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PubMed2003

Diagnostic significance and clinical applications of chimeric genes in Ewing's sarcoma.

Ewing's sarcoma (ES) is one of the most malignant bone and soft tissue tumors in childhood. Morphologically, ES belongs to the small round cell tumors (SRCT). ES, peripheral primitive neuroectodermal tumor (PNET), and Askin's tumor are classified as ES family tumors (ESFT) because they share a common chromosomal translocation. The EWS-FLI1 chimeric gene is generated by t (11; 22). Other reciprocal translocations resulting in formation of chimeric genes between EWS and ETS family genes (ERG, ETV1, E1AF, and FEV) are t (21; 22), t (7; 22), t (17; 22), and t (2; 22), respectively. Although it is generally difficult to distinguish ES from SRCT, we could easily and quickly distinguish ES from other SRCT by using reverse transcription polymerase chain reaction (RT-PCR). We looked for specific chimeric genes in 23 tumor samples, including three ES clinical samples. We detected five chimeric genes in the three ES samples. Three chimeric genes, all EWS-FLI1, were detected in one ES sample. Different chimeric genes, EWS-ERG and EWS-ETV1, were detected in the other two ES samples. Moreover, because we could not detect specific chimeric genes in samples from non-ESFT, it may be possible to use this technique to diagnose ESFT and to detect tumor cell contamination before hematopoietic stem cell transplantation.

Adolescent↗
PubMed2003

Advances in the diagnosis, molecular genetics, and treatment of pediatric embryonal CNS tumors.

Embryonal central nervous system (CNS) tumors are the most common group of malignant brain tumors in children. The diagnosis and classification of tumors belonging to this family have been controversial; however, utilization of molecular genetics is helping to refine traditional histopathologic and clinical classification schemes. Currently, this group of tumors includes medulloblastomas, supratentorial primitive neuroectodermal tumors, atypical teratoid/rhabdoid tumors, ependymoblastomas, and medulloepitheliomas. While the survival of older children with nonmetastatic medulloblastomas has improved considerably within the past two decades, the outcomes for infants and for those with metastatic medulloblastomas or other high-risk embryonal CNS tumors remain poor. It is anticipated that the emerging field of molecular biology will greatly aid in the future stratification and therapy for pediatric patients with malignant embryonal tumors. In this review, recent advances in the diagnosis, molecular genetics, and treatment of the most common pediatric embryonal CNS tumors are discussed.

Central Nervous System Neoplasms↗
PubMedDate not supplied

Samarium-153 ethylenediamine tetramethylene phosphonate therapy for bone pain palliation in skeletal metastases.

BACKGROUND: Systemic therapy with radionuclides may be used for the treatment of patients with painful skeletal metastases owing to its efficacy, low cost and low toxicity. Imported radionuclides for pain palliation, like Strontium-89 are expensive; particularly for developing countries. In the Indian scenario, Samarium-153 (Sm-153) is produced in our own reactors and as a result, it is readily available and economical. AIM: We undertook this study to determine the efficacy and toxicity of single-dose Sm-153 ethylenediamine tetramethylene phosphonate as a palliative treatment for painful skeletal metastases. MATERIALS AND METHODS: Eightysix patients with painful skeletal metastases from various primaries, were treated with Sm-153 EDTMP at a dose of 37 MBq/kg. The effects were evaluated according to change in visual analogue pain score, analgesic consumption, Karnofsky performance score, mobility score and blood count tests, conducted regularly for 16 weeks. STATISTICS: Repeated measures analysis. RESULTS: The overall response rates were 73%, while complete response was seen in 12.4%. Reduction in analgesic consumption with improvement in Karnofsky performance score and mobility score, was seen in all responders. Response rates were 80.3 and 80.5% in breast and prostate cancer, respectively. One case, each of Wilms tumor, ovarian cancer, germ cell tumor testis, multiple myeloma, primitive neuroectodermal tumor and oesophageal cancer, did not respond to therapy. No serious side-effects were noted, except for fall in white blood cell, platelet and haemoglobin counts, which gradually returned to normal levels by six-eight weeks. CONCLUSION: Sm-153 EDTMP provided effective palliation in 73% patients with painful bone metastases: the major toxicity was temporary myelosuppression.

Adolescent↗
PubMedDate not supplied

Activity of bortezomib in glioblastoma.

