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W L Gerald

Publications and source records attributed to W L Gerald.

At least 55 records · Page 3Linked to original sources
PubMed1996

International neuroblastoma staging system stage 1 neuroblastoma: a prospective study and literature review.

PURPOSE: To gain insight into the management of non-metastatic neuroblastoma by examining clinical and biologic features of International Neuroblastoma Staging System (INSS) stage 1 tumors. METHODS: Patients were staged by both the INSS and the Evans staging system and were evaluated for biologic prognostic factors. Patients with INSS stage 1 received no cytotoxic therapy. The literature was reviewed for clinical and biologic data about INSS stage 1. RESULTS: We evaluated 10 consecutive patients (median age, 17.5 months) with INSS stage 1; all remain disease-free (median follow-up duration, > 5 years). Tumors were in the abdomen (n = 6), chest (n = 3), or pelvis (n = 1). Neuroblastoma involved margins of resection in six tumors. Poor-prognostic biologic findings included tumor-cell diploidy (n = 2) and unfavorable Shimada histopathology (n = 2). Two patients were to receive chemotherapy for, respectively, a tumor deemed unresectable and a tumor classified as Evans stage III; second opinions resulted in surgical management alone in each case. Published reports confirm that some INSS stage 1 patients (1) are at risk for overtreatment, and (2) have poor-prognostic biologic findings yet do well. CONCLUSION: Surgery alone suffices for INSS stage 1 neuroblastoma, even if biologic prognostic factors are unfavorable, microscopic disease remains after surgery, and tumor size is suggestive of "advanced-stage" status in other staging systems. Attempts to resect regionally confined neuroblastomas should take precedence over immediate use of cytotoxic therapy; otherwise, some patients may receive chemotherapy or radiotherapy unnecessarily.

Adolescent↗
PubMed1996

Analysis of p21WAF1/CIP1 in primary bladder tumors.

The p21WAF1/CIP1 gene is regulated by p53 and encodes a cyclin-dependent kinase (Cdk)-inhibitor involved in senescence and cell quiescence. The role of p21 as a negative regulator of cell proliferation suggests that it may function as a tumor suppressor gene. However, only a few mutations of the p21WAF1/CIP1 gene have been reported to date. In order to assess potential p21WAF1/CIP1 gene alterations in human bladder cancer, we have examined this gene and its encoded product in a well-characterized cohort of 27 primary bladder tumors. Mobility shifts by single-strand conformation polymorphism in the p21WAF1/CIP1 gene were identified in 2 cases. Sequencing analyses revealed that one of these cases had point mutations in the 3' untranslated region, while the other case had a frame shift mutation at positions 322 (C to A) and a deletion of 8 nucleotides (323-->331; CCG-->ACG, codon 81 Arg-->Thr) that produced a stop signal at codon 83 (Gly--Stop). This tumor had a p21-negative phenotype by immunohistochemistry, but did not lose any allele. We further characterized these cases by the study of TP53 mutations using single-strand conformation polymorphism (PCR-SSCP) and sequencing, as well as immunohistochemical assays. Seven mobility shifts were identified and seven cases showed p53 nuclear accumulation. The two cases displaying mutated p21WAF1/CIP1 had wild-type TP53. It is concluded that p21WAF1/CIP1 gene aberrations are infrequent in bladder carcinoma but may be occasionally identified in primary bladder tumors.

Aged↗
PubMed1995

Characterization of the genomic breakpoint and chimeric transcripts in the EWS-WT1 gene fusion of desmoplastic small round cell tumor.

Desmoplastic small round cell tumor is a recently recognized distinctive tumor shown to be associated with a recurrent translocation, t(11;22)(p13;q12), and rearrangement of the genes for Ewing sarcoma (EWS) and Wilms tumor (WT1). A genomic DNA fragment containing the EWS-WT1 gene fusion has been isolated from a desmoplastic small round cell tumor, and the breakpoint has been characterized. The breakpoints involve the intron between EWS exons 7 and 8 and the intron between WT1 exons 7 and 8. Chimeric transcripts corresponding to the fusion gene were detected in four of six cases studied. Analysis of these transcripts show an in-frame fusion of RNA encoding the amino-terminal domain of EWS to both alternatively spliced forms of the last three zinc fingers of the DNA-binding domain of WT1. Desmoplastic small round cell tumor represents the third tumor type associated with translocation of EWS and the first tumor associated with consistent translocation of WT1. The chimeric products are predicted to modulate transcription at WT1 target sites and contribute to development of this unique tumor.

