 cervical SCC, n=406 cervical adenocarcinoma, and n=473 vulvar SCC) and population based controls (1,111). We calculated log‐additive odds ratios (ORs) and 95% confidence intervals (CIs) for the association between tagSNP and cancer risk using a pseudo‐likelihood based method which combined genotype information on cases, parents, and population controls. After correction for multiple comparisons, we identified several statistically significant SNP associations. Cervical SCC risk was associated with the minor alleles of the IL10RA rs9610 3’ UTR SNP (OR=1.76, 95% CI=1.15–2.68) and two synonymous IL12RB2 SNPs (rs4297265, OR=0.46, 95% CI=0.26–0.82; rs2229546, OR=0.43, 95% CI=0.21–0.87). Cervical adenocarcinoma risk was associated with the minor alleles of the IL10RA rs4252314 intronic SNP (OR=2.23, 95% CI=1.26–3.96) and IL12RB1 rs11575934 non‐synonymous SNP (OR=1.51, 95% CI=1.12–2.05). Finally, the minor allele of the IL12B rs3181224 3’ UTR SNP was associated with a reduced risk of vulvar SCC (OR=0.30, 95% CI=0.12–0.74). These results raise the possibility that a shift in the balance of the immune response due to genetic variants in key cytokine genes could influence the development of cervical and vulvar cancer.     

IL6, aspirin, nonsteroidal anti-inflammatory drugs, and breast cancer risk in women living in the southwestern United States.

Interleukin-6 is a cytokine thought to be involved in inflammation, insulin, and estrogen-related pathways. We evaluate genetic variation in the IL6 gene with risk of breast cancer. We also evaluate breast cancer associations with aspirin and nonsteroidal anti-inflammatory drugs. A breast cancer case-control study (n = 1,527 non-Hispanic white cases, 1,601 non-Hispanic white controls, 798 Hispanic/Native American cases, and 924 Hispanic/Native American controls) was conducted among women living in the southwestern United States (4-Corner's Breast Cancer Study). Five IL6 single nucleotide polymorphisms (SNP) and IL6 haplotypes based on these SNPs were evaluated. Allele frequencies were significantly different between non-Hispanic white and Hispanic/Native American women. Among postmenopausal women not recently exposed to hormones, the AG/GG genotypes of rs1800797 (-596A>G) and the GC/CC genotypes of rs1800795 (-174G>C) significantly reduced risk of breast cancer among non-Hispanic white women [odds ratio (OR), 0.69; 95% confidence interval (95% CI), 0.48-1.00 and OR, 0.68; 95% CI, 0.47-0.99, respectively] and Hispanic/Native American women (OR, 0.48; 95% CI, 0.28-0.83 and OR, 0.44; 95% CI, 0.26-0.99, respectively). Haplotypes of the five IL6 SNPs further defined these associations. Recent aspirin use significantly decreased risk of breast cancer among postmenopausal Hispanic/Native American women not recently exposed to hormones (OR, 0.56; 95% CI, 0.33-0.96). Among non-Hispanic white, the inverse association with aspirin was not statistically significant. IL6 genotype and haplotype significantly modified the association between aspirin and breast cancer, with the greatest effect modification being among women not recently exposed to hormones [P interaction = 0.06 (for non-Hispanic white) and 0.04 (for Hispanic/Native American) and SNP rs1800796 or -572G>C]. These data suggest that IL6 is associated with breast cancer risk and modifies the association between estrogen and aspirin and breast cancer risk.     

