CASE REPORT: A 24-year-old male presented with painless hardening of the right testis. There was no gynaecomastia, and serum levels of human chorionic gonadotropin and α-fetoprotein were normal. Ultrasound depicted hyperechogenic, clearly demarcated intratesticular lesion. Partial orchiectomy was performed. Macroscopically, tumour appeared as almost entirely calcified round mass, measuring 10 mm. Histopathological evaluation showed well-circumscribed, unencapsulated tumour composed of massive calcified geographic formations, surrounded with tumour cells. Neoplastic cells were large, polygonal, with abundant eosinophilic cytoplasm, and formed irregular cords, pseudo tubular structures, and nests in a fibrous and myxoid stroma, surrounded with lymphocytes. Other forms of calcification were also present: Needle-like deposits and lamellar, mulberry-like structures. There was no necrosis, mitotic activity and nuclear pleomorphism. Immunohistochemical study was positive for inhibin α and negative for Melan A, EMA, synaptophysin, chromogranin and AFP.
DISCUSSION: LCCSCT needs to be differentiated from other, more frequent, sex cord stromal tumours. Clinical and genetical evaluation of these patients had to be performed, due to connection of LCCSCT with genetic abnormalities. In evidently benign cases, organ-sparing surgery should be considered for younger patients, followed by long term follow-up.
CASE REPORT: We report a case that revealed significant intra-abdominal haemorrhage at autopsy. The source of haemorrhage was at the spleen hilum and histology established rupture of splenic artery aneurysm. There was no associated obstetric cause found.
CONCLUSION: Knowledge of spontaneous rupture of splenic artery aneurysm in late pregnancy is essential for monitoring maternal and foetal, morbidity and mortality. However, in the eventuality of death a comprehensive forensic autopsy is the only investigation to recognise such calamity and clear clinical confusion.
RECENT FINDINGS: p53 plays a major physiological role in embryonic development, by controlling cell proliferation, differentiation and responses to cellular stress. Tumor suppressor function of p53 is commonly lost in adult cancers through genetic alterations. However, both somatic and germline p53 mutations are rare in childhood blastomas, suggesting that in these cancers, p53 may be inactivated through other mechanisms than mutation. In this review, we summarize current knowledge about p53 pathway inactivation in childhood blastomas (specifically neuroblastoma, retinoblastoma and Wilms' tumor) through various upstream mechanisms. Laboratory evidence and clinical trials of targeted therapies specific to exploiting p53 upstream regulators are discussed.
SUMMARY: Despite the low rate of inherent TP53 mutations, p53 pathway inactivation is a common denominator in childhood blastomas. Exploiting p53 and its regulators is likely to translate into more effective targeted therapies with minimal late effects for children. (see Video Abstract, Supplemental Digital Content 1, http://links.lww.com/COON/A23).
MATERIALS AND METHODS: A systematic online search was conducted according to PRISMA statement for publications reporting on UR after RC. From initial 802 results, 14 articles including 6169 patients were included finally after exclusion of ineligible studies.
RESULTS: The incidence rate of UR was 4.4% (1.3%-13.7%). It was significantly lower with neobladder diversion (odds ratio = 0.44, 95% CI: 0.24-0.79, P = 0.006). Muscle invasion (hazard ratio = 1.18, 95% CI: 0.86-1.62, P = 0.31), carcinoma in situ (hazard ratio 0.97, 95% CI: 0.64-1.47, P = 0.88), prostatic stromal involvement (hazard ratio = 2.26, 95% CI: 0.01-627.75, P = 0.78), and prostatic urethral involvement (hazard ratio = 2.04, 95% CI: 0.20-20.80, P = 0.55) have no significant effect on UR. Men displayed tendency toward higher incidence of UR (odds ratio = 2.21, 95% CI: 0.96-5.06, P = 0.06). Absence of recurrence displayed tendency toward better disease specific survival, yet not significant (hazard ratio = 0.84, 95% CI: 0.66-1.08, P = 0.17). These results are limited by the retrospective nature of the included studies.
CONCLUSION: Muscle invasion, carcinoma in situ and prostatic stromal or urethral involvement at time of RC have no significant effect on UR. Orthotopic neobladder is associated with a significant lower risk of UR after RC.