NOD1 and NOD2 Genetic Variants in Association with Risk of Gastric Cancer and Its Precursors in a Chinese Population

BackgroundGenetic variants of nucleotide-binding oligomerization domain-containing protein (NOD) may influence the outcome of Helicobacter pylori (H. pylori) infection and gastric carcinogenesis. To explore genetic variants of NOD1 and NOD2 in association with gastric cancer (GC) and its precursors, a population-based study was conducted in Linqu County, China.MethodsTagSNPs of NOD1 and NOD2 were genotyped by Sequenom MASS array in 132 GCs, and 1,198 subjects with precancerous gastric lesions, and were correlated with evolution of gastric lesions in 766 subjects with follow-up data.ResultsAmong seven tagSNPs, NOD1 rs2709800 and NOD2 rs718226 were associated with gastric lesions. NOD1 rs2709800 TG genotype carriers had a decreased risk of intestinal metaplasia (IM, OR: 0.53; 95% CI: 0.31–0.92), while NOD2 rs718226 G allele (AG/GG) showed increased risks of dysplasia (DYS, OR: 2.96; 95% CI: 1.86–4.71) and GC (OR: 2.35; 95% CI: 1.24–4.46). Moreover, an additive interaction between rs718226 and H. pylori was found in DYS or GC with synergy index of 3.08 (95% CI: 1.38–6.87) or 3.99 (95% CI: 1.55–10.22), respectively. The follow-up data indicated that NOD2 rs2111235 C allele (OR: 0.52; 95% CI: 0.32–0.83) and rs7205423 G allele (OR: 0.56; 95% CI: 0.35–0.89) were associated with decreased risk of progression in H. pylori-infected subjects.ConclusionsNOD1 rs2709800, NOD2 rs718226, rs2111235, rs7205423 and interaction between rs718226 and H. pylori infection may be related to risk of gastric lesions.     

Lack of Association between IL-6 Polymorphisms and Haplotypes with Gastric Cancer

The process of combating neoplasms and mononuclear cells, and during H. pylori infection, several pro-inflammatory and anti-inflammatory cytokines are synthesized. In view of the involvement of the IL-6 law and the presence of H. pylori in the development of gastric diseases, the present study aimed to characterize the promoter-region polymorphism −597 (G/A) (rs1800797), −572 (C/G) (rs1800796), and −174 (G/C) (rs1800795) by PCR-RFLP in 375 gastric biopsy specimens from patients with peptic symptoms. A total of 375 samples were analyzed: 87 patients (without lesion without gastric tissue); 236 patients with gastritis and 52 patients with gastric cancer analyzed the PCR-RFLP techniques. All the results were normalized in relation to the presence of H. pylori. The frequencies of the three polymorphisms were compared in the Control vs Gastritis groups and a statistically significant test observed: −174 (G/C) (OR: 1.27; 95% CI: 0.84–1.93; P = 0.26), 572 (C/G) (OR: 1.42; 95% CI: 0.78–2.59; P = 0.25), and 597 (G/A) (OR: 0.98; 95% CI, 0.64–1.52; P = 0.94). Similar results were obtained when the gastric cancer group was compared to the control group: −174 (G/C) (OR: 1.27; 95% CI: 0.66–2.47; P = 0.47), −572 (C/G) (OR: 1.07; 95% CI: 0.43–2.68; P = 0.88), and −597 (G/A) (OR: 1.01; 95% CI, 0.5–0.9; P = 0.99). The haplotypes were and were not observed statistically significant differences. In conclusion, we found no correlations between any of the three polymorphisms in the IL-6 gene analyzed in this study and a higher risk of gastritis or gastric cancer.     