Interleukin-1beta gene in esophageal, gastric and colorectal carcinomas

Interleukin (IL)-1 gene polymorphisms are associated with development of gastric atrophy and with increased risk of gastric carcinoma. A -31C to T base transition in the promoter region of this gene is involved in carcinogenic changes within the stomach, especially in Helicobacter pylori infected individuals. We examined association between IL-1 locus polymorphisms and risk of esophageal, gastric and colorectal carcinomas in Japanese patients with H. pylori infection. IL-1B and IL-1RN polymorphisms were analyzed in 136 controls, 75 patients with esophageal carcinoma, 186 patients with gastric carcinoma, 69 patients with colorectal carcinoma, and 18 patients with ulcerative colitis (UC). For IL-1B-511 and -31 polymorphisms were determined by fluorescence-based polymerase chain reaction single-strand conformation polymorphism analysis. For IL-1 receptor antagonist gene (IL-1RN), penta-allelic variable number of tandem repeats (VNTR) was determined by PCR-standard agarose gel electrophoresis. For gastric carcinoma, IL-1B-511 heterozygotes (OR, 0.48; 95% CI, 0.3-0.9; p=0.0115) and T carriers (OR, 0.52; 95% CI, 0.3-1.0; p=0.0185) had a significantly reduced risk of carcinoma. For colorectal carcinoma, IL-1B-511 heterozygotes (OR, 0.34; 95% CI, 0.2-0.7; p=0.0028) and T carriers (OR, 0.43; 95% CI, 0.2-0.9; p=0.0015) had a significantly low risk of carcinoma. No significant difference was observed in the frequencies of IL-1B-31C/T and IL-1RN genotypes between controls and the esophageal carcinoma patients. Our results shows that IL-1B-511C/T and T carrier state may indicate less risk for gastric and colorectal carcinoma in the Japanese population.     

Obesity, adipokines, and prostate cancer in a prospective population-based study.

BACKGROUND: The purpose of this investigation was to examine the association of obesity and the adipokines leptin, adiponectin, and interleukin-6 (IL-6) with prostate cancer risk and aggressiveness. METHODS: One hundred twenty-five incident prostate cancer cases and 125 age-matched controls were sampled from among participants in the original San Antonio Center for Biomarkers of Risk of Prostate Cancer cohort study. The odds ratios (OR) of prostate cancer and high-grade disease (Gleason sum >7) associated with the WHO categories of body mass index (kg/m(2)) and with tertiles of serum concentrations of adiponectin, leptin, and IL-6 were estimated using multivariable conditional logistic regression models. RESULTS: Body mass index was not associated with either incident prostate cancer [obese versus normal; OR, 0.75; 95% confidence interval (95% CI), 0.38-1.48; P(trend) = 0.27] or high-grade versus low-grade disease (OR, 1.17; 95% CI, 0.39-3.52; P(trend) = 0.62). Moreover, none of the three adipokines was statistically significant associated with prostate cancer risk or high-grade disease, respectively: leptin (highest versus lowest tertile; OR, 0.77; 95% CI, 0.28-1.37; P(trend) = 0.57; OR, 1.20; 95% CI, 0.48-3.01; P(trend) = 0.85); adiponectin (OR, 0.87; 95% CI, 0.46-1.65; P(trend) = 0.24; OR, 1.93; 95% CI, 0.74-5.10; P(trend) = 0.85); IL-6 (OR, 0.84; 95% CI, 0.46-1.53; P(trend) = 0.98; OR, 0.84; 95% CI, 0.30-2.33; P(trend) = 0.17). CONCLUSIONS: Findings from this nested case-control study of men routinely screened for prostate cancer and who had a high prevalence of overweight and obesity do not provide evidence to support that prediagnostic obesity or factors elaborated by fat cells strongly influence prostate cancer risk or aggressiveness. However, due to the small sample population, a small or modest effect of obesity and adipokines on these outcomes cannot be excluded.     

The MDM2 promoter SNP285C/309G haplotype diminishes Sp1 transcription factor binding and reduces risk for breast and ovarian cancer in Caucasians

MDM2 plays a key role in modulating p53 function. The MDM2 SNP309T > G promoter polymorphism enhances Sp1 binding and has been linked to cancer risk and young age at diagnosis although with conflicting evidence. We report a second MDM2 promoter polymorphism, SNP285G > C, residing on the SNP309G allele. SNP285C occurs in Caucasians only, where 7.7% (95% CI 7.6%-7.8%) of healthy individuals carry the SNP285C/309G haplotype. In?vitro analyses reveals that SNP309G enhances but SNP285C strongly reduces Sp1 promoter binding. Comparing MDM2 promoter status among different cohorts of ovarian (n?= 1993) and breast (n?= 1973) cancer patients versus healthy controls (n?= 3646), SNP285C reduced the risk of both ovarian (OR 0.74; CI 0.58-0.94) and breast cancer (OR 0.79; CI 0.62-1.00) among SNP309G carriers.     

