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Introduction: The introduction of universal health insurance coverage aims to provide equal accessibility and affordability of health care, but whether such a policy eliminates health inequalities has not been conclusively determined. This research aims to examine the healthcare outcomes of oral cancer and determine whether the universal coverage system in Taiwan has reduced health inequality. Methods: Linking the databases of the National Cancer Registry with the National Mortality Registry in Taiwan, we stratified patients with oral squamous cell carcinoma by gender and income to estimate the incidence rate, cumulative incidence rate aged from 20 to 79 (CIR20-79), life expectancy, and expected years of life lost (EYLL). The difficulties with asymmetries and short follow-up periods were resolved through applying survival analysis extrapolation methods. Results: While all people showed a general improvement in life expectancy after the introduction of the NHI, the estimated change in EYLL’s of the high-, middle-, and low-income female patients were found to have +0.3, -0.5 and -7 years of EYLL, respectively, indicating a reduction in health inequality. Improvements for the male patients were unremarkable. There was no drop in the CIR20-79 of oral cancer in disadvantaged groups as in those with higher incomes. Conclusions: Universal coverage alone may not reduce health inequality across different income groups for oral cancer unless effective preventive measures are implemented for economically disadvantaged regions. [ABSTRACT FROM AUTHOR]

Background: Oral squamous cell carcinoma (OSCC) is the fourth leading cause of male cancer death in Taiwan. Exposure to environmental carcinogens is the primary risk factor for developing OSCC. CD44, a well-known tumor marker, plays a crucial role in tumor cell differentiation, invasion, and metastasis. This study investigated CD44 single-nucleotide polymorphisms (SNPs) with environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. Methodology/Principal Findings: Real-time polymerase chain reaction (PCR) was used to analyze 6 SNPs of CD44 in 599 patients with oral cancer and 561 cancer-free controls. We determined that the CD44 rs187115 polymorphism carriers with the genotype AG, GG, or AG+GG were associated with oral cancer susceptibility. Among 731 smokers, CD44 polymorphisms carriers with the betel-nut chewing habit had a 10.30–37.63-fold greater risk of having oral cancer compared to CD44 wild-type (WT) carriers without the betel-nut chewing habit. Among 552 betel-nut chewers, CD44 polymorphisms carriers who smoked had a 4.23–16.11-fold greater risk of having oral cancer compared to those who carried the WT but did not smoke. Finally, we also observed that the stage III and IV oral cancer patients had higher frequencies of CD44 rs187115 polymorphisms with the variant genotype (AG+GG) compared with the wild-type (WT) carriers. Conclusion: Our results suggest that gene–environment interactions between the CD44 polymorphisms and betel quid chewing and tobacco smoking increase the susceptibility to oral cancer development. Patients with CD44 rs187115 variant genotypes (AG+GG) were correlated with a higher risk of oral cancer development, and these patients may possess greater chemoresistance to advanced- to late-stage oral cancer than WT carriers do. The CD44 rs187115 polymorphism has potential predictive significance in oral carcinogenesis and also may be applied as factors to predict the clinical stage in OSCC patients. [ABSTRACT FROM AUTHOR]