BACKGROUND: Chemotherapy is the commonly accepted standard therapy for most types of brain tumor, especially in medulloblastoma, primitive neuroectodermal tumor and astrocytoma. However, no efficient therapy has been established to date for glioblastoma multiforme. The aim of the present study was to analyze the activity of bortezomib in glioblastoma cell lines in comparison with that in a pediatric acute lymphoblastic leukemia cell line. MATERIALS AND METHODS: Glioblastoma multiforme T98G, glioblastoma-astrocytoma U373M and T-lineage acute lymphoblastic leukemia CCRF-CEM cell lines were used. Proteasome inhibitor, bortezomib and 14 other anticancer drugs were tested using the MTT assay. RESULTS: Compared to the acute lymphoblastic cell line, both glioblastoma cell lines showed relatively good sensitivity to bortezomib, as well as to cisplatin, carboplatin, etoposide and actinomycin-D. The lines showed intermediate sensitivity to thiotepa and daunorubicin, but were highly resistant to first-line drugs used in the therapy of acute lymphoblastic leukemia, such as prednisolone, L-asparaginase, vincristine, doxorubicin and cytarabine. Bortezomib, which is not a substrate for PGP and MRP1, did not show cross resistance to drugs transported by these proteins. CONCLUSION: Our results support the necessity for further research on the role of bortezomib in the therapy of glioblastoma.

Antineoplastic Agents↗
PubMed1993

Cytogenetic evaluation of childhood neoplasms.

The cytogenetics of childhood neoplasms are reviewed. Chromosome abnormalities specific for various pediatric neoplasms can provide diagnostic, prognostic, and scientific information of value to the pathologist, clinician, and molecular biologist. Karyotypes of acute leukemia have independent prognostic significance. Chromosome aberrations associated with several of the small round blue-cell tumors of childhood can clarify the diagnosis. Recurring abnormalities in several tumors, such as hepatoblastomas, primitive neuroectodermal tumors, fibrosarcomas, and other tumor types, suggest interesting questions about pathogenesis and histogenetic relationships. Several tumor-specific chromosome aberrations, mostly in the acute leukemias, have been characterized at a molecular level.

Child↗
PubMed1996

EWS/FLI-1 antagonists induce growth inhibition of Ewing tumor cells in vitro.

Among primitive neuroectodermal tumors, Ewing tumors are characterized by a gene rearrangement recombining the 5'-EWS gene portion with one of two ETS-related proto-oncogenes, FLI-1 or ERG, in roughly 90 and 10% of cases, respectively. We attempted to antagonize EWS/FLI-1 function in Ewing tumor cell lines. As a control, a cell line derived from another small round cell tumor of neuroectodermal origin, neuroblastoma, was used. This cell line was found to express almost identical patterns of ETS proteins except for EWS/FLI-1 and a novel, ELF-related gene product. Stable expression of antisense EWS/FLI-1 cDNA resulted in decreased endogenous EWS/FLI-1 RNA levels and growth reduction of ET cells but not of neuroblastoma cells. DNA-binding FLI-1 derivatives localizing to the nucleus in which the 5'-EWS regulatory domain was replaced by bacterial beta-galactosidase dominantly modulated transcriptional transactivation from a degenerate ETS-binding motif. Transient transfection of these dominant-negative recombinants resulted in a significant decrease in the relative number of mitoses in four Ewing tumor cell lines tested but not in the neuroblastoma cell line. The presented evidence for modulation of tumor cell proliferation by EWS/FLI-1 antagonists suggests a causal role for EWS/FLI-1-mediated gene activation in the malignant transformation of the enigmatic Ewing tumor-precursor cell.

Blotting, Northern↗
PubMed2004

Imatinib mesylate (STI571) interference with growth of neuroectodermal tumour cell lines does not critically involve c-Kit inhibition.

