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Background Angiotensin‐converting enzyme (ACE) plays a pivotal role in several pathologies including cancers. The association of insertion/deletion (I/D) polymorphism of the ACE gene with prostate cancer (PC) risk remains controversial. We aimed to investigate for the first time, to our Knowledge, in North Africa the potential relationship between ACE I/D polymorphism with PC susceptibility and clinical outcomes of PC patients. Methods This case‐control study included 143 healthy individuals and 124 patients diagnosed with PC. Using genomic DNA, the samples were genotyped for ACE I/D polymorphism by polymerase chain reaction (PCR). Results We found that The D allele is significantly associated with an increased risk of PC and D/D + D/I genotypes were at 3 times increased risk of PC ([p = 0.005], OR = 2.95, IC 95% = 1.26–7.09) compared with I/I genotype (p = 0.003, OR = 0.3, IC 95% = 0.12–0.74). We observed an association between D/D and D/I genotypes with advanced age (≥70 years) (p = 0.014; r2 = 0.22). Furthermore, there is a significant prediction of advanced Gleason score ≥8 based on epidemiological parameters and ACE genotype (p = 0.000; R2 = 0.349), although no significant association was observed with stage and metastasis. Conclusion The ACE I/D polymorphism is likely to predispose to PC and could play a role in PC progression and aggressiveness.

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Background Minor histocompatibility antigens (mHAgs) are endogenous immunogenic peptides initially identified due to complications detected in several contexts of HLA geno‐identical hematopoietic stem cell transplantation (HSCT). In this study, we chose to examine the molecular polymorphism of the mHAgs HA‐8 and PANE1 in the Tunisian population. Material and Methods This study was conducted on 150 healthy and unrelated individuals. The DNA extraction and Sequence‐Specific Primers PCR (PCR‐SSP) methods were used for the molecular genotyping of the selected SNPs: PUM3 (rs2173904) and CENPM (rs5758511). Results Our results show that, 94% of Tunisians are carriers of the PANE1R allele (immunogenic variant of the PANE1 mHAg) and 68% of Tunisians are carriers of the HA‐8R allele (immunogenic variant of the HA‐8 mHAg). Furthermore, this study shows that about 5% of the Tunisians are carrier of the PANE1R antigen and its HLA molecule of presentation (the PANE1R/HLA‐A*0301 combination). However, only 2% of Tunisians are carrier of the HA‐8R/HLA‐A*0201 combination, that is, the HA8 immunogenic variant and its specific HLA molecule of presentation. Conclusion Our results are close to those reported in Caucasian, Asiatic, and African populations, this may be explained by the historical events experienced by Tunisia for millennia. These results could be used for further clinical and anthropological studies.

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