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Biomedical subjects

A L Boynton

Publications and source records attributed to A L Boynton.

At least 37 records · Page 2Linked to original sources
PubMed1998

Method for identifying prostate cells in semen using flow cytometry.

BACKGROUND: Prostate-specific antigen (PSA) cannot differentiate benign prostatic hyperplasia (BPH), from prostatitis, or prostate cancer in the range of 4.0-10 ng/ml. An accurate cytologic or histologic assessment is necessary to confirm the proper diagnosis. The nature of a biopsy tends to make it a selective test not frequently repeated. We are reporting a technique employing semen as a source for the differential diagnosis of prostate epithelial cells. METHODS: Eleven vasectomized and nonvasectomized prostate cancer patients provided semen samples (stage T1 to T2). Two patients provided repeat samples. In addition, 15 vasectomized or nonvasectomized individuals without evidence of disease provided semen samples. Three million cells fixed with 50% ethanol were stained by an antibody (7E11.C5) to prostate-specific membrane antigen (PSMA), Hybritech Antibody (399) to PSA, and cytokeratin 8 and 18. In addition to the antibodies described, a DNA stain To-Pro 3 was used to identify 2n-4n DNA containing cells. A dual laser, Becton Dickinson FACSCaliber cytometer, was used to analyze the samples. RESULTS: All semen specimens contained diploid, cytokeratin 18-positive epithelial cells regardless of disease status. A clear difference between prostate cancer and normal prostate cell samples was observed using staining with 7E11.C5. The ratio of prostatic cells in the total epithelial cell population (PSMA:cytokeratin ratios) was calculated for each specimen. A retrospective study of sixteen semen samples from 11 prostate cancer patients had a mean PSMA:cytokeratin ratio of 0.57, whereas the samples from 15 patients without evidence of cancer had a mean PSMA:cytokeratin ratio of 0.11. This difference was significant. PSA staining was variable and inconsistent. CONCLUSIONS: This report demonstrates that human semen contains prostate cells that can be characterized and used in the clinical diagnosis of prostate cancer.

Adult↗
PubMed1998

Evaluation of phase I/II clinical trials in prostate cancer with dendritic cells and PSMA peptides.

BACKGROUND: A phase I trial involving patients with advanced prostate cancer was conducted to assess the safe administration of dendritic cells (DC) and HLA-A0201-specific prostate-specific membrane antigen (PSMA) peptides (PSM-P1 or -P2). Thirty-three of the phase I participants were subsequently enrolled in a phase II trial, which involved six infusions of DC pulsed with PSM-P1 and -P2 peptides. METHODS: Clinical monitoring was conducted up to 770 days from the start of the phase I study. Data collected included: complete blood count, bone and total alkaline phosphatase, prostate markers, physical examination, performance status, bone scan, ProstaScint scan, and chest X-ray, as well as assays to monitor cellular immune responses. RESULTS: Nine partial responders were identified in the phase II study based on National Prostate Cancer Project (NPCP) criteria, plus 50% reduction of prostate-specific antigen. Four of the partial responders were also responders in the phase I study, with an average response duration of 225 days. Their combined average total response period was over 370 days. Five other responders were nonresponders in the phase I study. Their average partial response period was 196 days. CONCLUSIONS: The responses observed in the phase I and II clinical trials were significant and of long duration. The partial-responder group included patients who continued to respond from phase I, as well as those who started to respond during the phase II trial.

Alkaline Phosphatase↗
PubMed1998

Cell adhesion molecule Nr-CAM is over-expressed in human brain tumors.

Using the technique of differential display-polymerase chain reaction (DD-PCR), we isolated a cDNA fragment that is over-expressed in glioblastoma multiforme tissue as compared to normal brain tissue. Sequence analysis indicated that this sequence is identical to the previously isolated human neuron-glia-related cell adhesion molecule hNr-CAM. Gene-specific RT-PCR analysis indicated that hNr-CAM is over-expressed in high-grade astrocytomas, gliomas and glioblastoma tumor tissues as compared to normal brain tissue. High levels of hNr-CAM expression also were observed in cell lines derived from astrocytomas, gliomas and glioblastoma multiforme tumors. Low levels of hNr-CAM expression were observed in neuroblastoma, meningiomas, melanoma, normal breast and prostate tumor tissues. Northern blot analysis showed an alternatively spliced mRNA of 1.4 kb in several tumors as compared to the 7.5 kb transcript found in normal brain tissue. Genomic Southern blot analysis of DNA from 3 brain tumor cell lines showed that over-expression of hNr-CAM in brain tumors was not due to gene amplification. In situ hybridization analysis indicated that 11 of the 20 human brain tumor samples studied showed hNr-CAM over-expression. Our results suggest that hNr-CAM is over-expressed in malignant brain tumors and can serve as a novel marker for brain tumor detection and perhaps therapy.