A therapeutic role of STI571 (imatinib mesylate) has been anticipated in patients with c-Kit positive neuroectodermal tumors. We examined the efficacy of STI571 to inhibit expansion of c-Kit positive neuroectodermal tumor cell lines in vitro and in a mouse model inoculated with ES (Ewing sarcoma) derived tumor cells, and investigated the molecular mechanism of STI571 action. Eleven tumor lines of ES, PNET (primitive neuroectodermal tumors) and NB (neuroblastoma) were assayed in the presence of 1, 5, 10, 15, 20 or 30 micro M STI571 for 24, 48, 72 h and 7 days. The mechanism of STI571 action was investigated using a microphysiometer cytosensor that determines cellular metabolic rates in the presence of STI571. c-Kit and global protein phosphorylation was assayed by immunoprecipitation and a direct enzyme-linked immunoadsorbent assay after 72 h of 10 micro M STI571. Apoptosis was investigated by propidium iodide (PI), Annexin V staining and by enzymatic activity of caspase-3. Moreover, apoptotic gene expression was investigated using microarray technology. In nude mice, tumor volume and histology were analyzed in STI571 treated and untreated mice, and apoptotic gene expression analysis was performed on tumor masses. A decrease in cell proliferation and increase of cell apoptosis was caused by STI571 in a concentration- and time-dependent manner. Cytosensor microphysiometer and immunoprecipitation experiments demonstrated a time- and concentration-dependent decrease of cellular metabolic activity and global protein dephosphorylation after STI571 exposure. The inhibition by STI571 appeared at least to some extent independent of c-Kit inhibition since cells remained sensitive to SCF stimulation. Tumor volume was significantly reduced in STI571-treated mice compared to tumors from control inoculated non-treated mice. The apoptosis pathway in response to STI571 appeared not to be dependent on caspase activation, while gene expression profiles suggested accumulation of reactive oxygen species (ROS) resulting in cell death after exposure to STI571. The results point to the potential relevance of STI157 for neuroectodermal tumor therapy in view of its inhibitory effect on tumor cell growth, in spite of the observation that the inhibition of the c-Kit signaling pathway is not critically involved.

Animals↗
PubMed2003

Malignant peripheral nerve sheath tumor of small round cell type with pleomorphic spindle cell sarcomatous areas.

An unusual case of malignant peripheral nerve sheath tumor (MPNST) arising in the posterior mediastinum of a 59-year-old man is reported. Histopathologically, the tumor showed an admixture of a dense proliferation of small round cells resembling a primitive neuroectodermal tumor (PNET) and a pleomorphic spindle cell sarcomatous area. Abortive rosettes, primitive neural tube-like structures, and a few glandular structures were found in the small round cell area. Small round cells were immunoreactive for neural cell adhesion molecule and synaptophysin, but were not immunoreactive for MIC2 and neuron-specific enolase. Pleomorphic spindle cells were occasionally arranged in a storiform pattern and were diffusely immunoreactive for S-100 protein. The MPNST of small round cell type is distinguishable from PNET by its negative immunoreactivity for MIC2, and the present tumor is assumed to be derived from primitive neuroectodermal cells in the peripheral nerve capable of bidirectional (neuron and Schwann cell) differentiation.

Biomarkers, Tumor↗
PubMed1999

Neuroectodermal differentiation in Ewing's sarcoma family of tumors does not predict tumor behavior.

The observation that neuroectodermal differentiation imparts a worse prognosis to the Ewing family of tumors has been suggested by some studies and refuted by others. To assess whether the diagnosis of Ewing's sarcoma versus peripheral primitive neuroectodermal tumor (PNET) affects prognosis, we analyzed tumors from 63 analogously treated pediatric and young adult patients from the National Cancer Institute and St Jude Children's Research Hospital and retrospectively compared the results with clinical outcomes. The tumors were assessed using standard light microscopy and immunohistochemical stains for neuron-specific enolase, CD57, S100 protein, neurofilament protein, and synaptophysin with or without antigen retrieval. Ultrastructural evaluation was also performed in 39 tumors. Classification was performed using Kiel criteria as well as a modified classification. Kaplan-Meier analyses, with Mantel-Haenzel evaluation of the significance of the differences, were performed separately for localized or metastatic tumors. Using the Kiel classification on a subset of 60 cases, 39 tumors qualified as PNET and 21 as Ewing's sarcoma. Using the modified classification on a subset of 61 cases, 14 were classified as PNET, 21 as atypical Ewing's sarcoma, and 26 as Ewing's sarcoma. The addition of electron microscopy to the diagnostic armamentarium significantly increased the likelihood of identifying PNET. No significant differences in event-free or overall survival were seen using either the modified or Kiel classification, regardless of the ancillary diagnostic techniques employed. In this exploratory analysis, neuroectodermal differentiation did not play a role in clinical outcome. Confirmation of this finding will require a larger, separate study of similarly treated patients, and it may not apply to older patients.

Adolescent↗
PubMed1989

Primary intracranial neoplasms in the first year of life.

