Paratesticular desmoplastic small round cell tumors: A case report and review of the literature

Desmoplastic small round cell tumor (DSCRT) is a rare malignancy most often seen in the abdomen or pelvis of young men. Unfortunately, this disease is usually metastatic at diagnosis and has dismal outcomes. We describe a case of isolated paratesticular DSCRT in a 14â yearâ old male successfully treated with surgical resection, chemotherapy, and adjuvant radiation, and we present a review of the relevant literature. It appears that isolated, paratesticular DSCRTs have a markedly better outcome than the classic abdominal or pelvic location. We hypothesize that this is due to earlier detection and the relative ease of surgical resection.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138864/1/pbc26631.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138864/2/pbc26631_am.pd

Resolution of mandibular fibrous dysplasia following imatinib therapy in Noonan syndrome

http://deepblue.lib.umich.edu/bitstream/2027.42/175984/2/Pediatric Blood Cancer - 2023 - Goldman - Resolution of mandibular fibrous dysplasia following imatinib therapy in Noonan.pdfArticle in PressDescription of Pediatric Blood Cancer - 2023 - Goldman - Resolution of mandibular fibrous dysplasia following imatinib therapy in Noonan.pdf : Published versio

Bcl-2 and N-Myc Coexpression Increases IGF-IR and Features of Malignant Growth in Neuroblastoma Cell Lines

The bcl-2 and c-myc oncogenes cooperate to transform multiple cell types. In the pediatric malignancy NB(2), Bcl-2 is highly expressed. In tumors with a poor prognosis, N-Myc, a protein homologous to c-Myc, is overexpressed as a result of gene amplification. The present study was designed to determine whether Bcl-2 cooperates with N-Myc to bestow a tumorigenic phenotype to neuroblastoma (NB) cells. NB cell lines that at baseline express neither Bcl-2 nor N-Myc were stably transfected to express these gene products. In this model, we found Bcl-2 rescues N-Myc-expressing cells from apoptosis induced by serum withdrawal. Coexpression of Bcl-2 and N-Myc supports growth in low serum conditions and anchorage-independent growth in soft agar. Similarly, in vivo tumorigenic and angiogenic activity was dependent on coexpression. Our data further suggests that the mechanism underlying these changes involves the receptor for insulin growth factor type I (IGF-IR)