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Hemangiomas are benign blood vessel and capillary tumor growths which are widespread in many organs but extremely rare in the bladder, making up just 0.6% of all bladder tumors. To the best of our knowledge, few cases of bladder hemangioma are associated with pregnancy in the literature, and no bladder hemangiomas have been discovered incidentally after abortion. The use of angioembolization is well established; however, postoperative follow-up is crucial to identify tumor recurrence or residual disease. Case presentation: In 2013, a 38-year-old female was referred to a urology clinic with an incidental finding after an abortion of a large bladder mass identified incidentally using ultrasound (US). The patient was recommended for CT, which reported a polypoidal hypervascular lesion, as previously described arising from the urinary bladder wall. Diagnostic cystoscopy showed a large, bluish-red, pulsatile, vascularized submucosal mass with large dilated submucosal vessels, a wide-based stalk, and no active bleeding in the posterior wall of the urinary bladder, measuring about 2 × 3 cm, with negative urine cytology. Due to the vascular nature of the lesion and no active bleeding, the decision was made not to biopsy. The patient underwent angioembolization and scheduled for US every six months with regular diagnostic cystoscopy. In 2018, at 5 years of follow-up, the patient developed recurrence after a successful pregnancy. The angiography revealed recanalization of the previously embolized left superior vesical arteries from the anterior division of the left internal iliac artery, resulting in arteriovenous malformation (AVM). The second angioembolization was performed, with the total exclusion of AVM without residual. By the end of 2022, the patient had remained asymptomatic and without recurrence. Conclusion: Angioembolization is a safe treatment technique, minimally invasive, and has less effect on the quality of life, especially in young patients. Long-term follow-up is essential for detecting tumor recurrence or residual disease. Full article

The role of deficiency of oxoguanine glycosylase 1 (Ogg1) Mmh homolog, a repair enzyme of the 8-hydroxy-2’-deoxyguanosine (8-OHdG) residue in DNA, was investigated using the multiorgan carcinogenesis bioassay in mice. A total of 80 male and female six-week-old mice of C57BL/6J background carrying a mutant Mmh allele of the Mmh/Ogg1 gene (Ogg1^−/−) and wild type (Ogg1^+/+) mice were administered N-diethylnitrosamine (DEN), N-methyl-N-nitrosourea (MNU), N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), N-bis (2-hydroxypropyl) nitrosamine (DHPN) and 1,2-dimethylhydrazine dihydrochloride (DMH) (DMBDD) to induce carcinogenesis in multiple organs, and observed up to 34 weeks. Significant increase of lung adenocarcinomas incidence was observed in DMBDD-treated Ogg1^−/− male mice, but not in DMBDD-administered Ogg1^+/+ animals. Furthermore, incidences of lung adenomas were significantly elevated in both Ogg1^−/− males and females as compared with respective Ogg1^−/− control and DMBDD-treated Ogg1^+/+ groups. Incidence of total liver tumors (hepatocellular adenomas, hemangiomas and hemangiosarcomas) was significantly higher in the DMBDD-administered Ogg1^−/− males and females. In addition, in DMBDD-treated male Ogg1^−/− mice, incidences of colon adenomas and total colon tumors showed a trend and a significant increase, respectively, along with significant rise in incidence of simple hyperplasia of the urinary bladder, and a trend to increase for renal tubules hyperplasia in the kidney. Furthermore, incidence of squamous cell hyperplasia in the forestomach of DMBDD-treated Ogg1^−/− male mice was significantly higher than that of Ogg1^+/+ males. Incidence of small intestine adenomas in DMBDD Ogg1^−/− groups showed a trend for increase, as compared to the wild type mice. The current results demonstrated increased susceptibility of Ogg1 mutant mice to the multiorgan carcinogenesis induced by DMBDD. The present bioassay could become a useful tool to examine the influence of various targets on mouse carcinogenesis. Full article