Previous studies have reported an association between hot tea drinking and risk of esophageal cancer, but no study has examined this association using prospectively and objectively measured tea ...drinking temperature. We examined the association of tea drinking temperature, measured both objectively and subjectively at study baseline, with future risk of esophageal squamous cell carcinoma (ESCC) in a prospective study. We measured tea drinking temperature using validated methods and collected data on several other tea drinking habits and potential confounders of interest at baseline in the Golestan Cohort Study, a population‐based prospective study of 50,045 individuals aged 40–75 years, established in 2004–2008 in northeastern Iran. Study participants were followed‐up for a median duration of 10.1 years (505,865 person‐years). During 2004–2017, 317 new cases of ESCC were identified. The objectively measured tea temperature (HR 1.41, 95% CI 1.10–1.81; for ≥60°C vs. <60°C), reported preference for very hot tea drinking (HR 2.41, 95% CI 1.27–4.56; for “very hot” vs. “cold/lukewarm”), and reported shorter time from pouring tea to drinking (HR 1.51, 95% CI 1.01–2.26; for <2 vs. ≥6 min) were all associated with ESCC risk. In analysis of the combined effects of measured temperature and amount, compared to those who drank less than 700 ml of tea/day at <60°C, drinking 700 mL/day or more at a higher‐temperature (≥60°C) was consistently associated with an about 90% increase in ESCC risk. Our results substantially strengthen the existing evidence supporting an association between hot beverage drinking and ESCC.
What's new?
Previous studies have indicated that hot tea may increase the risk of esophageal cancer. In this large, prospective study, the authors found that drinking hot tea is indeed associated with an increased risk of esophageal squamous cell carcinoma (ESCC). Furthermore, a preference for “very hot” tea more than doubled this risk. It may thus be a reasonable public‐health measure to extrapolate these results to all types of beverages, and to advise the public to wait for beverages to cool to <60°C before consumption.
A recent study showed an association between hookah/opium use and gastric cancer but no study has investigated the relationship with gastric precancerous lesions. We examined the association between ...hookah/opium and gastric precancerous lesions and subsequent gastric cancer. In a population‐based cohort study, 928 randomly selected, healthy, Helicobacter pylori‐infected subjects in Ardabil Province, Iran, were followed for 10 years. The association between baseline precancerous lesions and lifestyle risk factors (including hookah/opium) was analyzed using logistic regression and presented as odds ratios (ORs) and 95% confidence intervals (CIs). We also calculated hazard ratios (HRs) and 95% CIs for the associations of lifestyle risk factors and endoscopic and histological parameters with incident gastric cancers using Cox regression models. Additionally, the proportion of cancers attributable to modifiable risk factors was calculated. During 9,096 person‐years of follow‐up, 36 new cases of gastric cancer were observed (incidence rate: 3.96/1,000 persons‐years). Opium consumption was strongly associated with baseline antral (OR: 3.2; 95% CI: 1.2–9.1) and body intestinal metaplasia (OR: 7.3; 95% CI: 2.5–21.5). Opium (HR: 3.2; 95% CI: 1.4–7.7), hookah (HR: 3.4; 95% CI: 1.7–7.1) and cigarette use (HR: 3.2; 95% CI: 1.4–7.5), as well as high salt intake, family history of gastric cancer, gastric ulcer and histological atrophic gastritis and intestinal metaplasia of body were associated with higher risk of gastric cancer. The fraction of cancers attributable jointly to high salt, low fruit intake, smoking (including hookah) and opium was 93% (95% CI: 83–98). Hookah and opium use are risk factors for gastric cancer as well as for precancerous lesions. Hookah, opium, cigarette and high salt intake are important modifiable risk factors in this high‐incidence gastric cancer area.
What's new?
Gastric cancer strikes Iranian men more often than any other cancer, and previous studies report a connection between gastric cancer and hookah, a traditional smoking device in the region. This study probed the factors associated with precancerous lesions and gastric cancer, including hookah and opium use. They found that both hookah and opium use increased the likelihood of developing cancer, as did high salt intake and cigarette smoking.
Detecting pre-clinical bladder cancer (BC) using urinary biomarkers may provide a valuable opportunity for screening and management. Telomerase reverse transcriptase (TERT) promoter mutations ...detectable in urine have emerged as promising BC biomarkers.
We performed a nested case-control study within the population-based prospective Golestan Cohort Study (50,045 participants, followed up to 14 years) and assessed TERT promoter mutations in baseline urine samples from 38 asymptomatic individuals who subsequently developed primary BC and 152 matched controls using a Next-Generation Sequencing-based single-plex assay (UroMuTERT) and droplet digital PCR assays.