Diet, vegetarian food and prostate carcinoma among men in Taiwan

In a case-control study in a veterans hospital in Taiwan, we compared 237 histology-confirmed prostate carcinoma cases with 481 controls, frequency matched by age, for their consumption of vegetarian food, namely soybean products, rice, wheat protein and other vegetables. The multivariable logistic regression analysis showed a significant association with such food (odds ratio (OR)=0.67, 95% confidence interval (CI)=0.47, 0.94). This beneficial effect presented for men with body mass index (BMI) < or =25 kg m(-2) (OR=0.50, 95% CI=0.32, 0.76) but not for men with greater BMI. The OR of prostate carcinoma for men with BMI < or =25 kg m(-2) was 1.74 (95% CI=1.21, 2.51), compared with men with higher BMI (>25 kg m(-2)). Other significant risk factors associated with the disease included higher income (OR=2.40, 95% CI=1.07, 5.42), physical activity (OR=1.75, 95% CI=1.08, 2.83), being married (OR=2.49, 95% CI=1.40, 4.43) and coffee consumption (OR=1.88, 95% CI=1.07, 3.30). Stratified analysis also showed that the consumption of fish/shellfish had an adverse association for men with higher BMI. This study suggests that the intake of the low fat local vegetarian food has a protective effect against prostate carcinoma for thin men in this study population.     

Plasma carotenoid, alpha-tocopherol and retinol concentrations and risk of colorectal adenomas: A case-control study in Japan

To investigate associations between plasma carotenoids, alpha-tocopherol and retinol with colorectal adenomas risk, we measured concentrations in 224 asymptomatic colorectal adenoma cases and 230 population-based controls matched for age and sex. After adjustment for age, history of colorectal adenomas and cancers, BMI, smoking, drinking status, multivitamin consumption and plasma total cholesterol, the risk of colorectal adenomas in the highest quartile was approximately half of that of men in the lowest quartile for alpha-carotene (OR=0.38; 95% CI: 0.18-0.84; P(trend)=0.01), beta-carotene (OR=0.51; 95% CI: 0.24-1.07; P(trend)=0.03) and total carotenoids (OR=0.48; 95% CI: 0.22-1.03; P(trend)=0.04). In addition, a protective association for alpha-carotene in women was also indicated, but which did not reach statistical significance (OR=0.53; 95% CI: 0.19-1.52; P(trend)=0.35). Our findings suggest a protective effect of carotenoids against the development of colorectal adenomas.     

Association study of prostate cancer susceptibility variants with risks of invasive ovarian, breast, and colorectal cancer

Several prostate cancer susceptibility loci have recently been identified by genome-wide association studies. These loci are candidates for susceptibility to other epithelial cancers. The aim of this study was to test these tag single nucleotide polymorphisms (SNP) for association with invasive ovarian, colorectal, and breast cancer. Twelve prostate cancer-associated tag SNPs were genotyped in ovarian (2,087 cases/3,491 controls), colorectal (2,148 cases/2,265 controls) and breast (first set, 4,339 cases/4,552 controls; second set, 3,800 cases/3,995 controls) case-control studies. The primary test of association was a comparison of genotype frequencies between cases and controls, and a test for trend stratified by study where appropriate. Genotype-specific odds ratios (OR) were estimated by logistic regression. SNP rs2660753 (chromosome 3p12) showed evidence of association with ovarian cancer [per minor allele OR, 1.19; 95% confidence interval (95% CI), 1.04-1.37; P(trend) = 0.012]. This association was stronger for the serous histologic subtype (OR, 1.29; 95% CI, 1.09-1.53; P = 0.003). SNP rs7931342 (chromosome 11q13) showed some evidence of association with breast cancer (per minor allele OR, 0.95; 95% CI, 0.91-0.99; P(trend) = 0.028). This association was somewhat stronger for estrogen receptor-positive tumors (OR, 0.92; 95% CI, 0.87-0.98; P = 0.011). None of these tag SNPs were associated with risk of colorectal cancer. In conclusion, loci associated with risk of prostate cancer may also be associated with ovarian and breast cancer susceptibility. However, the effects are modest and warrant replication in larger studies.     