Abdominal Neoplasms↗
PubMed1995

Desmoplastic small round cell tumor of the pleura.

Three cases of desmoplastic small round cell tumor (DSRCT) with multiphenotypic differentiation, primary in the pleura, are presented. This is a previously unrecognized site for this tumor type. Two patients were male and one female aged 29, 24, and 17 years. All presented with chest pain and were found to have pleural-based tumors associated with pleural effusion. Abdominal involvement was not present in any of the cases. Histologically, the tumor showed the characteristic features of intra-abdominal DSRCT, including angulated nests of small cells embedded in a vascular fibroblastic stroma, focal rhabdoid phenotype, and areas of central necrosis. The neoplastic cells showed evidence of epithelial, mesenchymal, and neural differentiation with characteristic dot-like positivity for vimentin and desmin topographically corresponding to perinuclear aggregates of intermediate filaments identified on electron microscopy in one case. Two patients died of disease 2 years and 15 months after presentation, respectively, and one patient is alive with disease 18 months after presentation. The histogenesis of DSRCT is unknown. Most previously reported cases involved the peritoneum or tunica vaginalis, suggesting a histogenetic relationship to the mesothelium. The occurrence of these tumors in the pleura lends further support to this theory.

Adolescent↗
PubMed1995

Very-high-dose short-term chemotherapy for poor-risk peripheral primitive neuroectodermal tumors, including Ewing's sarcoma, in children and young adults.

PURPOSE: To improve the prognosis of patients with poor-risk peripheral primitive neuroectodermal tumors (pPNETs; including peripheral neuroepithelioma and Ewing's sarcoma), while testing the feasibility of intensive use in adolescents and young adults of high-dose cyclophosphamide, doxorubicin, and vincristine (HD-CAV). PATIENTS AND METHODS: This report concerns previously untreated patients with newly diagnosed pPNET deemed poor-risk because of a tumor volume more than 100 cm3 or metastases to bone or bone marrow. The P6 protocol consists of seven courses of chemotherapy. Courses 1, 2, 3, and 6 include 6-hour infusions of cyclophosphamide on days 1 and 2 for a total of 4,200 mg/m2 per course (140 mg/kg per course for patients < 10 years old), plus 72-hour infusions of doxorubicin 75 mg/m2 and vincristine 2.0 mg/m2 beginning on day 1 (HD-CAV). Courses 4, 5, and 7 consist of 1-hour infusions of ifosfamide 1.8 g/m2/d and etoposide (VP-16) 100 mg/m2/d, for 5 days. Granulocyte colony-stimulating factor (G-CSF) and mesna are used. Courses start after neutrophil counts reach 500/microL and platelet counts reach 100,000/uL. Surgical resection follows course 3 and radiotherapy follows completion of all chemotherapy. RESULTS: Among the first 36 consecutive assessable patients (median age, 17 years), HD-CAV achieved excellent histopathologic or clinical responses in 34 patients and partial responses (PRs) in two patients. For 24 patients with locoregional disease, the 2-year event-free survival rate was 77%; adverse events were two locoregional relapses, one distant relapse, and one secondary leukemia. All six patients with metastatic disease limited to lungs achieved a complete response (CR) and did not relapse; one is in remission 36+ months from diagnosis, but the other patients are not assessable in terms of long-term efficacy of the P6 protocol because of short follow-up time (n = 3), additional systemic therapy (bone marrow transplantation), or septic death (autopsy showed no residual pPNET). All six patients with widespread metastases had major responses, including eradication of extensive bone marrow involvement, but distant relapses ensued. Myelosuppression was severe, but most patients received the first three courses of HD-CAV within 6 to 7 weeks. Major nonhematologic toxicities were mucositis and peripheral neuropathy. CONCLUSION: Excellent antitumor efficacy and manageable toxicity support the dose-intensive use of HD-CAV for pPNET in children, as well as in young adults. Consolidation of remissions of pPNET metastatic to bone and bone marrow remains a therapeutic challenge.

Adolescent↗
PubMed1995

Detection of circulating tumor cells in patients with localized and metastatic prostatic carcinoma: clinical implications.