Prognostic and clinical significance of focal adhesion kinase expression in breast cancer: A systematic review and meta-analysis

BackgroundThe prognostic significance of focal adhesion kinase (FAK) in breast cancer remains controversial. Here, we conducted a meta-analysis to explore the prognostic value of FAK expression in breast cancer.Materials and methodsPossible prognostic significance of protein or mRNA expression of FAK in breast cancer was investigated with searches of electronic databases for relevant publications. Pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs) were extracted from eligible studies.ResultsA total of eight eligible studies which included 2604 participants were analyzed in this meta-analysis. Increased expression of FAK protein was found to significantly correlate with shorter overall survival (OS) (HR = 1.43, 95% CI: 1.12–1.83; P = 0.004), and not with disease-free survival (HR = 1.31, 95% CI: 0.92–1.85; P = 0.14). Elevated FAK protein expression was also associated with negative estrogen receptor (ER) expression (OR, 1.34; 95% CI, 1.06–1.68; P = 0.01), negative progesterone receptor (PR) expression (OR, 1.54; 95% CI, 1.22–1.93; P < 0.001), positive human epidermal growth factor receptor 2 (HER2) expression (OR, 1.64; 95% CI, 1.28–2.09; P < 0.001), triple-negative breast cancer (TNBC) (OR, 1.57; 95% CI, 1.14–2.17; P = 0.006), high nuclear grade (OR, 1.70; 95% CI, 1.05–2.78; P = 0.03), high Ki-67 expression level (OR, 2.87; 95% CI, 1.94–4.24; P < 0.001), and positive p53 status (OR, 2.28; 95% CI, 1.58–3.29; P < 0.001).ConclusionOur meta-analysis identifies an association between increased FAK protein expression and worse OS among breast cancer patients. Moreover, enhanced FAK expression is associated with negative ER expression, negative PR expression, positive HER2 expression, TNBC, high nuclear grade, high Ki-67 expression level, and positive p53 status in breast carcinoma.     

Risk factors associated with gastric cancer in patients with a duodenal ulcer

Background: Although gastric cancer (GC) and duodenal ulcer (DU) are both strongly associated with Helicobacter pylori infection, a DU is negatively associated with the risk of GC. The aim of the study is to evaluate histologic risk factors for GC among patients with a DU. Materials and Methods: A total of 541 consecutive patients with GC were prospectively evaluated for the presence of a DU. Control patients with only a DU (n = 89) were recruited from health screening population. Histologic grading was assessed using the updated Sydney system for six gastric biopsies from three regions. GC risk among patients with a DU was evaluated using logistic regression analysis. Results: Among patients with GC, 7.6% (41/541) had a concomitant DU or an ulcer scar. Corpus‐predominant/pangastritis were more frequently found in concomitant GC patients with a DU (90%) than in patients with a DU alone (62%) (p = .001). In patients with a DU, moderate–severe chronic inflammation at the lesser and greater curvatures of corpus was associated with GC risk (OR, 3.70; 95% CI, 1.46–9.36, and OR, 7.72; 95% CI, 3.18–18.7, respectively). Additionally, moderate–severe intestinal metaplasia (IM) at the antrum and corpus lesser curvature was associated with GC risk (OR, 7.52; 95% CI, 3.06–18.5, and OR, 9.25, 95% CI, 2.39–35.8, respectively). Conclusions: A DU is not rare in patients with GC in a high‐risk region of GC. Patients with a DU with chronic corpus gastritis and IM have an increased risk of GC, thus those patients should be followed up for GC development.     

Demographic,social and lifestyle risk factors for cancer registry-notified cancer of unknown primary site (CUP)