MDM2 SNP309 and cancer risk: a combined analysis

A paper by Bond et al. reported that a single-nucleotide polymorphism (SNP) in the intronic promoter region of the mouse double minute 2 (MDM2) gene (called SNP309) can significantly change the expression of MDM2 and thereby suppress the p53 pathway. Furthermore, it was shown that SNP309 accelerates tumor formation in Li-Fraumeni patients. This initial report aroused the attention of many researchers, which investigated the role of SNP309 for the risk and the onset of cancer in different tissues. To provide a more robust estimate of the effect of this polymorphism on cancer risk, we combined the available genotype data for breast, colorectal and lung cancers. For breast cancer, we combined the data from 11 studies including 5737 cases and 6703 controls. For colorectal cancer, we combined the data from five studies with 1620 cases and 886 controls. For lung cancer, we performed a fixed-effect meta-analysis from seven studies including 4276 cases and 5318 controls. Our results suggest that the SNP309 variant does not have an impact on the risk of breast [odds ratio (OR) = 0.97, 95% confidence interval (CI) = 0.87-1.08] or colorectal cancers (OR = 0.97, 95% CI = 0.76-1.25). However, the combined estimate of the ORs for lung cancer revealed an increased risk for GG versus TT (OR = 1.27, 95% CI = 1.12-1.44). The data show that SNP309 alone has little or no effect on the risk of common cancers, but it might modify the time of tumor onset and prognosis.     

Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study.

The association between plasma carotenoids and prostate cancer risk was investigated in a case-control study nested within the prospective Health Professionals Follow-up Study. We matched 450 incident prostate cancer cases diagnosed from 1993-1998 to 450 controls by age, time, month, and year of blood donation. Modest inverse, but not statistically significant, associations were observed among plasma alpha-carotene, beta-carotene, and lycopene concentrations, and overall risk of prostate cancer diagnosis [odds ratio (highest versus lowest quintile; OR), alpha-carotene: OR, 0.67 [95% confidence interval (CI), -0.40-1.09]; beta-carotene: OR, 0.78 (95% CI, 0.48-1.25); lycopene: OR, 0.66 (95% CI, 0.38-1.13)]. The inverse association between plasma lycopene concentrations and prostate cancer risk was limited to participants who were 65 years or older (OR, 0.47; 95% CI, 0.23-0.98) and without a family history of prostate cancer (OR, 0.48; 95% CI, 0.26-0.89). Combining, older age and a negative family history provided similar results (OR, 0.43; 95% CI, 0.18-1.02). Inverse associations between beta-carotene and prostate cancer risk were also found among younger participants (<65 years of age; OR, 0.36; 95% CI, 0.14-0.91; P(trend) = 0.03). Combining dietary intake and plasma data confirmed our results. We found a statistically significant inverse association between higher plasma lycopene concentrations and lower risk of prostate cancer, which was restricted to older participants and those without a family history of prostate cancer. This observation suggests that tomato products may exhibit more potent protection against sporadic prostate cancer rather than those with a stronger familial or hereditary component. In addition, our findings also suggest that among younger men, diets rich in beta-carotene may also play a protective role in prostate carcinogenesis.     