PURPOSE: To determine the frequency with which prostate-specific antigen (PSA)-positive cells can be detected in the peripheral blood of patients with prostatic cancer in different stages and with different sensitivities to hormonal therapy. PATIENTS AND METHODS: Peripheral blood from 107 men with prostatic cancer and 27 non-prostate cancer controls was analyzed for PSA mRNA using reverse-transcriptase polymerase chain reaction (RT-PCR) and Southern blotting. RESULTS: The lower limit of detection was one PSA-producing cell diluted into 1 x 10(6) blood mononuclear cells. The test detected PSA mRNA in four of 25 patients (16%) with clinically organ-confined (T1-2) disease, three of 10 (30%) with T3-4 or N+ tumors, and 25 of 72 (35%) with distant metastases. None of the control samples were positive. An increase in positivity was observed with increasing PSA levels. Within the subgroup of patients with distant metastases, positivity was observed in six of 16 patients (38%) with normal or undetectable PSA levels after hormonal therapy and, overall, in 37% of patients (21 of 57) with androgen-independent disease. CONCLUSION: An RT-PCR-based assay for PSA mRNA can detect circulating cells in the peripheral blood of patients with prostatic cancer. The frequency of positivity increases with tumor stage. A unique observation was the detection of cells in patients with no measurable PSA on hormonal therapy. This suggests that continued seeding of distant sites may still be occurring in these patients, despite seemingly successful therapy. The relationship between continued seeding, disease progression, and survival will require further study.

Base Sequence↗
PubMed1995

Detection of chimeric transcripts in desmoplastic small round cell tumor and related developmental tumors by reverse transcriptase polymerase chain reaction. A specific diagnostic assay.

Desmoplastic small round cell tumor is a recently described entity associated with fusion of the EWS and WT1 genes and with expression of a chimeric transcript. To investigate the structure and potential diagnostic utility of the detection of EWS-WT1 chimeric RNA in desmoplastic small round cell tumor, 12 examples of this entity and 49 other tumors that enter in its differential diagnosis were studied by reverse transcriptase polymerase chain reaction for the presence of EWS-WT1, EWS-FLI-1, PAX3-FKHR, and PAX7-FKHR chimeric transcripts. EWS-WT1 was detected in 11 of 12 desmoplastic small round cell tumors but not in any other tumor type studied, including 17 Wilms' tumors, 10 Ewing's sarcomas/primitive neuroectodermal tumors, 13 alveolar rhabdomyosarcomas, and 9 embryonal rhabdomyosarcomas. One desmoplastic small round cell tumor was found to have a variant EWS-WT1 chimeric product that included exon 8 of EWS EWS-FLI-1 chimeric RNA was present in all Ewing's sarcoma/primitive neuroectodermal tumor and not identified in any other tumor types, including desmoplastic small round cell tumor. PAX3/PAX7-FKHR chimeras were present in 9 of 13 alveolar rhabdomyosarcomas but not in any other tumors. Detection of chimeric transcripts by reverse transcriptase polymerase chain reaction is a very specific aid in differential diagnosis of developmental tumors and further establishes desmoplastic small round cell tumor as a distinct entity.

Adolescent↗
PubMed1995

Molecular diagnosis of synovial sarcoma and characterization of a variant SYT-SSX2 fusion transcript.

The translocation t(X;18)(p11;q11) is seen in > 80% of synovial sarcomas (SS) with informative karyotypes. The breakpoints of the t(X;18) have been cloned and shown to involve two novel genes, SSX (at Xp11) and SYT (at 18q11), which produce a chimeric SYT-SSX transcript as a result of the translocation. Recently, SSX has been shown to be duplicated, with both copies, SSX1 and SSX2, located within distinct subregions of Xp11. We performed a reverse transcriptase polymerase chain reaction (RT-PCR) assay for both chimeric SYT-SSX transcripts in a series of 35 SS (29 monophasic, 6 biphasic) to assess its usefulness in molecular diagnosis and to evaluate the incidence of molecular variants. Of the 35 cases, 29 (83%) showed a specific SYT-SSX RT-PCR product, using a consensus primer for SSX1 and SSX2 Upon excluding three negative cases that had poor quality RNA, the proportion of positives rose to 91% (29/32). The 29 positive cases were further studied using primers specific for either SSX1 or SSX2; 19 cases were positive for SYT-SSX1 and 10 for SYT-SSX2. The relationship of histological subtype (monophasic versus biphasic) to SSX1 or SSX2 involvement was not statistically significant. In a single histologically unremarkable monophasic SS, a slightly larger SYT-SSX2 RT-PCR product was observed. Sequencing of this novel variant showed a 129-bp segment inserted between the usual SYT and SSX2 fusion points, of which 126 bp were derived from a more proximal (5') portion of SSX2 The 3 bp immediately 5' to the fusion point could not be assigned to either SYT or SSX2 and may represent an insertion-deletion or a cryptic splicing event. This fragment maintains the reading frame of the chimeric product and encodes a predicted protein larger by 43 amino acids, which nevertheless replaces the region homologous to the transcriptional repression domain Kruppel-associated box, recently recognized in the 5' portion of the SSX genes, with all but the 3' end of the SYT transcript. Thus, a diagnosis of SS may be confirmed in > 90% of cases using RT-PCR detection of the chimeric transcript resulting from the t(X;18), and the incidence of molecular variants appears low.