BackgroundLittle is known about the risk factors for cancer of unknown primary site (CUP). We examined the demographic, social and lifestyle risk factors for CUP in a prospective cohort of 266,724 people aged 45 years and over in New South Wales, Australia.MethodsBaseline questionnaire data were linked to cancer registration, hospitalisation, emergency department admission, and mortality data. We compared individuals with incident cancer registry-notified CUP (n = 327) to two sets of controls randomly selected (3:1) using incidence density sampling with replacement: (i) incident cancer registry-notified metastatic cancer of known primary site (n = 977) and (ii) general cohort population (n = 981). We used conditional logistic regression to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs).ResultsIn a fully adjusted model incorporating self-rated overall health and comorbidity, people diagnosed with CUP were more likely to be older (OR 1.05, 95% CI 1.04–1.07 per year) and more likely to have low educational attainment (OR 1.77, 95% CI 1.24–2.53) than those diagnosed with metastatic cancer of known primary. Similarly, compared to general cohort population controls, people diagnosed with CUP were older (OR 1.10, 95% CI 1.08–1.12 per year), of low educational attainment (OR 1.69, 95% CI 1.08–2.64), and current (OR 3.42, 95% CI 1.81–6.47) or former (OR 1.95, 95% CI 1.33–2.86) smokers.ConclusionThe consistent association with educational attainment suggests low health literacy may play a role in CUP diagnosis. These findings highlight the need to develop strategies to achieve earlier identification of diagnostically challenging malignancies in people with low health literacy.     

The clinical significance and prognostic value of Xenopus kinesin-like protein 2 expressions in human tumors: A systematic review and meta-analysis

Targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a microtubule-associated protein that plays a pivotal part in the formation of spindles. There is accumulating evidence that the expression of TPX2 is upregulated in many kinds of human cancers and that this protein is involved in the occurrence and progression of tumors. The purpose of this meta-analysis was to investigate the relationship between the overexpression of TPX2 and poor prognosis in cancer patients. A total of 18 eligible studies encompassing 3115 patients were included by searching relevant databases. Hazard ratios (HRs) or odds ratios (ORs) with 95% confidence intervals (CIs) were pooled under random-/fixed-effect models. After calculation, the results showed that patients with increased TPX2 expression had a significantly shorter overall survival (HR = 2.21; 95% CI: 1.70–2.86), and disease-free survival (HR = 2.10; 95% CI: 1.67–2.64). In addition, it was found that increased TPX2 expression was significantly associated with TNM stage (OR = 2.17; 95% CI:1.42–3.32), lymph node metastasis (OR = 2.98; 95% CI: 2.28–3.89), distant metastasis (OR = 2.25; 95% CI:1.03–4.92), and vascular invasion (OR = 2.22; 95% CI:1.26–3.91). Nevertheless, there was no significant correlation between increased expression of TPX2 and either gender, tumor differentiation, or tumor size. Thus, we can come to the conclusion that the overexpression of TPX2 is related to poor clinical outcomes and can be used as a biomarker for the prognosis of patients with cancer.     

Association of pre-admission statin therapy and the inflammatory response in ST elevation myocardial infarction patients

Purpose: To demonstrate the possible association of statin therapy with C reactive protein (CRP) serial measurements in ST elevation myocardial infarction (STEMI) patients.

Materials and methods: STEMI patients between 2008 and 2016 with available CRP data from admission were divided into two groups according to pre-admission statin therapy. A second CRP measurement was noted following primary coronary intervention (within 24?h from admission). The difference between the two measurements was designated ΔCRP.

Results: The cohort consisted of 1134 patients with a median age of 61 (IQR52–70), 81% males. Patients on statins prior to admission (336/1134, 26%) were more likely to have CRP levels within normal range (≤5?mg/l) compared to patients without prior treatment, both at admission (75 vs. 24%, p?=?0.004) and at 24?h (70 vs. 48%, p?=?0.029). The prevalence of patients with pre-admission statin therapy decreased as ΔCRP increased (p?=?0.004; n?=?301). The likelihood of ΔCRP to be above 5?mg/l in patients with pre-admission statin therapy was reduced after age and gender adjustments (OR 0.54, 95% CI 0.32–0.92, p?=?0.023) and in multivariate (OR 0.57, 95% CI 0.33–0.99, p?=?0.048) analysis.

Conclusions: Pre-admission statin therapy is associated with a less robust inflammatory response in STEMI patients, highlighting statin’s pathophysiological importance.     