Family history of cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium

Alcohol and tobacco consumption are well-recognized risk factors for head and neck cancer (HNC). Evidence suggests that genetic predisposition may also play a role. Only a few epidemiologic studies, however, have considered the relation between HNC risk and family history of HNC and other cancers. We pooled individual-level data across 12 case-control studies including 8,967 HNC cases and 13,627 controls. We obtained pooled odds ratios (OR) using fixed and random effect models and adjusting for potential confounding factors. All statistical tests were two-sided. A family history of HNC in first-degree relatives increased the risk of HNC (OR=1.7, 95% confidence interval, CI, 1.2-2.3). The risk was higher when the affected relative was a sibling (OR=2.2, 95% CI 1.6-3.1) rather than a parent (OR=1.5, 95% CI 1.1-1.8) and for more distal HNC anatomic sites (hypopharynx and larynx). The risk was also higher, or limited to, in subjects exposed to tobacco. The OR rose to 7.2 (95% CI 5.5-9.5) among subjects with family history, who were alcohol and tobacco users. A weak but significant association (OR=1.1, 95% CI 1.0-1.2) emerged for family history of other tobacco-related neoplasms, particularly with laryngeal cancer (OR=1.3, 95% CI 1.1-1.5). No association was observed for family history of nontobacco-related neoplasms and the risk of HNC (OR=1.0, 95% CI 0.9-1.1). Familial factors play a role in the etiology of HNC. In both subjects with and without family history of HNC, avoidance of tobacco and alcohol exposure may be the best way to avoid HNC.     

Interleukin-18 gene promoter polymorphisms and the risk of esophageal squamous cell carcinoma

Background. Esophageal squamous cell carcinoma (ESCC) is multifactorial, and the genetic background may be a crucial etiologic factor. Interleukin-18 (IL-18) is a multifunctional cytokine that induces interferon (IFN)-gamma secretion and plays an important role in antitumor immunity. Variations in the DNA sequence in the IL-18 gene promoter may lead to altered IL-18 production and/or activity, and so this can modulate an individual's susceptibility to ESCC. To test this hypothesis, we investigated the relationship of IL-18 gene promoter -137 G/C and -607 C/A polymorphisms and their haplotypes with the risk of ESCC in a Chinese population. Methods. Two hundred and thirty five patients with ESCC and 250 age- and sex-matched controls, using sequence specific primers-polymerase chain reaction (PCR-SSP). Results. Two polymorphisms, -137 G/C and -607 C/A were in strong linkage disequilibrium (LD). There were significantly differences in the genotype and allele distribution of -137 G/C polymorphism of the IL-18 gene among cases and controls. The -137 GC and CC genotypes were associated with a significantly increased risk of ESCC as compared with the -137 GG genotypes (OR = 1.91, 95% CI, 1.29-2.82, p = 0.001 and OR = 2.95, 95% CI, 1.23-7.04, p = 0.012, respectively). Consistent with the results of the genotyping analyses, the -137 C/ - 607 A haplotype was associated with a significantly increased risk of ESCC as compared with the -137G/ - 607 C haplotype (OR = 1.61; 95% CI, 1.16-2.23; p = 0.004). Conclusion. This study shows for the first time an association between IL-18 gene promoter -137 G/C polymorphism may contribute represent a genetic risk factor for ESCC in a Chinese population.     

Cancer in first-degree relatives and risk of glioma in adults.