Adolescent↗
PubMed1994

Immunohistochemical detection of cathepsin D in T2N0M0 breast carcinoma.

Recent studies have reported significant but inconsistent correlations between tumor cathepsin D (CD) concentration and prognosis in breast carcinoma. To investigate the tissue distribution and a prognostic utility of CD in breast carcinoma, 159 cases of T2N0M0 breast carcinoma with a minimum of 10 years' follow-up were studied for CD expression by immunohistochemistry. This group of patients was chosen for study because of current interest in prognostic markers for stage I breast carcinoma and the likelihood that there would be sufficient recurrences in this group to detect significant differences. Seventy-two carcinomas (45%) showed prominent staining of cells composing the tumor. Neoplastic cell staining for CD correlated with well-differentiated architecture, and lack of neoplastic cell CD expression correlated with high nuclear grade and the medullary carcinoma category. Stromal cell (primarily histiocyte) staining in carcinomas was the major contributor to CD expression in 67 of the 159 cases (42%). Intense intratumoral stromal cell staining correlated with absence of estrogen receptors and the medullary carcinoma subtype. There was no significant correlation between disease-free or overall survival and (a) intensity of overall staining for CD, (b) staining of carcinoma cells alone, or (c) staining of nonneoplastic cells within the region of the carcinoma. These results show that a significant proportion of CD activity detected within a tumor by immunohistochemistry may be contributed by nonneoplastic cells, and there is no significant correlation between survival and immunohistochemical detection of CD in T2N0M0 breast cancer.

Analysis of Variance↗
PubMed1994

Solitary fibrous tumor. Consistent CD34 immunoreactivity and occurrence in the orbit.

The distinction of solitary fibrous tumors (SFTs) from histologically similar neoplasms relies heavily on a characteristic microscopic appearance. No discriminating ultrastructural or immunohistochemical features are known. We evaluated 22 SFTs and 118 other tumors often considered in the differential diagnosis for immunoreactivity using a monoclonal antibody directed against the human hematopoietic progenitor cell antigen, CD34. All the SFTs (22 of 22, 100%) demonstrated strong CD34 immunoreactivity, irrespective of tumor site and histologic grade. Strong and generalized CD34 positivity was also found in most dermatofibrosarcoma protuberans (11 of 12, 92%) and occasional smooth-muscle tumors (leiomyomas 2 of 11, 18%; leiomyosarcomas 2 of 11, 18%). Variable numbers of CD34 positive cells were present in all neurofibromas (9 of 9, 100%) and focally present in most schwannomas (8 of 9, 89%). Some of the hemangiopericytomas (7 of 16, 44%) exhibited CD34 immunoreactivity, however, generally with weak intensity and patchy distribution. CD34 immunoreactivity was not observed in mesotheliomas (0 of 20, 0%), synovial sarcomas (0 of 13, 0%), fibrosarcomas (0 of 12, 0%), or spindle-cell thymomas (0 of 5, 0%). We conclude that CD34 immunoreactivity is a sensitive marker for SFT and, in conjunction with an appropriate immunohistochemical panel, may be useful in discriminating SFTs from other histologically similar neoplasms. The observation that some mesenchymal stromal cells and SFTs share a CD34-positive immunophenotype suggests a histogenetic relationship. The inclusion in this study of two cases of SFTs arising in the orbit establishes another site of origin for this tumor and provides further support for a mesenchymal histogenesis.