Forty-one infants with histologically verified primary intracranial neoplasms were studied who had been diagnosed and treated during the first year of life at the Hospital for Sick Children during the years 1975-1986. Forty-one percent of tumors were astrocytomas, 22% were primitive neuroectodermal tumors, and 20% were choroid plexus papillomas. Seventy-one percent were located in the supratentorial compartment and 29% in the infratentorial compartment. Thirty percent were in the cerebral hemisphere, 12% in the optic pathway-hypothalamic region, 5% in the thalamus, 17% in the cerebellum, 5% in the brain stem, 12% in the lateral ventricles, 12% in the III ventricle, and 7% in the IV ventricle. The most common presenting features in this series of patients were vomiting and increasing head size. The symptoms and signs before diagnosis were present for 2 months or less in 87% of cases. Forty-four percent of the tumors were totally resected while only a partial resection or biopsy was carried out in 56%. Sixty-six percent of the patients required a CSF diversionary shunt. Twenty-nine percent of patients received radiotherapy. Slightly more than half of these received radiotherapy immediately after surgery, whereas delayed radiation therapy was performed in the remainder. The surgical mortality was 7.3%. Of the entire group, 39% have died, with most dying within 6 months of surgery. Treatment, survival relative to histologic type, psychomotor development, and neurologic function of the survivors are discussed.

Age Factors↗
PubMedDate not supplied

Pediatric core needle biopsy: strengths and limitations in evaluation of masses.

Needle core biopsies (NCB) are widely used in adults but are less often used for the evaluation of pediatric tumors. To determine the diagnostic utility of NCB for pediatric tumors, we performed a retrospective analysis. Fifty NCB of masses from 1992 to 1998, subsequent pathologic specimens, and medical records were reviewed. All patients were less than 21 years of age. Of the NCB 78% (39/50) were diagnostic of a neoplasm, 8% (4/50) were nondiagnostic in cases where a tumor was subsequently diagnosed, and 14% (7/50) revealed inflammatory or reactive lesions, with no subsequent diagnosis of a neoplasm according to medical record review. In cases in which a neoplasm was present, NCB was diagnostic in 91% (39/43). For cases in which there was a previous diagnosis of a tumor, 100% (9/9) of NCB were diagnostic of a recurrence or metastasis. In cases of NCB for primary tumor diagnosis, 88% (30/34) were diagnostic. The most common problems encountered were related to specimen adequacy, such as insufficient tissue, crush artifact, and tumor necrosis. Tumor diagnoses were as follows: primitive neuroectodermal tumor (PNET)/Ewing sarcoma (12), malignant lymphoma/Hodgkin's disease (8), rhabdomyosarcoma (4), germ cell tumor (3), Wilms' tumor (3), neuroblastoma (1), sarcoma, not otherwise specified (4), and other neoplasms (8). There were no complications of the procedure. NCB of pediatric tumors is an effective diagnostic tool and can be used to obtain diagnostic material quickly and safely. NCB was diagnostic in 90% of cases in this series. When NCB provide sufficient material for immunohistochemical, cytogenetic, flow cytometric, and other ancillary studies, the diagnostic efficacy is enhanced. The major limitations in this series were related to sampling problems and specimen adequacy for comprehensive pathologic evaluation.

Adolescent↗
PubMed2005

Differentiating imaging findings in primary and secondary tumors of the jugular foramen.

The preoperative diagnosis of a jugular foramen tumor may be challenging, since a large variety of unusual lesions may be located in this region. These tumors may be classified as primary lesions (which are located in the jugular foramen or extend from the jugular foramen into the surrounding structures) and as secondary lesions (that extend from the surrounding structures into the jugular foramen). Primary tumors include glomus jugulare tumors, schwannomas, meningiomas and peripheral primitive neuroectodermal tumors, while secondary tumors comprise chordomas, chondrosarcomas, chondroblastomas, giant-cell tumors, cholesterol granulomas, giant cholesterol cyst, endolymphatic sac tumors, reactive myofibroblastic tumors, temporal bone carcinomas and metastases. Accurate preoperative radiological suspicion is of great value for preoperative patient counseling and has a direct impact on the surgical planning in these cases. The present study describes and discusses the main differentiating imaging features of lesions involving the jugular foramen, whose accurate preoperative radiological evaluation is essential for proper surgical planning.

Brain Neoplasms↗
PubMed2000

Preliminary individual adjuvant therapy for gliomas based on the results of molecular biological analyses for drug-resistance genes.