Prevalence and clinicopathologic characteristics of gastric cardia cancer in South Korea

Background and Aim: Western reports have suggested that the prevalence of gastric cardia cancer (GCC) has been increasing, and indicated some differences between GCC and gastric noncardia cancer (GNCC). However, few studies have been conducted in Asia. The aims of this study were to estimate the prevalence of GCC and to evaluate differences of clinicopathologic characteristics between GCC and GNCC in South Korea. Methods: This study was single‐center case–control study. A total of 829 patients with gastric cancer and 270 controls were enrolled between 2003 and 2011. Baseline characteristics, Helicobacter pylori (H. pylori) infection status, and histologic characteristics were compared among three groups (GCC, GNCC, and control). Results: Sixty cases (7.2%) of gastric cancer were located in cardia. Multivariate analysis showed that male odds ratio (OR, 5.72; 95% CI, 1.72–19.07; p = .005) and cigarette smoking (OR, 5.38; 95% CI, 1.39–20.90; p = .015) were risk factors of GCC in comparison with control group, but H. pylori infection rate was not significant. In the case of GNCC, cigarette smoking (OR, 3.87; 95% CI, 1.81–8.29; p < .001), past alcohol intake (OR, 2.82; 95% CI, 1.28–6.20; p = .010), intestinal metaplasia (OR, 3.22; 95% CI, 2.00–5.17; p < .001), and H. pylori infection (OR, 3.06; 95% CI, 1.90–4.93; p < .001) were risk factors of GNCC. Gastroesophageal reflux disease symptoms were higher in the GNCC (21.2%) than control group (13.5%) (p = .008). However, in the case of GCC, they were similar between the GCC (12.7%) and control group (p = .872). According to multivariate analysis, history of H. pylori eradication (OR, 0.34; 95% CI, 0.19–0.61; p < .001) was associated with a protective effect on GNCC. GCC showed higher depth of invasion (p = .038) and frequent distant metastasis (p = .012) than GNCC. Conclusion: In this referral center based study, the prevalence of GCC was 7.2% in South Korea. Risk factors and clinicopathologic characteristics for GCC and GNCC were different, supporting that the pathophysiology is different in the development of GCC and GNCC.     

Reconsidering the relation between serum homocysteine and red blood cell distribution width: a cross-sectional study of a large cohort

Purpose: In a recent small sample study, red blood cell distribution width (RDW) was suggested as a predictor of homocysteine levels. The current study was aimed to reexamine this association in a large scale sample.

Methods: A retrospective cross-sectional study of healthy adults, conducted at Rabin Medical Center, during 2000–2014. Data were retrieved from the medical charts and a logistic regression controlling for interfering factors was carried out. Sensitivity analysis was implemented by exclusion of individuals with anaemia.

Results: Five thousand, five hundred fifty-four healthy individuals were included. Mean serum homocysteine level was 10.10 (SD 2.72) μmol/L. 34.4% of the study population had a homocysteine level higher than the upper limit of normal (10.8?μmol/L). Homocysteine showed no association with RDW (OR 1.00; 95% CI 0.97–1.03), but increased with age (OR 1.05; 95% CI 1.04–1.06) and decreased with a rise in haemoglobin (OR 0.77; 95% CI 0.71–0.83), and in the mean corpuscular volume (OR 0.86; 95% CI 0.85–0.88). Exclusion of individuals with anaemia did not reveal an association between homocysteine and RDW but found a somewhat smaller association between haemoglobin and RDW [OR 0.82; 95% CI 0.73–0.91].

Conclusions: In our large scale sample we did not find an association between RDW and serum homocysteine.     

Effect of Helicobacter pylori eradication on gastric precancerous lesions: A systematic review and meta-analysis

Background

The question of whether eradication of Helicobacter pylori (Hp) can reverse gastric precancerous lesions, including intestinal metaplasia, remains uncertain, leading to ongoing debate. Therefore, a meta-analysis was performed to evaluate the effect of Hp eradication on gastric precancerous lesions.

Materials and Methods

PubMed, Embase, Cochrane Library, Web of Science, Scopus database, and ClinicalTrials.gov were systematically searched from inception to April 2023 for studies that explored the impact of Hp eradication on gastric precancerous lesions. Risk ratios (RRs) and their 95% confidence intervals (95% CIs) were selected as the effect size. We used the random-effects model to assess pooled data. We also performed quality assessments, subgroup analyses, and sensitivity analyses.