Base Sequence↗
PubMed1998

Application of the differential hybridization of Atlas Human expression arrays technique in the identification of differentially expressed genes in human glioblastoma multiforme tumor tissue.

BACKGROUND AND OBJECTIVES: Several molecular biology techniques are utilized to study changes in gene expression during the genesis of human tumors. Our objective was to identify genes that showed altered expression between normal brain tissue (NBT) and glioblastoma multiforme tumor tissue (GMTT). METHODS: The technique of differential hybridization of two Atlas Human cDNA expression array was used. In this technique, dCTP32-labeled complimentary DNA from NBT and GMTT was hybridized to two identical human cDNA expression array membranes containing 588 known genes. RESULTS: Autoradiographic analysis showed that of the 588 genes analyzed, 52 are overexpressed in GMTT and 57 in NBT. A gene-specific semiquantitative reverse transcription polymerase chain reaction (RT-PCR) method was used to confirm the expression pattern of seven known genes. RT-PCR results demonstrate that the expression pattern of a majority of genes agreed with the expression pattern observed on expression array. The known tumor suppressor genes retinoblastoma (RB) and p53 showed loss of expression in GMTT compared with NBT. CONCLUSIONS: We conclude that the differential hybridization technique of Atlas Human cDNA expression array can be a useful method in identifying genes that are differentially expressed either in NBT or GMTT.

Autoradiography↗
PubMed1998

CXCR-4, a chemokine receptor, is overexpressed in and required for proliferation of glioblastoma tumor cells.

BACKGROUND AND OBJECTIVES: Using the technique of differential hybridization of Atlas Human cDNA expression arrays, we previously reported the isolation of a G protein coupled receptor, CXCR-4, which is overexpressed in glioblastoma multiforme tumor tissue (GMTT) compared to normal brain tissue (NBT). METHODS: Using gene specific reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization, we studied its expression in a variety of brain and breast tumor tissue samples. To demonstrate the requirement of CXCR-4 in glioblastoma cell proliferation an antisense construct was overexpressed. Glioblastoma cells were also treated with antibodies against CXCR-4 and its ligand, SDFbeta-1. RESULTS: Expression analysis indicated that CXCR-4 is overexpressed in 57% of the primary glioblastoma tissues and in 88% of the glioblastoma cell lines analyzed. Overexpression of CXCR-4 in glioblastoma cell lines enhanced their soft agar colony-forming capability. Expression of anti-sense CXCR-4 in glioblastoma cell lines caused neurite outgrowth and cellular differentiation. Treatment of glioblastoma cell lines with CXCR-4 and SDFbeta-1 specific antibodies caused inhibition of glioblastoma cell proliferation. CONCLUSIONS: On the basis of these results, we conclude that CXCR-4 gene is required for the proliferation of human glioblastoma tumors.

Brain Neoplasms↗
PubMed1998

Molecular characterization of CXCR-4: a potential brain tumor-associated gene.

BACKGROUND AND OBJECTIVES: We have previously reported the isolation of a G protein-coupled receptor, CXCR-4, that is overexpressed in glioblastoma multiforme tumor tissue (GMTT), as compared to normal brain tissue (NBT). METHODS: Gene-specific RT-PCR, Northern blotting, and in situ hybridization techniques were used to study its expression in a variety of normal tissues, tumor tissues, and cell lines, as well as during development. Antisense CXCR-4 was overexpressed in glioblastoma cells to study its effect on cell proliferation. RESULTS: Gene-specific RT-PCR analysis indicated that the CXCR-4 gene is overexpressed in several malignant glioma tissues, breast tumor tissues and cell lines. Northern blot analysis indicated that CXCR-4 is expressed at high levels in certain leukemias, uterine cancer, and Burkitt's lymphoma cell line. The occipital and temporal lobe showed high levels of CXCR4 in normal human brain. The CXCR-4 gene was expressed in all organs in the early stages of development (days 8-10). In adult mouse, CXCR-4 is expressed only in brain, spinal cord, bone marrow, and pituitary gland. Antisense CXCR-4 overexpression in glioblastoma cells caused inhibition of cell proliferation and induction of cellular differentiation in vitro. This suggests that CXCR-4 expression may play an important role during embryonic development and also in the genesis of human gliomas. CONCLUSIONS: On the basis of CXCR4 expression data and antisense overexpression data, we conclude that CXCR-4 plays an important role in the tumorigenic properties of brain, breast, and other tumor types. On the basis of its unique expression during mouse development, we conclude that it may play an important role in the normal functioning of brain, spinal cord, and bone marrow during development.

