Low grade papillary transitional cell carcinoma pelvic recurrence masquerading as high grade invasive carcinoma, ten years after radical cystectomy

BACKGROUND: Tumor recurrence following radical cystectomy for a low-grade superficial transitional cell carcinoma (TCC) is exceedingly uncommon and has not been reported previously. CASE PRESENTATION: We describe a case of a young male presenting with anorexia, weight loss and a large, painful locally destructive pelvic recurrence, ten years after radical cystoprostatectomy. The pathology was consistent with a low-grade urothelial carcinoma. After an unsuccessful treatment with cisplatin-based chemotherapy, the patient underwent a curative intent hemipelvectomy with complete excision of tumor and is disease free at one year follow-up. CONCLUSION: A literature review related to this unusual presentation is reported and a surgical solutions over chemotherapy and radiotherapy is proposed

Low grade papillary transitional cell carcinoma pelvic recurrence masquerading as high grade invasive carcinoma, ten years after radical cystectomy

Abstract Background Tumor recurrence following radical cystectomy for a low-grade superficial transitional cell carcinoma (TCC) is exceedingly uncommon and has not been reported previously. Case presentation We describe a case of a young male presenting with anorexia, weight loss and a large, painful locally destructive pelvic recurrence, ten years after radical cystoprostatectomy. The pathology was consistent with a low-grade urothelial carcinoma. After an unsuccessful treatment with cisplatin-based chemotherapy, the patient underwent a curative intent hemipelvectomy with complete excision of tumor and is disease free at one year follow-up. Conclusion A literature review related to this unusual presentation is reported and a surgical solutions over chemotherapy and radiotherapy is proposed.</p

Novel t(1;2)(p36.1;q23) and t(7;19)(q32;q13.3) chromosomal translocations in ischemic fasciitis: expanding the spectrum of pseudosarcomatous lesions with clonal pathogenetic link

Abstract Background Ischemic fasciitis is a distinctive pseudosarcomatous entity with a marked predilection for elderly and physically debilitated or immobilized patients. The etiology of these lesions is unknown but felt to be related to ischemic vascular events. Case presentation Herein, we report for the first time, two cytogenetic translocations, t(1;2)(p36.1;q23) and t(7;19)(q32;q13.3) in a 75 year-old ambulating female with a history of left total hip arthroplasty 20 years ago. Conclusion These translocations suggest a possible clonal pathogenetic link though their significance remains to be established

MYC amplification and polysomy 8 in chondrosarcoma: array comparative genomic hybridization, fluorescent in situ hybridization, and association with outcome. J Clin Oncol

A B S T R A C T Purpose To identify recurrent regions of genomic gain or loss in chondrosarcoma in a clinically relevant and statistically valid fashion. Materials and Methods Array comparative genomic hybridization (CGH) results of 15 frozen tumor samples of high-grade chondrosarcoma for chromosome 8 are presented. A separate subset of 116 cartilaginous tumors with outcome data was used for validation. Results Array CGH identified gain at 8q24.12-q24.13, the region of the MYC (c-Myc) oncogene, as a frequent change in high-grade chondrosarcoma. In the validation arm of 116 cartilaginous tumors, MYC was frequently amplified in G2 (15%), G3 (20%), and dedifferentiated (21%) chondrosarcomas. No amplification was identified in samples of enchondroma and grade 1 chondrosarcoma. In samples without MYC amplification, polysomy 8 was a frequent finding in grade 1 (18%), grade 2 (31%), grade 3 (80%), and dedifferentiated (29%) chondrosarcomas, but was not found in any samples of enchondroma. MYC protein expression was identified in all samples with amplification, but was also frequent in the remaining samples without amplification or polysomy 8. Kaplan-Meier survival curves for overall survival showed a statistically significant difference for patients with MYC amplification or polysomy 8 (P ϭ .034). Univariate analysis involving Cox proportional hazards models showed that grade (P ϭ .003), polysomy 8 (P ϭ .045), and MYC amplification (P ϭ .053) correlated with shorter overall survival. By multivariate analysis, grade of chondrosarcoma (P ϭ .026) was the only factor to reach statistical significance. Conclusion MYC amplification and polysomy 8 can be used as markers of prognostic importance in chondrosarcoma. Molecular targeting of MYC expression may have therapeutic potential in the future for subsets of chondrosarcoma. J Cli