Policymakers require estimates of the future number of cancer patients in order to allocate finite resources to cancer prevention, treatment and palliative care. We examine recent cancer incidence trends in Iran and present predicted incidence rates and new cases for the entire country for the year 2025. We developed a method for approximating population‐based incidence from the pathology‐based data series available nationally for the years 2008 to 2013, and augmented this with data from the Iranian National Population‐based Cancer Registry (INPCR) for the years 2014 to 2016. We fitted time‐linear age‐period models to the recent incidence trends to quantify the future cancer incidence burden to the year 2025, delineating the contribution of changes due to risk and those due to demographic change. The number of new cancer cases is predicted to increase in Iran from 112 000 recorded cases in 2016 to an estimated 160 000 in 2025, a 42.6% increase, of which 13.9% and 28.7% were attributed to changes in risk and population structure, respectively. In terms of specific cancers, the greatest increases in cases are predicted for thyroid (113.8%), prostate (66.7%), female breast (63.0%) and colorectal cancer (54.1%). Breast, colorectal and stomach cancers were the most common cancers in Iran in 2016 and are predicted to remain the leading cancers nationally in 2025. The increasing trends in incidence of most common cancers in Iran reinforce the need for the tailored design and implementation of effective national cancer control programs across the country.
The Helicobacter pylori duodenal ulcer promoting (dupA) gene has been previously described as a risk marker for duodenal ulcer (DU) development and a protective factor against gastric cancer (GC). Recent studies which have assessed the application of dupA in the prediction of clinical outcomes have been controversial. In the current study, the association of dupA with the clinical outcomes and histopathological changes following H. pylori infection was evaluated in Iranian patients. A total of 157 H. pylori-infected patients with DU (n530), gastric ulcer (n523), gastritis (n568) or GC (n536) were assessed. The presence of jhp0917 and jhp0918 genes was determined by gene specific PCR. Gastric histopathological changes were recorded according to the updated Sydney system. Seventy-eight (49.7 %) and 71 (45.2 %) of the 157 tested strains, respectively, were positive and negative for both genes. The remaining 8 (5.09 %) of the 157 strains were jhp0917-positive/jhp0918-negative. Univariate analysis showed inverse associations between dupA and histological features including dysplasia as the penultimate stage of GC and lymphoid follicles as a consequence of relatively long-standing H. pyloriassociated gastritis. The degrees of nucleotide sequence identity of Iranian strains to Colombian, Brazilian and Indian strains ranged from 86.1 to 100 % for the aligned regions of jhp0917, from 88 to 98.8 % for jhp0918 and from 93.4 to 99.5 % for the partial sequences of the dupA gene. Despite the fact that possession of the dupA gene showed no association with any disease category in our population as reported in several other countries, association of dupA-negative strains of H. pylori with pre-malignant lesions calls for additional studies to evaluate the role of this gene as a protective marker against GC.
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