New adjuvant therapy individualized by the results of reverse transcription-polymerase chain reaction (RT-PCR) for drug-resistance genes has been used to treat malignant gliomas. Protocol studies for malignant gliomas were not so encouraging in their therapeutic results because of heterogeneity and the various drug-sensitivities of the tumors. Individualization of glioma therapy is recommended. Drug-resistance genes messenger ribonucleic acid (mRNA) expressions were investigated in drug-resistant human glioma cell lines derived from U87MG and 46 frozen samples of retrospectively examined neuroepithelial tumors (12 low grade neuroepithelial tumors, 16 Grade III gliomas, 11 glioblastomas, and 7 other malignant neuroepithelial tumors such as medulloblastomas and primitive neuroectodermal tumors) by RT-PCR with the specific primers for O6-methylguanine DNA methyltransferase (MGMT), multidrug-resistance gene 1 (MDR1), multidrug-resistance-associated protein (MRP), and glutathione-S-transferase-pi (GST-pi). Thirty-seven preliminary individual adjuvant therapies (IAT) based on RT-PCR results, mainly in MGMT expression, were performed on 30 consecutive patients with neuroepithelial tumors. In the retrospectively examined series, the initial response to 1-(4-amino-2-methyl-5-pyrimidynyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) was correlated most significantly to the MGMT mRNA expression among 11 independent prognostic factors (p = 0.0037) in multivariate logistic regression analysis. In the preliminary IAT, 17 of 32 evaluable therapies had a partial or complete response (53.1% response rate). Our IAT based on RT-PCR seemed to be more effective than conventional therapies for malignant gliomas.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Mutation analysis of human cytokeratin 8 gene in malignant rhabdoid tumor: a possible association with intracytoplasmic inclusion body formation.

The rhabdoid cell, which is typically observed in malignant rhabdoid tumor (MRT) and other malignant neoplasms, has an eosinophilic cytoplasm containing a spheroid perinuclear inclusion body. This distinct cell is known to act as a highly aggressive indicator in many types of malignant tumors and is characterized by aggregates of intermediate filaments, comprising both vimentin and cytokeratin (CK) 8, which is mainly expressed in simple-type epithelium such as liver and intestine. To clarify the cause of the inclusion body formation, we analyzed the alteration of the complete human CK8 gene (KRT 8: 1724 base pairs) in seven samples of MRT (three from frozen materials and four from cultured cell lines) by reverse-transcriptase polymerase chain reaction, followed by direct sequencing. In addition, the two cell lines, Huh7 and HeLa, which lacked rhabdoid feature, six pediatric malignant tumors, including three cases of primitive neuroectodermal tumor (PNET) and three of Wilms' tumor; and 15 normal liver tissue (as a control) were also analyzed. All MRT samples had missense mutations in the human KRT 8 gene, i.e., Arg89 --> Cys (5/7); Arg --> Cys251 (3/7); Glu267 --> Lys (6/7); Ser290 --> Ile, Met; (7/7) and Arg301 --> His(4/7), none of which was detected in any control samples. Among these mutations, the most noteworthy findings were that Arg89 belongs to the H1 subdomain of the head domain and that Arg251 belongs to the short nonhelical linker segment, or L1-2. Both these mutations are noted for their relationships to lateral protofilament-protofilament interactions. In addition, Ser290 has been previously reported to be a phosphorylation site, which has been recognized to play an important role in filament organization, leading to conformational change of the CK8 filaments. In conclusion, mutated codons of CK8 gene in MRT were located in the important region involved in the conformational change of intermediate filament.

Amino Acid Sequence↗
PubMed2006

Clonality analysis of pediatric multiple tumors: two case reports and laboratory investigation.

We examined the possibility of using microsatellite and mitochondrial DNA polymorphisms as markers to detect the clonal origin of tumor cells found in the same patient. We considered two children with complex tumor diseases: one with supratentorial primitive neuroectodermal tumors (PNET) and a hepatic rhabdoid tumor and another with brain and abdominal rhabdoid tumors. In the first patient we found an mtDNA cytosine insertion both in the normal tissue and in the primary tumor, whereas in the hepatic tumor we detected an insertion of 2 cytosine. In the second child, who had a constitutional mutation of hSNF5/INI-1, we identified the same mtDNA pattern both in normal tissue and in the abdominal tumor but not in the brain tumor, which presented three different mtDNA polymorphisms. Thus, we demonstrated the same clonal origin for tumors in the first patient and different clonal origins of the tumors in the second patient. At times it is very difficult to discriminate two neoplastic lesions or metastatic diseases by using only histopathologic techniques. Molecular examination of clonality is a useful tool to obtain information about the origin of synchronous and/or metachronous tumors found in the same patient.