Results

Fifteen studies were included. Compared with placebo, Hp eradication could significantly prevent the progression of gastric precancerous lesions (RR = 0.87, 95% CI: 0.81–0.94, p < 0.01) and reverse them (RR = 1.32, 95% CI: 1.17–1.50, p < 0.01). Then, specific precancerous lesions were further explored. The progression of intestinal metaplasia was significantly prevented by Hp eradication compared to placebo or no treatment (RR = 0.80, 95% CI: 0.69–0.94, p < 0.01). Moreover, compared with placebo or no treatment, Hp eradication also improved chronic atrophic gastritis (RR = 1.84, 95% CI: 1.30–2.61, p < 0.01) and intestinal metaplasia (RR = 1.41, 95% CI: 1.15–1.73, p < 0.01). However, in terms of preventing dysplasia progression (RR = 0.86, 95% CI: 0.37–2.00) and improving dysplasia (RR = 0.89, 95% CI: 0.47–1.70), Hp eradication had no advantage compared to placebo or no treatment.

Conclusions

Hp eradication therapy could prevent the progression of gastric precancerous lesions and reverse them. Notably, intestinal metaplasia can be reversed, but this may only be appropriate for patients with epigenetic alterations and milder lesions.     

Long-term statin therapy affects the severity of chronic gastritis

Background: Helicobacter pylori (H. pylori) is a major cause of chronic gastritis. Statins have several pleotropic effects and their mechanisms of action could be related to anti‐inflammatory, antioxidants, and immunomodulatory effects. Aim: To determine whether statin therapy affects the severity of chronic gastritis. Materials and Methods: In a retrospective study, we evaluated 516 patients who underwent upper endoscopy. One‐hundred and ninety‐eight patients had chronic gastritis, The 198 patients with chronic gastritis were divided into two groups: group 1 comprised patients with a history of statin therapy and group 2 comprised patients with no history of statin therapy. Both groups were compared for age, gender, body mass index (BMI), underlying diseases, drug therapy, alcohol consumption, smoking and the serum levels of C‐reactive protein (CRP). The presence of H. pylori was determined by gastric biopsy and rapid urease test. The grade and severity of gastritis were assessed using the updated Sydney classification system in two gastric biopsy specimens that were taken from each participant in each group. Results: Of the 198 patients with chronic gastritis, 49% of the patients had mild gastritis and 51% had moderate to severe gastritis. From the results of a multiple logistic regression analysis after adjusting for confounding variables that included age, gender, and BMI, we found that elevated serum CRP levels (odds ratio (OR) 2.33; 95% confidence interval (CI) = 0.8–2.6, p = .02), H. pylori (OR 1.99; CI 0.14–2.4, p = .04), and the use of statin (OR 1.64; CI = 0.71–1.77, p = .05) independently predict the severity of chronic gastritis. Conclusion: Long‐standing statin therapy may reduce the severity of chronic gastritis. Mild increased CRP levels in absence of obvious source can predict the severity of chronic gastritis. Further researches are needed to assess the effect of statin in chronic gastritis.     

High parental occupational social contact and risk of childhood hematopoietic,brain and bone cancers

BackgroundThe etiology of childhood cancer is largely unknown, though some research suggests an infectious origin of hematopoietic, central nervous system (CNS) and bone cancers.MethodsWe examined parental occupational social contact as a proxy for exposure to infectious agents and risk of childhood cancer. This population-based case-control study utilized a linkage of four Danish data-registries, and included 3581 cases (<17 years, diagnosed 1973–2012) and 358,100 age-matched controls. We examined the risks of leukemia, lymphoma, CNS and bone cancer related to high occupational social contact from (1) conception to birth and (2) birth to diagnosis.ResultsAcute lymphoblastic leukemia (ALL) and bone cancer were inversely associated with high maternal social contact from conception to birth (OR: 0.86, 95% CI: 0.67–1.10) and birth to diagnosis (OR: 0.54, 95% CI: 0.34–0.86). Children of fathers with high social contact from birth to diagnosis had an increased risk of bone cancers, particularly in rural areas (OR: 1.65, 95% CI: 1.03–2.63). Parental social contact was associated with increased risk of astrocytoma, with strongest associations found in first-born children (maternal: OR: 1.54, 95% CI: 1.02–2.32; paternal: OR: 1.82, 95% CI: 1.05–3.17).ConclusionOur results support the notion of a role of infections for some cancer types.     