Animals↗
PubMed1998

Report of immune monitoring of prostate cancer patients undergoing T-cell therapy using dendritic cells pulsed with HLA-A2-specific peptides from prostate-specific membrane antigen (PSMA).

BACKGROUND: In this paper we describe our program for the immune monitoring of phase II participants given dendritic cell (DC)/prostate-specific membrane antigen (PSMA)-based immunotherapy, and we also present some initial findings. METHODS: Phase II subjects received six administrations of autologous dendritic cells exogenously pulsed with two peptides derived from PSMA. Prior to the initial infusion, and following each treatment, peripheral blood mononuclear cells (PBMC) were collected for the generation of dendritic cells as well as for comprehensive immune monitoring. RESULTS: Thus far, an increase in PSMA-peptide-specific as well as overall cellular reactivity has been observed in several patients receiving DC plus PSM-P1 and -P2, as measured by delayed-type hypersensitivity (DTH) test and enzyme-linked immunosorbant assay (ELISA). CONCLUSIONS: Our initial observations using an ELISA and DTH test indicate that we are enhancing cellular immunity in prostate cancer patients following infusion with DC plus PSMA-derived peptides. Several methods are underway to comprehensively monitor both cell-mediated and humoral immune responsiveness, including: determining anti-PSMA serum antibody titers, testing immunogen-restricted responder-cell proliferation and cytotoxicity, assessing aberrations in signal transduction, antigen processing, and presentation, and measuring soluble factors that may promote tumor outgrowth.

Antigens, Neoplasm↗
PubMed1998

Rapid disruption of gap junctional communication and phosphorylation of connexin43 by platelet-derived growth factor in T51B rat liver epithelial cells expressing platelet-derived growth factor receptor.

Gap junctional communication (GJC) between contacting cells has been postulated to be involved in the regulation of cell proliferation. This suggestion stems from numerous studies showing modulation of GJC by agents that influence cellular proliferation. Platelet-derived growth factor (PDGF), a strong mitogen, inhibits GJC in many cell types. To understand the molecular nature of the signal transduction pathway responsible for the GJC blockade, T51B rat liver epithelial cells, which lack endogenous PDGF receptor (PDGFr), were infected with a retrovirus containing either wild-type full-length cDNA of human PDGFr beta (Kin+) or a mutant PDGFr beta lacking receptor tyrosine kinase activity (Kin-). PDGF caused a complete but transient interruption of cell communication in Kin+ cells within 15-20 min of addition. This interruption of GJC was not associated with a gross destabilization of gap junction plaques but with the phosphorylation of connexin43 (Cx43), the only known gap junction protein expressed in these cells. These effects were exhibited in either control T51B cells or in Kin- cells, indicating a requirement of the receptor tyrosine kinase activity. Further examination revealed that the newly phosphorylated Cx43 then undergoes a rapid degradation utilizing the lysosomal pathway resulting in a decreased total Cx43 protein level. The re-establishment of GJC following PDGF treatment was dependent on protein synthesis. This report describes a suitable cell system which is currently being utilized for the characterization of the PDGF signaling pathway responsible for the inhibition of GJC.

Animals↗
PubMed1998

Platelet-derived growth factor-induced disruption of gap junctional communication and phosphorylation of connexin43 involves protein kinase C and mitogen-activated protein kinase.