Antibodies, Monoclonal↗
PubMed1994

Highly effective induction therapy for stage 4 neuroblastoma in children over 1 year of age.

PURPOSE: To test the efficacy of a protocol for poor-risk neuroblastoma that builds on the following: (1) our favorable previously reported results with dose-intensive use of cyclophosphamide; (2) our retrospective analysis of neuroblastoma chemotherapy reports, which supported the value of high-dose cisplatin and etoposide (VP-16); and (3) the Goldie-Coldman hypothesis that rapid cytoreduction plus the use of non-cross-resistant chemotherapy combinations will decrease the risk of drug resistance. PATIENTS AND METHODS: The N6 protocol included seven courses of high-dose chemotherapy plus surgical resection of bulk disease. Courses 1, 2, 4, and 6 consisted of 6-hour intravenous infusions of cyclophosphamide 70 mg/kg/d on days 1 and 2 (ie, 140 mg/kg per course), a 72-hour intravenous infusion of doxorubicin 75 mg/m2 and vincristine 0.1 mg/kg beginning day 1, and vincristine 1.5 mg/m2 intravenous bolus on day 9. Courses 3, 5, and 7 consisted of 2-hour intravenous infusions of VP-16 200 mg/m2/d on days 1 to 3 (ie, 600 mg/m2 per course), and 1-hour intravenous infusions of cisplatin 50 mg/m2/d on days 1 to 4 (ie, 200 mg/m2 per course). Courses were to start after neutrophil counts reached 500/microL and platelet counts reached 100,000/microL. Response was defined by international criteria. RESULTS: Among 24 consecutive previously untreated patients diagnosed with stage 4 neuroblastoma at more than 1 year of age, 21 patients achieved a complete or very good partial remission; one patient had no evidence of disease except by iodine-131-metaiodobenzylguanidine (MIBG) scan, which was markedly improved; and one patient had resolution of extensive metastatic disease, but still had an incompletely resected primary tumor. The sole patient to have a poor response had clinical features at diagnosis that are atypical for neuroblastoma, namely, 8 years of age and an unknown primary tumor. Severe toxicities included myelosuppression, mucositis, and hearing deficits. CONCLUSION: The N6 approach reliably achieves significant cytoreduction against stage 4 neuroblastoma. This may eventuate in an improved cure rate, since consolidative treatments using myeloablative therapy, immunotherapy, or biologic response modifiers such as cis-retinoic acid are most likely to be effective against minimal residual disease.

Abdominal Neoplasms↗
PubMed1994

The molecular genetics of Wilms tumor: a paradigm of heterogeneity in tumor development.

The evidence that genes on chromosome 11 are involved in Wilms tumor development is convincing; however, it is also evident that the mechanisms of tumorigenesis are more complex than the two-mutation model originally proposed. Potentially several genetic loci participate in Wilms tumor development. This should not be too surprising considering the complexity of pathways regulating growth and differentiation in nephrogenesis. It is possible that these various genes act at different points in the differentiation pathway and disruption of their normal function contributes to tumorigenesis. In fact, these loci may interact with one another in tumor formation. Certain types of genetic alterations may be the rate-limiting steps, but other changes may also contribute or be necessary for tumor development. Homozygous inactivation of specific genes, combinations of mutated alleles, and relaxation of genetic imprinting, or even interactions between different mutated alleles may all be part of the process for individual tumors. It has been found that some patients with the WAGR syndrome who are hemizygous for WT1 at 11p13 have in addition loss of heterozygosity within 11p15, and a sporadic tumor has been shown to have a WT1 mutation and loss of heterozygosity at loci at both 11p15 and 11p13 (59,85). These observations suggest the potential for interaction among the various Wilms tumor loci. Not only are there likely to be a number of different genetic loci linked to Wilms tumor development, but the mechanisms underlying altered gene function may be more variable than originally believed. It is probably not correct to think of Wilms tumor as a homogeneous entity. Mutations at different loci or various combinations of genetic lesions could well be responsible for the different categories of Wilms tumors. This apparent genetic complexity of Wilms tumor development is a concept that can very likely be applied to many other types of neoplasms. A complete understanding of Wilms tumorigenesis awaits identification of all members of the Wilms tumor gene family and the functional significance of their alterations.