Hypomethylation of repetitive elements in blood leukocyte DNA and risk of gastric lesions in a Chinese population

BackgroundTo explore the association between hypomethylation of repetitive elements (LINE-1, Sat2, and ALU) in blood leukocyte DNA and risks of gastric lesions, and development of gastric cancer (GC), a population-based study was conducted in a high-risk area of GC in China.MaterialsMethylation levels were determined by MethyLight in 902 subjects with various gastric lesions from two cohort studies at baseline and 276 subjects with long-term follow-up data.ResultsThe frequency of LINE-1 or Sat2 hypomethylation was significantly increased in subjects with dysplasia (DYS) compared with superficial gastritis/chronic atrophic gastritis. The odds ratios (ORs) were 2.22 [95% confidence interval (CI): 1.45–3.40] for LINE-1 and 1.58 (95% CI: 1.14–2.21) for Sat2. A dose–response pattern was found for the risk of DYS and LINE-1 hypomethylation (P-trend < 0.001). Further stratified analysis indicated that the frequency of LINE-1 or Sat2 hypomethylation was higher in subjects with Helicobacter pylori infection. The ORs were 1.83 (95% CI: 1.12–2.99) for LINE-1 and 1.44 (95% CI: 1.01–2.05) for Sat2. The follow-up data indicated that the risk of progression to GC was increased in intestinal metaplasia (IM) subjects with LINE-1 hypomethylation (OR = 2.82; 95% CI: 1.17–6.77) or Sat2 hypomethylation (OR = 2.78; 95% CI: 1.15–6.74). The risk of progression to GC was also increased in DYS subjects with Sat2 hypomethylation (OR = 5.24; 95% CI: 2.00–13.74).ConclusionsThese findings suggest that hypomethylation of repetitive elements in blood leukocytes is associated with the risks of advanced gastric lesions and development of GC.     

New scoring system combining the FIB-4 index and cytokeratin-18 fragments for predicting steatohepatitis and liver fibrosis in patients with nonalcoholic fatty liver disease

Purpose: To establish a new scoring system as a noninvasive tool for predicting steatohepatitis and liver fibrosis in patients with nonalcoholic fatty liver disease (NAFLD).

Methods: A total of 170 patients histologically diagnosed with nonalcoholic steatohepatitis (NASH) (n?=?130) or nonalcoholic fatty liver (NAFL) (n?=?40) were enrolled. We analyzed receiver operating characteristic (ROC) curves and performed multivariate analysis to predict steatohepatitis and liver fibrosis.

Results: Multivariate analysis showed that cytokeratin-18 fragment (CK18-F) levels (≥278?U/L) (odds ratio [OR], 4.46; 95% confidence interval [CI], 1.42–14.00; p?=?0.010) and the FIB-4 index (≥1.46) (OR, 4.54; 95% CI, 1.93–29.50; p?=?0.004) were independently associated with prediction of NASH. We then established a new scoring system (named the FIC-22 score) for predicting NASH using CK18-F levels and FIB-4 index. The areas under the ROC curve (AUROCs) of the FIC-22 score and NAFIC score were 0.82 (95% CI, 0.75–0.89) and 0.71 (95% CI, 0.62–0.78) (p?=?0.044). Additionally, the AUROC of the FIC-22 score for predicting the presence of fibrosis (F?≥?1) was 0.78 (95% CI, 0.70–0.85).