Results were obtained for 30 cases and 101 controls. TERT promoter mutations were detected in 14 pre-clinical cases (sensitivity 46·67%) and none of the controls (specificity 100·00%). At an estimated BC cumulative incidence of 0·09% in the cohort, the positive and negative predictive values were 100·00% and 99·95% respectively. The mutant allelic fractions decreased with the time interval from urine collection until BC diagnosis (p = 0·033) but the mutations were detectable up to 10 years prior to clinical diagnosis.
Our results provide the first evidence from a population-based prospective cohort study of the potential of urinary TERT promoter mutations as promising non-invasive biomarkers for early detection of BC. Further studies should validate this finding and assess their clinical utility in other longitudinal cohorts.
French Cancer League, World Cancer Research Fund International, Cancer Research UK, Tehran University of Medical Sciences, the International Agency for Research on Cancer, and the U.S. National Cancer Institute.
Primary pancreatic lymphoma is an unlikely malignancy accounting for less than 0.5% of pancreatic tumors. Clinical presentation is often nonspecific and may be clinically misdiagnosed as pancreatic ...adenocarcinoma. Here we present an Iranian case of primary pancreatic lymphoma in a 47-year-old male suffering from jaundice and 20% weight loss. Endoscopic ultrasound revealed a mixed echoic mass lesion at the head of pancreas. The patient underwent endoscopic ultrasound-guided fine needle aspiration of solid pancreatic mass and histopathologic diagnosis revealed granuloma. Computed tomography-guided core needle biopsy was performed and eventually histological examination showed granuloma that was coherent with the diagnosis of primary pancreatic lymphoma. Primary pancreatic lymphoma is a rare entity presenting with nonspecific symptoms, laboratory and radiological findings. Computed tomography results in combination with clinical and radiological studies generally provide guidance for appropriate investigation.
EUS-guided fine-needle biopsy sampling (EUS-FNB) has largely replaced FNA for tissue diagnosis of pancreatobiliary mass lesions. However, the optimal number of passes required for the diagnosis of ...malignancy is not clear. We aimed to compare the per-pass performance of 2 types of fine-needle biopsy (FNB) needles for the detection of malignancy.
One hundred fourteen patients referred for EUS evaluation of solid pancreatobiliary mass lesions underwent randomization between biopsy sampling with a Franseen needle and a 3-prong tip needle with an asymmetric cutting surfaces. Four passes of EUS-FNB were taken from each mass lesion. Two pathologists blinded to needle type analyzed the specimens. The final diagnosis of malignancy was made based on FNB specimen pathology, surgery, or a follow-up of at least 6 months after EUS-FNB. The sensitivity of EUS-FNB to diagnose malignancy was compared between the 2 groups. The cumulative sensitivity of detection of malignancy by EUS-FNB was calculated after each pass in each arm. Other characteristics of the specimens including cellularity and blood contents were also compared between the 2 groups. In the primary analysis, lesions categorized as suspicious on EUS-FNB were considered nondiagnostic for malignancy.
Ninety-eight patients (86%) had a final diagnosis of malignancy, and 16 patients (14%) had benign disease. Four passes of EUS-FNB with the Franseen needle detected malignancy in 44 of 47 patients (sensitivity, 93.6%; 95% confidence interval CI, 82.5-98.7) and with the 3-prong asymmetric-tip needle in 50 of 51 patients (sensitivity, 98%; 95% CI, 89.6-99.9; P = .35). Two passes of EUS-FNB detected malignancy with a sensitivity of 91.5% (95% CI, 79.6-97.6) with the Franseen needle and 90.2% (95% CI, 78.6-96.7) with the 3-prong asymmetric-tip needle. The cumulative sensitivities at pass 3 were 93.6% (95% CI, 82.5-98.6) and 96.1% (95% CI, 86.5-99.5), respectively. Samples collected with the Franseen needle had significantly higher cellularity than samples collected with the 3-prong asymmetric-tip needle (P < .01). However, no difference as found between the 2 types of needles in term of specimen bloodiness.
No significant differences were found in the diagnostic performance of the Franseen needle versus the 3-prong asymmetric-tip needle in patients with suspected pancreatobiliary cancer. However, the Franseen needle yielded higher cellularity of the specimen. Two passes of EUS-FNB are required to detect malignancy with at least 90% sensitivity with either type of needle. (Clinical trial registration number: NCT04975620.)