Chromosomes, Human, Pair 11↗
PubMed1993

Viral gene detection in oral neoplasms using the polymerase chain reaction.

Eighty-four squamous cell proliferative lesions of the oral cavity and six examples of normal oral squamous mucosa were investigated for the presence of human papillomavirus (HPV) by the polymerase chain reaction (PCR) using universal primers and type specific probes. Human papillomavirus was identified in 1 of 6 histologically normal biopsy specimens, 2 of 4 hyperplasias, 2 of 5 inflammatory lesions, 9 of 36 cases of dysplasia or carcinoma in situ, and 7 of 39 carcinomas. All of the specimens found positive for HPV using the PCR were confirmed using slot blot hybridizations. All HPV-positive cases contained HPV 16. In addition, 2 were co-infected with HPV 11 and 1 was co-infected with HPV 18. Types 6 and 33 were not found. The same genotypes that infect the uterine cervix also were found in the oral cavity. This is the first time universal primers that allow for the detection of HPV types 6, 11, 16, 18, 31, 33, 35, 39, 40, 42, 45, 51-59, and at least 25 other novel types have been used on oral tumors, and represents the largest number of oral samples analyzed by the PCR at this time. Due to lack of clear correlation between HPV infection and histologic findings, however, the role of this virus in oral carcinogenesis remains uncertain.

Carcinoma, Squamous Cell↗
PubMed1993

Desmoplastic small cell tumor with multi-phenotypic differentiation.

Desmoplastic small cell tumor (DSCT) is a distinctive, poorly understood malignant tumor with a complex phenotype. The main features of the 46 cases presented here include a mean age of 20.8 years (range 7-48), male predominance (37 M:9 F), primary intraabdominal location (except for 2 cases), characteristic histologic pattern consisting of tumor cell nests surrounded by a cellular desmoplastic stroma, immunohistochemical reactivity for markers of epithelial, muscle and neural differentiation, and association with a unique cytogenetic abnormality. These findings suggest that this tumor is a distinct neoplastic process and that it probably belongs to the family of primitive small round cell developmental tumors. It is proposed that DSCT arises during development from a progenitor cell with potential for multiphenotypic differentiation.

Adolescent↗
PubMed1992

Expression of the 11p13 Wilms' tumor gene, WT1, correlates with histologic category of Wilms' tumor.

Homozygous inactivation of WT1, a Wilms' tumor gene located on chromosome 11 at p13, is believed to predispose to Wilms' tumor and therefore may be a common occurrence in this cancer. The expression of this gene in primary Wilms' tumors was examined by northern and quantitative RNA slot blot analysis and compared with clinical, histologic, and molecular features of each case. The characteristic 3.2 kb RNA was readily detected in most primary tumors although there was marked variation in the level of WT1-specific transcripts. No abnormal-sized RNA products were detected and expression of WT1 was not coordinated with that of several other oncofetal genes: N-myc, insulinlike growth factor 2 (IGF-2), and c-myc. The relative abundance of WT1-specific RNA did correlate with the histologic category of Wilms' tumor such that those tumors with heterologous differentiation have, in general, lower relative levels of WT1 transcripts than those tumors without heterologous differentiation. These results further establish the heterogeneity of Wilms' tumor with respect to the expression of tumor-associated oncofetal genes and suggest a relationship between WT1 expression and cellular differentiation.

Antigens, Neoplasm↗
PubMed1991

Intra-abdominal desmoplastic small round-cell tumor. Report of 19 cases of a distinctive type of high-grade polyphenotypic malignancy affecting young individuals.

Nineteen cases of a distinctive type of malignant small-cell tumor are presented. The main features of the entity are as follows: a predilection for adolescent males (mean age: 18.6 years); predominant or exclusive intra-abdominal location, with only inconstant and secondary organ involvement; nesting pattern of growth; focal rhabdoid features; intense desmoplastic reaction; immunohistochemical reactivity for epithelial [keratin, epithelial membrane antigen (EMA)], neural [neuron-specific enolase (NSE)], and muscle (desmin) markers; and highly aggressive behavior. It is proposed that this represents yet another member of the continuously enlarging and evolving family of small round (blue) cell tumors of infancy and childhood that features, more than any other member of this group, the capacity for simultaneous multidirectional phenotypical expression.

Abdominal Neoplasms↗