Relatively few studies have examined glioma risk in relation to history of cancer in first-degree relatives. We sought to describe such risks in a large hospital-based case-control study. Histologically confirmed incident adult glioma cases (n = 489) were identified at three regional referral hospitals between June 1994 and August 1998. Controls (n = 799) admitted to the same hospitals for nonmalignant conditions were frequency-matched on age, sex, race/ethnicity, hospital, and proximity of residence to hospital. Participants received a personal interview, including questions regarding cancer in family members. Odds ratios (ORs) were calculated to estimate the risk of glioma associated with a history of cancer in a first-degree relative using conditional logistic regression and compared with standardized incidence ratios among relatives of cases versus relatives of controls. Among participants reporting a family history of a brain cancer or a brain tumor, risk of glioma was 1.6 [95% confidence interval (CI), 0.5-5.3; n = 5] and 3.0 (95% CI, 0.9-10.8; n = 7), respectively, in comparison with those without such family histories. Participants who had a family history of stomach (OR, 2.2; 95% CI, 1.0-4.6), colon (OR, 1.4; 95% CI, 0.9-2.2), or prostate cancer (OR, 2.1; 95% CI, 1.1-3.8) or Hodgkin disease (OR, 2.4; 95% CI, 0.9-6.3) had an increased glioma risk. OR estimates were similar to the ratios of standardized incidence ratios for cancer in relatives of cases versus controls. Shared environmental or genetic factors in families may influence glioma risk. Our findings suggest that individuals with a family history of specific cancers other than glioma may have an increased glioma risk.     

Dietary fish intake and risk of leukaemia, multiple myeloma, and non-Hodgkin lymphoma.

This study aimed to determine whether fish intake was protective against leukemia, multiple myeloma, and non-Hodgkin lymphoma (NHL), and if our previous finding of a protective effect of fish-related occupations on the risk of these diseases was due to dietary intake of fish. We used data from a population-based case-control study undertaken in Canada in 1994-1998. Dietary information was available for 919 leukemia cases, 287 myeloma cases, 1418 NHL cases, and 4202 controls. The risk of each of the three cancers was determined using multiple logistic regression analysis according to quartiles of weekly fresh fish intake, percentage of total energy intake from fresh fish, and percentage of total fat intake from fresh fish. After adjusting for age, sex, smoking, BMI, and proxy status, people who consumed greater proportions of their total energy intake from fresh fish had a significantly lower risk of each of the three types of cancer, and there was a significant dose-response for risk of leukemia and NHL. Those in the highest quartile for percentage of fat intake from fish were at lowest risk: leukemia odds ratio (OR) 0.72, 95% confidence interval (CI) 0.58-0.89; multiple myeloma OR 0.64, 95% CI 0.45-0.90; NHL OR 0.71, 95% CI 0.60-0.85; and all LH cancers combined OR 0.70, 95% CI 0.61-0.81. The protective effect previously observed for working with fish on the risk of leukemia and lymphoma was independent of fish intake. These findings suggest that a diet high in fish may be protective against lymphohematopoietic cancers and confirm the reduced risk among fish workers.     

Pediatric Plasma Cell Neoplasms: A Population-Based Study

IntroductionPlasma cell neoplasms are exceptionally rare in the pediatric population; the demographic characteristics and the clinical outcomes of plasma cell neoplasms in this population are currently poorly understood. The aim of this study was to provide a comprehensive analysis of pediatric plasma cell neoplasms, based on the United-States Surveillance, Epidemiology, and End Results (SEER) program registries.Materials and MethodsAll pediatric patients (aged less than 20 years) diagnosed with a malignant plasma cell neoplasm were retrieved from the SEER Program database (18 registries), collecting patient records between 2000 and 2018. The plasma cell neoplasm type, sex, age at diagnosis, year of diagnosis, race and origin, primary disease site, follow-up duration, and vital status at the last known contact were retrieved and analyzed.ResultsThe age-adjusted incidence rate of plasma cell neoplasms for 1,000,000 person-years was 0.06 for the pediatric population (compared with 90.6 for the adult population). The types of pediatric plasma cell neoplasms predominantly consisted of plasmacytomas, with 11 solitary extraosseous plasmacytoma (42.3%) and 7 solitary bone plasmacytoma (26.9%), while plasma cell myelomas represented only a minority of the neoplasms (8 patients; 30.8%). Most plasmacytomas were localized in the head and neck region. Hispanic patients represented 50% of the pediatric plasma cell neoplasm cases (but only 11.1% of adult cases, P < .01). Female-to-Male ratio was 1.36. Five-year overall survival rates were 88.2% (95% confidence interval [95% CI]: 74.2%-100%) for pediatric plasmacytoma and 36.5% (95% CI: 12.4%-100%) for pediatric plasma cell myeloma (P = .013).ConclusionThis first population-based study of pediatric plasma cell neoplasms underlines the rarity of this entity and demonstrates its unique characteristics, including the significant predominance of plasmacytomas, of female patients, and of patients from hispanic origin, and the poor clinical outcomes of pediatric plasma cell myeloma patients.     