Previously we showed a rapid and transient inhibition of gap junctional communication (GJC) by platelet-derived growth factor (PDGF) in T51B rat liver epithelial cells expressing wild-type platelet-derived growth factor beta receptors (PDGFrbeta). This action of PDGF correlated with the hyperphosphorylation of the gap junction protein connexin43 (Cx43) and required PDGFrbeta tyrosine kinase activity, suggesting the participation of protein kinases and phosphatases many of which are activated by PDGF treatment. In the present study, two such kinases, namely protein kinase C (PKC) and mitogen-activated protein kinase (MAPK), are investigated for their possible involvement in PDGF-induced closure of junctional channels and Cx43-phosphorylation. Down-regulation of PKC-isoforms by 12-O-tetradecanoylphorbol-13-acetate or pretreatment with the PKC inhibitor calphostin C, completely blocked PDGF action on GJC and Cx43. Activation of MAPK correlated with PDGF-induced Cx43 phosphorylation, and prevention of MAPK activation by PD98059 eliminated the PDGF effects. Interestingly, elimination of GJC recovery by cycloheximide was associated with a sustained activated-MAPK level. Based on these results we postulate that the activation of PKC and MAPK are required in PDGF-mediated Cx43 phosphorylation and junctional closure.

Animals↗
PubMed1998

Measurement of serum prostate-specific membrane antigen, a new prognostic marker for prostate cancer.

OBJECTIVES: To describe current results with Western blot assay for prostate specific membrane antigen (PSMA) using 7E11.C5 antibody and the development of an additional antibody measurement for PSMA by a new sandwich immunoassay. METHODS: A population of patients from a screening group, from a difficult diagnostic group, from a pre- and postoperative radical prostatectomy group, and from a group with metastatic disease followed for a serial period, provided the serum values for a prospective assessment of PSMA by Western blot assay. A new monoclonal antibody was sought, reacting to the C-terminal region of PSMA in order to develop a sandwich radioimmunoassay. RESULTS: PSMA values in screened patients correlate with the more advanced stage of the cancers determined. In postprostatectomy patients, the PSMA value corresponds more with preoperative values and with the values of those with a poor clinical course. In difficult diagnostic cases, the PSMA value is increased, specifically in hormone-refractory cases and particularly in those cases judged by other criteria, such as the National Prostatic Cancer Project, to be in clinical progression compared with those judged to be in clinical remission. The level of PSMA value appears to be independent of homogeneous tumor volume and to be more related to that of prior hormone treatment, or to where prostate cancer cells can be documented to be outside the prostate. A new monoclonal antibody, 3F5.4G6, reacts with the extracellular domain of PSMA near the C-terminal region. This is in contrast to the previously measured antibody 7E11.C5, which reacts with an N-terminal epitope. 3F5.4G6 recognizes the same PSMA protein as does 7E11.C5. The epitopes are essentially at opposite ends of the molecule. The 3F5.4G6 antibody reacts with the LNCaP line but not with DU145, or PC3. These two antibodies to PSMA are well suited for use in a new sandwich immunoassay. CONCLUSIONS: PSMA provides a prostatic cancer serum test by using Western blot, which suggests a clinical prognostic value not seen with other markers. New antibodies, such as 3F5.4G6, reacting with the extracellular domain of PSMA combined with 7E11.C5, appear to offer an opportunity for a new sandwich immunoassay.

Antibodies, Monoclonal↗
PubMed1998

Isolation and characterization of monoclonal antibodies specific for the extracellular domain of prostate specific membrane antigen.

PURPOSE: Monoclonal antibodies specific for protein epitopes of prostate specific membrane antigen (PSMA) expressed on the external surface of prostatic epithelial cells were prepared to provide material for use in the diagnosis or treatment of prostatic cancer. MATERIALS AND METHODS: Mice were immunized with LNCaP cell membranes followed by purified PSMA before fusion. Hybridomas were screened by reactivity with purified PSMA. Resulting antibodies were characterized by enzyme-linked immunosorbent assay, Western blot and fluorescence-activated cell sorter analyses. RESULTS: Monoclonal antibody producing hybridomas designated 3E11, 3C2, 4E10-1.14, 3C9 and 1G3 were obtained which displayed specificities for differing regions of the extracellular domain of the PSMA protein. These antibodies reacted strongly with PSMA from multiple sources and specifically stained unfixed PSMA expressing cells by flow cytometric analysis. CONCLUSIONS: The antibodies obtained displayed strong reactivity and specificity for extracellular epitopes of PSMA. These antibodies will have value in future diagnostic and therapeutic applications focusing on PSMA as a target antigen.