Adult↗
PubMed1994

Genetic aberrations in human brain tumors.

Over the last decade, much has been learned about the genetic changes that occur in human neoplasia and how they contribute to the neoplastic state. Oncogenes and tumor suppressor genes have been identified, and many powerful molecular genetic techniques have emerged. Brain tumors have been intensively studied as part of this process. Specific and recurring genetic alterations have been identified and are associated with specific tumor types. In astrocytomas, for example, losses of genetic material on chromosomes 10 and 17 and amplification of the epidermal growth factor receptor gene seem important in pathogenesis, with the loss of chromosome 10 and the amplification of epidermal growth factor receptor being strongly associated with glioblastoma multiforme. Meningiomas, on the other hand, have usually lost part or all of chromosome 22. Brain tumors also express growth factors and growth factor receptors that may be important in promoting tumor growth and angiogenesis. These include epidermal growth factor, transforming growth factor-alpha, platelet-derived growth factor, the fibroblast growth factors, and vascular endothelial growth factor. In this article, we review the genetic aberrations that occur in the major types of brain tumors, including glial tumors, meningiomas, acoustic neuromas, medulloblastomas, primitive neuroectodermal tumors, and pituitary tumors. Wherever possible, clinical correlations have been made concerning the prognostic and therapeutic implications of specific aberrations. We also provide some background about the cytogenetic and molecular genetic techniques that have contributed to the description and understanding of these alterations and speculate as to some clinical and basic science issues that might be explored in the future.

Brain↗
PubMed1998

Brain tumor in the first year of life: a single institute study.

Brain tumors in infants present special diagnostic and therapeutic challenges. To figure out the clinical features, pathological classification of the tumors and the treatment outcome of infantile brain tumors, 458 children (age<16) with brain tumors were reviewed retrospectively. Among them 21 cases (4.6%) were diagnosed during the first 12 months of life. Two tumors were definitely of congenital origin. The majority of infants with brain tumors presented with increased intracranial pressure. Fourteen tumors were located at the supratentorial area. Sixteen cases had neuroepithelial tumors; astrocytoma (optic pathway), supratentorial primitive neuroectodermal tumor (PNET) and medulloblastoma were found in three cases each. There were two treatment-related mortalities. Compared with the outcomes in older children, the treatment outcome was poorer in medulloblastoma and the optic pathway glioma which showed a higher growth potential. Because of the limited application of postoperative adjuvant therapy, radical surgical removal played a more important role in this age group. The prognosis of patients in whom the tumors could not be totally removed, largely depended on the pathological malignancy of the tumors. Though the treatment outcome was not always dismal, immaturity of the brain, higher growth potential, perioperative risks, limitations in adjuvant therapy, and pessimistic attitude on the part of parents made management more challenging.

Adolescent↗
PubMed1990

[Immunohistochemical study of placental form of glutathione S-transferase in human brain tumors and fetal brains].

The activity of glutathione S-transferase placental form (GST-pi) was examined in 100 cases including various histologic subtypes and grading of human brain tumors and 10 cases of fetal brains by immunohistochemical studies. The 69% of cases with brain tumors were shown to be positive for GST-pi. This activity in neuroepithelial tumors tended to increase in order to tumor grading, however, medulloblastoma and primitive neuroectodermal tumor (PNET) were not immunoreactive with GST-pi. Embryonal carcinoma showed strong staining, although fetal brains were negative. The metastatic brain tumors showed the same reactivity with GST-pi as those of original carcinomas. Moreover, the difference of GST-pi activity was investigated on some brain tumors treated with or without antitumor drug, such as 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU). The 85% of recurrent cases showed strong staining with GST-pi, and GST-pi activity seemed to be increased after treated with ACNU. The present study indicated that GST-pi might be a useful marker for human brain tumor, as the same conclusion was applicable to other neoplastic lesions examined previously. It is suggested that the increased GST-pi activity with malignancy of tumor may indicate the tendency to recurrence. The presence of such activity in tumor cells may also imply their acquired multidrug resistance. Our findings suggest that the evaluation of GST-pi activity in brain tumors will offer a predictive value for eventual behavior of the tumor.

Biomarkers, Tumor↗