Physical inactivity,energy intake,obesity and the risk of rectal cancer in Canada

We conducted a population-based case-control study of 1,447 incident rectal cancer cases and 3,106 population controls aged 20-76 years to assess the effect of recreational physical activity, energy intake and obesity on rectal cancer risk in 7 of 10 Canadian provinces in 1994-97. After adjustment for the effect of various potential confounding factors, total recreational physical activity in the highest quartile was associated with an odds ratio (OR) for rectal cancer risk of 0.88 (95% confidence interval [CI] = 0.64-1.20) in women and 1.15 (95% CI = 0.88-1.49) in men. Women and men in the highest quartile of caloric intake (> = 56,741 and > = 63,143 kJ/week) had ORs of 1.50 (95% CI = 1.00-2.25) and 1.61 (95% CI = 1.13-2.28), respectively. Total dietary fat intake was not associated with a risk of rectal cancer after adjustment for caloric intake. Obesity (BMI > = 30 kg/m(2)) was associated with an OR of 1.44 (95% CI = 1.06-1.95) for women and 1.78 (95% CI = 1.36-2.34) for men. Men and women with lifetime maximum body mass index (BMI) > = 30 kg/m(2) had respective ORs of 1.70 (95% CI = 1.30-2.23) and 1.26 (95% CI = 0.96-1.66). The greatest increase in rectal cancer risk was observed in men and women with simultaneous high energy intake, high BMI and low physical activity. Our study provides evidence that physical inactivity, high energy intake and obesity are associated with the risk of rectal cancer, and there is a probable synergic effect among the 3 risk factors.     

Association of markers of insulin and glucose control with subsequent colorectal cancer risk.

We evaluated the association of plasma insulin and other markers of insulin and glucose control with subsequent colorectal cancer. Incident colon (n = 132) and rectal (n = 41) cancer cases and matched controls (n = 346) were identified between baseline in 1989 and 2000 among participants in a community-based cohort in Washington County, Maryland. Circulating markers of insulin and glucose control were measured in baseline blood samples. Body mass index (BMI) and use of medications to treat diabetes mellitus were self-reported at baseline. Conditional logistic regression was used to estimate matched odds ratios (ORs). Compared with the lowest fourth, participants with insulin concentrations in the highest fourth were not at an increased risk of colorectal cancer [OR, 0.78; 95% confidence interval (CI), 0.45-1.35; P(trend) = 0.24]. Similarly, no associations were observed for the ratio of total cholesterol:HDL-cholesterol, triglycerides, and insulin-like growth factor binding protein 1. However, those in the highest fourth of glycosylated hemoglobin (HbA(1c)) level had a slightly increased risk of colorectal cancer (OR, 1.57; 95% CI, 0.94-2.60; P(trend) = 0.02). The OR of colorectal cancer was 1.70 (95% CI, 1.01-2.86; P(trend) = 0.08) comparing BMI >/=30 kg/m(2) to <25 kg/m(2). The OR of colorectal cancer was 2.43 (95% CI, 1.10-5.38) for the use of medications to treat diabetes. The associations of higher HbA(1c), higher BMI, and the use of medications to treat diabetes, with colorectal cancer lend support to the hypothesis that perturbations in insulin and glucose control may influence colorectal carcinogenesis. It is possible that HbA(1c), BMI, and the use of medications to treat diabetes, as a surrogate for protracted or severe type 2 diabetes mellitus, may have been better time-averaged indicators of hyperinsulinemia and hyperglycemia than the plasma markers that were measured once prediagnostically in a nonfasting population.