Animals↗
PubMed1997

A targeted library of small-molecule, tyrosine, and dual-specificity phosphatase inhibitors derived from a rational core design and random side chain variation.

Tyrosine phosphatases (PTPases) dephosphorylate phosphotyrosines while dual-specificity phosphatases (DSPases) dephosphorylate contiguous and semicontiguous phosphothreonine and phosphotyrosine on cyclin dependent kinases and mitogen-activated protein kinases. Consequently, PTPases and DSPases have a central role controlling signal transduction and cell cycle progression. Currently, there are few readily available potent inhibitors of PTPases or DSPases other than vanadate. Using a pharmacophore modeled on natural product inhibitors of phosphothreonine phosphatases, we generated a refined library of novel, phosphate-free, small-molecule compounds synthesized by a parallel, solid-phase combinatorial-based approach. Among the initial 18 members of this targeted diversity library, we identified several inhibitors of DSPases: Cdc25A, -B, and -C and the PTPase PTP1B. These compounds at 100 microM did not significantly inhibit the protein serine/threonine phosphatases PP1 and PP2A. Kinetic studies with two members of this library indicated competitive inhibition for Cdc25 DSPases and noncompetitive inhibition for PTP1B. Compound AC-alphaalpha69 had a Ki of approximately 10 microM for recombinant human Cdc25A, -B, and -C, and a Ki of 0.85 microM for the PTP1B. The marked differences in Cdc25 inhibition as compared to PTP1B inhibition seen with relatively modest chemical modifications in the modular side chains demonstrate the structurally demanding nature of the DSPase catalytic site distinct from the PTPase catalytic site. These results represent the first fundamental advance toward a readily modifiable pharmacophore for synthetic PTPase and DSPase inhibitors and illustrate the significant potential of a combinatorial-based strategy that supplements the rational design of a core structure by a randomized variation of peripheral substituents.

Binding, Competitive↗
PubMed1997

Comparison of serum PSMA, PSA levels with results of Cytogen-356 ProstaScint scanning in prostatic cancer patients.

BACKGROUND: Stored serum from clinical trial cases undergoing ProstaScint (CYT-356) scanning were available for Prostate Specific Membrane Antigen (PSMA) assay. Prostate Specific Antigen (PSA) levels had already been determined. This provided an opportunity to see what correlations existed between the serum markers and the ProstaScint scan. A group of patients had the studies preprostatectomy, whereas another group had the studies postprostatectomy. METHODS: The scan results, serum PSA, serum PSMA, and clinical data were separately analyzed. PSMA serum levels were determined by Western blot. RESULTS: Preoperatively, radical prostatectomy patients showed a correlation between serum PSA or PSMA levels and the ProstaScint scan in the total group (n = 86), or in an untreated group (n = 38). Preoperatively, PSMA correlated with the pathological stage, whereas PSA correlated with the scan. Postoperatively, only PSMA serum levels correlated with the scan in an untreated group (n = 40). CONCLUSIONS: Preoperatively or postoperatively, Western blot PSMA serum levels predict the stage of disease or local, regional, or distant metastases, as shown by ProstaScint scan. Both the scan and the serum tests provide prognostic information and evaluate the extent of disease to a more significant degree than previously possible.

Adult↗
PubMed1997

Follow-up evaluation of prostate cancer patients infused with autologous dendritic cells pulsed with PSMA peptides.

BACKGROUND: We recently conducted a phase I clinical trial administering autologous dendritic cells pulsed with prostate-specific membrane antigen (PSMA) peptides to advanced prostate cancer patients. Participants were divided into 5 groups receiving 4 or 5 infusions of peptides alone (PSM-P1 or -P2; groups 1 and 2, respectively), autologous DC (group 3), or DC pulsed with PSM-P1 or -P2 (groups 4 and 5, respectively). Seven partial responders were observed. Follow-up evaluation of these responders is presented in this report. METHODS: Clinical monitoring for hematological studies and prostate markers was conducted up to 370 days from the start of the phase I study. Data collected include: lymphocyte, hematocrit, alkaline phosphatase, prostate-specific antigen (PSA), free PSA, and PSMA levels. RESULTS: Groups 4 and 5 (patients infused with DC pulsed with PSM-P1 or -P2) represented 5/7 responders. The length of response was between 100 days (1 patient) to 200 days or above (6 patients). Four patients still remained responsive at the end of the period of observation. CONCLUSIONS: The responses observed in this phase I clinical trial are significant and of long duration. Most of the responders were in treatment groups infused with DC pulsed with PSM-P1 or -P2, suggesting the requirement of both components for effective immunotherapy.