Conclusions: In patients with NAFLD, the FIC-22 score had high predictive accuracy not only for steatohepatitis but also for the presence of liver fibrosis.     

Pre-diagnostic circulating p53 autoantibodies and subsequent lung cancer risk in low-income African and European Americans

IntroductionMutations of the TP53 gene lead to the production of autoantibodies against p53, a major tumor suppressor protein. Although studies have indicated the association of p53 autoantibodies with human cancers, epidemiologic evidence on lung cancer is still lacking.MethodsIn this nested case-control study conducted within the Southern Community Cohort Study, we investigated the association of circulating p53 autoantibodies with the subsequent risk of developing lung cancer. Using blood samples collected prior to any cancer diagnosis from 295 cases and their individually matched controls, seroreactivity to p53 was assessed by fluorescent bead-based multiplex serology. Conditional logistic regression models were used to estimate odds ratios (OR) and 95 % confidence intervals (CI) for lung cancer risk associated with p53 autoantibodies.ResultsAfter adjustment for potential confounders, p53 seropositivity was significantly associated with an increased risk of lung cancer (OR=2.98, 95 % CI: 1.10–8.06) among African Americans, but not among European Americans (OR=1.21, 95 % CI: 0.24–6.15). The positive associations were restricted to men (OR=4.59, 95 % CI: 1.30–16.16) and participants with a short interval (≤ 4 years) from blood collection to diagnosis (OR=4.30, 95 % CI: 1.33–13.89).ConclusionOur findings add to the evidence supporting p53 autoantibodies as a biomarker of lung cancer.     

Blood cadmium levels as a marker for early lung cancer detection

BackgroundWe assessed whether blood cadmium levels were associated with incident lung cancer and could be used in the context of a screening program for early-stage lung cancer.Material and methodsWe measured blood cadmium levels among 205 lung cancer patients and 205 matched controls. Cases and controls were matched for sex, age and smoking history (total pack-years, years since cessation for former smokers).ResultsThe odds ratio for those in the highest quartile of cadmium level (versus lowest) was four-fold (OR = 4.41, 95 % CI:2.01–9.67, p < 0.01). The association was present in former smokers (OR = 16.8, 95 % CI:3.96−71.2, p < 0.01), but not in current smokers (OR = 1.23, 95 % CI: 0.34–4.38) or in never smokers (OR not defined). Among former smokers, the association was present in both early- and late-stage lung cancer.ConclusionBlood cadmium levels may be a marker to help with the early detection of lung cancer among former smokers.     

Association of p53 Arg72Pro polymorphism with gastric cancer: a meta-analysis

Background: p53 tumor suppressor gene Arg72Pro polymorphism has been associated with gastric cancer. However, results were inconsistent. We performed this meta-analysis to estimate the association between p53 Arg72Pro polymorphism and gastric cancer.

Methods: An electronic search of PubMed was conducted to select studies. Studies containing available genotype frequencies of Arg72Pro were chosen, and the association was assess by pooled odds ratio (ORs) with 95% confidence interval (CIs).

Results: The meta-analysis suggested that the p53 Arg72Pro was associated with the gastric cancer risk (Additive model: OR = 1.149, 95% CI = 1.045–1.263, p = 0.004; Dominant model: OR = 1.18, 95% CI = 1.049–1.328, p = 0.006; Recessive model: OR = 1.202, 95% CI = 1.013–1.427, p = 0.035) in Asian subgroup.

Conclusion: This meta-analysis suggests that p53 Arg72Pro polymorphism is associated with increased risk of gastric cancer in Asians.     

