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PubMed2001

Ewing sarcoma and sinonasal neuroectodermal tumors as second malignant tumors after retinoblastoma and other neoplasms.

BACKGROUND: Excesses of various childhood cancers have been reported after retinoblastoma, including a trickle of Ewing sarcoma (ES) and perhaps histologically similar olfactory neuroblastoma, both of which are neural tumors. To update and advance this information, case reports were sought by an extensive review of the literature. PROCEDURE: The search was made through the use of PubMed, and the Web of Science (Citation Index Expanded), keying on primary references. Three sinonasal cancers diagnosed as ES were immunohistochemically stained for MIC-2 protein (positive in ES). RESULTS: Retinoblastoma occurred before ES in ten cases (seven bilateral). In four others, retinoblastoma (three bilateral) developed before sinonasal neural tumors (poorly differentiated). ES also occurred after 14 cancers other than retinoblastoma (five lymphomas, four leukemias, and one each of five miscellaneous cancers). The predominance of retinoblastoma prior to ES differs markedly from the low-frequency of retinoblastoma among childhood cancers in the general population. On the contrary, cancers other than retinoblastoma were proportionate to those in the general population. Previously, retinoblastoma followed by excesses of osteosarcoma and soft tissue sarcomas has been attributed to the action of the inherited RB-1 gene. The sinonasal tumors stained negative for MIC-2 protein. CONCLUSIONS: Heritable retinoblastoma may predispose to ES and perhaps to a subset of poorly differentiated neuroectodermal tumors in the sinonasal region that may be related to olfactory neuroblastoma.

Adolescent↗
PubMed2004

Expression of Fas ligand in retinoblastoma.

BACKGROUND: The importance of the Fas-Fas ligand (FasL) mechanism for the immune evasion by tumors provided a strong rationale for the examination of FasL expression in retinoblastoma. In an earlier publication, the authors reported that invasive retinoblastomas decreased Fas expression. Because to the authors' knowledge there is not much information regarding the effect of FasL expression on retinoblastoma, the authors studied the expression of FasL in retinoblastoma and correlated it with invasiveness. METHODS: Thirty-six archival retinoblastoma specimens were divided into 2 groups. Group A (n = 17) was comprised of specimens from tumors with no invasion and Group B (n = 19) was comprised of specimens from tumors with invasion of the choroid (focal, diffuse), optic nerve (laminar, postlaminar, surgical end), and orbit. Sections were immunostained with a monoclonal antibody to FasL and the immunoreactivity was assessed. RESULTS: In Group A, FasL was negative in 100% (17 of 17) of the tumor specimens. In Group B, FasL was expressed in 79% (15 of 19) of the tumor specimens (positive in 9 tumors and heterogeneous in 6 tumors). The difference in FasL expression between the two groups was significant (P < 0.001) CONCLUSIONS: Increased expression of FasL was observed in specimens taken from patients with aggressive tumors. Thus, Loss of Fas and gain of aberrant FasL expression were common features of malignant transformation. The data suggested that the Fas/FasL pathway is potentially immunosuppressive and may be involved in the escape of retinoblastoma cells from immune destruction.

Adolescent↗
PubMed2007

Risk factors for extraocular relapse following enucleation after failure of chemoreduction in retinoblastoma.

OBJECTIVE: To assess the outcome and determine risk factors for extraocular relapse in patients with retinoblastoma who had been enucleated after failure of chemoreduction. METHODS: Retrospective study (1995-2002) at three institutions. Pathological risk factors (PRF) were defined as invasion of the anterior segment, choroid, post-laminar optic nerve, subarachnoid space, or sclera according to the local pathology report. Extraocular relapse was defined as an event. RESULTS: One hundred twenty-two patients were included (17 had bilateral enucleation). Chemoreduction included vincristine, carboplatin, and etoposide (n=80, 65.6%), vincristine, and carboplatin (n=17, 13.9%), or carboplatin (n=25, 20.5%). Thirty-five also received external beam radiotherapy (28.7%). PRF included: 39 with choroidal involvement, 9 with anterior segment, 9 with scleral, and 2 with post-laminar optic nerve with subarachnoid invasion. Adjuvant chemotherapy was given to eight patients (6.5%) because of scleral invasion. Four patients had an extraocular relapse after enucleation, two of whom survive after intensive treatment including stem cell rescue. Five-year probability of event-free survival is 0.96. Only scleral invasion and bilateral enucleation were significantly associated with extraocular relapse. CONCLUSIONS: The risk of extraocular relapse is low after enucleation following failure of chemoreduction. Patients who underwent bilateral enucleation and those with scleral invasion are at higher risk of extraocular relapse.

Antineoplastic Agents↗
PubMed2006

The study of c-Src kinase and pStat3 protein expression in retinoblastoma.

We examine the immunoreactivity of the non-receptor tyrosine kinase, c-Src kinase and its downstream molecule, signal transducer and activator of transcription 3 (pStat3) in retinoblastoma (RB), and correlation with invasiveness and differentiation. Tumor samples from 40 patients with RB were available for the study. There were 18 tumors in group 1 (non-invasive) and 22 tumors in group 2 (invasive). The immunoreactivity of c-Src kinase and pStat3 was compared in the two groups of tumors. Group 1 (non-invasive) RB showed intermediate c-Src kinase immunoreactivity (Allred score 4-5) in 14/18 tumors and low immunoreactivity (Allred score 2-3) in 4/18 tumors. pStat3 was intermediate (Allred score 4-5) in 6/18 tumors and negative (Allred score 0) in 12/18 tumors. Group 2 (invasive) RB showed high c-Src kinase immunoreactivity (Allred score 6-8) in 22/22 tumors and high pStat3 (Allred score 6-8) in 19/22 tumors. The expression of c-Src kinase (P<0.001) and pStat3 (P<0.001) was significantly higher in group 2 RB. Src kinase expression (P<0.05) and pStat3 expression (P<0.05) was higher in the poorly differentiated tumors compared to moderately- and well-differentiated tumors. The increased expression of c-Src kinase and pStat3 expression could play a role in the invasiveness of group 2 tumors. Further characterization of the pathways involved in the pathogenesis of RB will shed light on fundamental mechanisms of tumorigenesis.

Biomarkers, Tumor↗