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Experimental studies indicate that gamma linolenic acid (GLA) and docosahexaenoic acid (DHA) may inhibit glioma cells growth but effects of oral consumption of these fatty acids on brain tumor fatty ...acid composition have not been determined in vivo.
GLA oil (GLAO; 72% GLA), DHA oil (DHAO; 73% DHA) were fed to adult wistar rats (1 mL/rat/day) starting one week prior to C6 glioma cells implantation and continued for two weeks after implantation. Control group were fed same amount of high linoleic acid safflower oil (74-77% linoleic acid). Fatty acid composition of tumor samples was determined in a set of 8-12 animals in each group and serum fatty acid in 6 animals per each group. Gene expression of tumor fatty acid binding protein 7 (FABP7), epidermal growth factor receptor (EGFR), peroxisome proliferator activated receptor gamma (PPAR-gamma) and retinoid x receptor-alpha (RXR-alpha) were determined in a set of 18 animals per group.
DHAO feeding increased EPA of brain tumors and decreased ratio of n-6/n-3 fatty acids. Serum levels of EPA were also increased in DHAO group. A similar trend in serum and tumor levels of DHA were observed in DHAO group but it did not achieve statistical significance. GLAO increased serum concentration of GLA but had no significant effect on tumor GLA or dihomo-gamma linolenic acid (DGLA) concentrations. Gene expression of FABP7 was up-regulated in tumors of DHAO group but no other significant effects were observed on EGFR, PPAR-gamma or RXR-alpha expression, and expression of these genes in tumors of GLAO were not different from SFO group.
Dietary supplementation of DHA containing oil could be an effective way to increase levels of long chain n-3 fatty acids in brain tumors and this increase may be mediated partly by up-regulation of FABP7 expression.
Red meat and processed meat are associated with some gastrointestinal cancers. Our study aims to investigate the association of different meat types with esophageal and gastric cancer (EC, GC) in a ...high‐risk population. The Golestan Cohort Study (GCS) is a population‐based cohort of 50 045 individuals aged 40 to 75 from northeast Iran. Detailed data on different exposures were collected using validated questionnaires. We considered quintiles of meat consumption, using grams and density (g/1000 kcal/day). We calculated intake of red, processed, organ and white meat, as well as total red meat, including the first three. We used proportional hazards regression models to estimate hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) for the association between meat types and cancer. During 12 years of follow‐up, out of 49 585 participants (57.4% women), 369 developed EC (48.2% women) and 368 developed GC (27.5% women), including 309 esophageal squamous cell, 20 esophageal adenocarcinomas, 216 cardia and 95 non‐cardia GC. No association was found for EC except for red meat among females (HR for one quintile increase 1.13, 95% CI = 1.00‐1.27). The risk of GC increased for intake of total red meat (HR 1.08, 95% CI = 1.00‐1.17) and red meat separately (HR 1.09, 95% CI = 1.00‐1.18). The HR for red meat and non‐cardia GC was 1.23 (95% CI = 1.02‐1.48). No associations were observed for other types of meat. In conclusion, in this high‐risk population red meat intake is associated with GC, but not EC, suggesting a substantial role of this modifiable factor in determining the burden of GC.
What's new?
While high intakes of red meat and processed meat are risk factors for certain cancer types, especially colorectal cancer, associations with esophageal cancer (EC) and gastric cancer (GC) remain uncertain. Here, meat intake and EC and GC risk were examined in a population in northeast Iran with overall low meat intake, except for high consumption of organ and chicken meat. Hazards regression modeling reveals associations between red meat intake and elevated GC risk, particularly non‐cardia GC. There was no association with EC or its subtypes. Further study is needed to determine possible etiological involvement of red meat in GC development.
Esophageal squamous cell carcinoma (ESCC) shows remarkable variation in incidence that is not fully explained by known lifestyle and environmental risk factors. It has been speculated that an unknown ...exogenous exposure(s) could be responsible. Here we combine the fields of mutational signature analysis with cancer epidemiology to study 552 ESCC genomes from eight countries with varying incidence rates. Mutational profiles were similar across all countries studied. Associations between specific mutational signatures and ESCC risk factors were identified for tobacco, alcohol, opium and germline variants, with modest impacts on mutation burden. We find no evidence of a mutational signature indicative of an exogenous exposure capable of explaining differences in ESCC incidence. Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC)-associated mutational signatures single-base substitution (SBS)2 and SBS13 were present in 88% and 91% of cases, respectively, and accounted for 25% of the mutation burden on average, indicating that APOBEC activation is a crucial step in ESCC tumor development.