Job strain and risk of esophageal and cardia cancers

BackgroundFew studies have investigated work-related stress in relation to esophageal or cardia cancers.MethodsOur nationwide Swedish population-based case-control study included 189 and 262 esophageal and cardia adenocarcinoma cases respectively, 167 esophageal squamous-cell carcinoma cases and 820 controls. We derived each study participant's occupation of longest duration from occupational histories and applied a psychosocial job-exposure matrix. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using conditional logistic regression, in multivariable models.ResultsJob strain was positively associated with risk of esophageal adenocarcinoma (OR 3.2, 95% CI 1.0–9.8) and squamous-cell carcinoma (OR 4.0, 95% CI 1.6–10.5), but not with cardia adenocarcinoma. No associations regarding demands, control, social support or iso strain were observed, except for a positive association between high control and risk of esophageal squamous-cell carcinoma (OR 1.5, 95% CI 1.0–2.3).ConclusionJob strain seems to increase the risk of both histological types of esophageal cancer.     

Insurance status as a modifier of the association between race and stage of prostate cancer diagnosis in Florida during 1995 and 2013

BackgroundCancer stage at diagnosis is a critical prognostic factor regarding a patient’s health outcomes. It has yet to be shown whether insurance status across different race has any implications on the stage of disease at the time of diagnosis. This study aimed to investigate whether insurance status was a modifier of the association between race and stage of previously undetected prostate cancer at the time of diagnosis in Florida between 1995 and 2013.MethodsSecondary data analysis of a cross-sectional survey using information from the Florida Cancer Data System (n = 224,819). Study participants included black and white males diagnosed with prostate cancer in Florida between 1995 and 2013. The main outcome variable was stage of prostate cancer at diagnosis. The main independent variable was race (black vs white). Adjusted logistic regression models were used to explore the association between race, insurance status and stage at diagnosis. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated.ResultsBlack males were more likely to be diagnosed with late stage prostate cancer (OR 1.31; 95% CI 1.27–1.35). Being uninsured (OR 2.28; 95% CI 2.13–2.45) or having Medicaid (OR 1.84; 95% CI 1.70–1.98) was associated with a diagnosis of late stage cancer. Stratified analysis for health insurance revealed that blacks had an increased risk for late stage cancer if uninsured (OR 1.29; 95% CI 1.07–1.55) and if having Medicare (OR 1.39; 95% CI 1.31–1.48).Conclusion: Insurance status may modify the effect of race on late stage prostate cancer in black patients.     

Association between Psoriasis Vulgaris and Coronary Heart Disease in a Hospital-Based Population in Japan

BackgroundPsoriasis vulgaris is a chronic inflammatory skin disease with an immune-genetic background. It has been reported as an independent risk factor for coronary heart disease (CHD) in the United States and Europe. The purpose of this study was to investigate the association between psoriasis and CHD in a hospital-based population in Japan.MethodsFor 113,065 in-hospital and clinic patients at our institution between January 1, 2011 and January 1, 2013, the diagnostic International Classification of Diseases (ICD)-10 codes for CHD, hypertension, dyslipidemia, diabetes, and psoriasis vulgaris were extracted using the medical accounting system and electronic medical record, and were analyzed.ResultsThe prevalence of CHD (n = 5,167, 4.5%), hypertension (n = 16,476, 14.5%), dyslipidemia (n = 9,236, 8.1%), diabetes mellitus (n = 11,555, 10.2%), and psoriasis vulgaris (n = 1,197, 1.1%) were identified. The prevalence of CHD in patients with hypertension, dyslipidemia, diabetes, and psoriasis vulgaris were 21.3%, 22.2%, 21.1%, and 9.0%, respectively. In 1,197 psoriasis patients, those with CHD were older, more likely to be male, and had more number of the diseases surveyed by ICD-10 codes. Multivariate analysis showed that psoriasis vulgaris was an independent associated factor for CHD (adjusted odds ratio [OR]: 1.27; 95% confidence interval [CI]: 1.01–1.58; p = 0.0404) along with hypertension (adjusted OR: 7.78; 95% CI: 7.25–8.36; p < 0.0001), dyslipidemia (adjusted OR: 2.35; 95% CI: 2.19–2.52; p < 0.0001), and diabetes (adjusted OR: 2.86; 95% CI: 2.67–3.06; p < 0.0001).ConclusionPsoriasis vulgaris was independently associated with CHD in a hospital-based population in Japan.