Alkaline Phosphatase↗
PubMed1997

Isolation and characterization of a novel gene from human glioblastoma multiforme tumor tissue.

Using the technique of DD-PCR (differential display-polymerase chain reaction) we isolated a novel gene (D2-2) that is overexpressed in glioblastoma multiforme tissue (GMT) as compared to normal brain tissue (NBT). D2-2 is also highly expressed in recurrent glioma, colon tumor metastatic to brain, breast tumors, prostate tumors and a prostate tumor cell line (LNCaP). Northern blot analysis showed that D2-2 is highly expressed in several tumor cell lines (MOLT lymphoblastic leukemia, SW480 colorectal adrenocarcinoma, A549 lung carcinoma, HL-60 promyelocytic leukemia, S3 HeLa cells, K-562 chronic myelogeneous leukemia and G361 melanoma) as compared to NBT. Additionally, D2-2 is very highly expressed in cell lines derived from glioblastomas, grade IV astrocytomas, normal human fetal astrocytes (NHFA) and glioma. D2-2 is moderately expressed in neuroblastoma, neuroectodermal and medulloblastoma tumor cell lines. D2-2 expression is localized to the frontal lobe, occipital lobe and the cerebellum in the normal brain. Normal tissues such as thyroid, stomach, adrenal cortex, small intestine and pancreas show high expression of D2-2. We also show that D2-2 is expressed 28-fold higher in fetal brain (20 weeks) than in adult brain. Sequence analysis of a 2.0-kb fragment for D2-2 shows no homology to known sequences in the data base.

Amino Acid Sequence↗
PubMed1997

Monoclonal antibody 7E11.C5 staining of viable LNCaP cells.

BACKGROUND: Prostate-specific membrane antigen (PSMA) is a transmembrane glycoprotein defined by the monoclonal antibody 7E11.C5. The 7E11.C5 antibody forms the basis of an in vivo diagnostic imaging agent (ProstaScint, Cyt-356) for identification of metastatic prostate cancer. The epitope on PSMA recognized by 7E11.C5 has been determined to be the first 6 amino acids from the N-terminal, expressed on the cytoplasmic side of the plasma membrane. Thus, the basis for 7E11.C5 specificity in imaging studies remains unclear. METHODS: Fluorescence-activated cell sorter (FACS) analysis of fixed and viable cultured cells was used to determine the staining intensity with FITC-labeled antibodies. RESULTS: The results indicate that FITC-labeled 7E11.C5 antibody is taken up and specifically labels viable LNCaP cells in vitro. Labeling intensity of viable cells after 2 hr of antibody incubation was similar to that of fixed cells. No labeling of cells that do not express PSMA was observed, nor was labeling observed with LNCaP cells treated with an isotype-matched irrelevant antibody. CONCLUSIONS: Uptake and labeling of PSMA by FITC-labeled 7E11.C5 in viable cells in vitro strongly suggest that this is a major basis for effectiveness of the 7E11.C5 antibody during in vivo imaging applications with 111In-labeled antibody (ProstaScint, Cyt-356).

Antibodies, Monoclonal↗
PubMed1997

Characterization of C4-2 as a tumor-suppressor gene in human brain tumors.

BACKGROUND: Brain tumors claimed the lives of 13,300 people in 1995. Our objective was to isolate and characterize unique tumor-suppressor genes from human brain tumors derived from patients in the United States. METHODS: Differential display-polymerase chain reaction was used to isolate tumor suppressor genes. RESULTS: Clone C4-2 was isolated and is expressed in normal adult human brain, but not in brain tissue from glioblastoma multiforme tumors. C4-2 has 66% homology to the previously isolated ARPP-16 (cAMP-regulated phosphoprotein of Mr = 16,000) based on limited sequencing. C4-2 is expressed at high levels in normal brain and is not expressed or expressed at low levels in several brain tumor cell lines. Expression of C4-2 was also either not expressed or expressed at low levels in meningioma, B-cell lymphoma, recurrent glioma, LNCAP (prostate tumor cell line), breast tumor, or prostate tumor tissue. CONCLUSION: We conclude that C4-2 may function as a potential tumor-suppressor gene.

Adult↗