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At least 19 recordsLinked to original sources
PubMed1999

Localization and function of Bam protein require the benign gonial cell neoplasm gene product.

Division of a female Drosophila stem cell produces a daughter stem cell and a cystoblast. The cystoblast produces a syncytial cluster of 16 cells by precisely four mitotic divisions and incomplete cytokinesis. Mutations in genes required for cystoblast differentiation, such as bag-of-marbles, block syncytial cluster formation and produce a distinctive "tumorous" or hyperplastic germ cell phenotype. In this paper, we compare the oogenic phenotype of benign gonial cell neoplasm mutations to that of mutations in bam. The data indicate that, like bam, bgcn is required for cystoblast development and that germ cells lacking bgcn become trapped in a stem cell-like state. One indication that germ cells lacking bgcn cannot form cystoblasts is that bgcn stem cells resist genetic ablation by Bam misexpression. Misexpression of Bam eliminates wild-type stem cells, apparently by inducing them to divide as cystoblasts. bgcn stem cells remain active when Bam is misexpressed, probably because they cannot adopt the cystoblast fate. Bgcn activity is not required for Bam protein expression but is essential for the localization of Bam protein to the fusome. Together, the results suggest that Bam and Bgcn cooperatively regulate cystoblast differentiation by controlling localization of Bam protein to the fusome.

Animals↗
PubMed2000

Characterization of the human EPLIN (Epithelial Protein Lost in Neoplasm) gene reveals distinct promoters for the two EPLIN isoforms.

EPLIN is a novel LIM domain protein that co-localizes to the actin stress fibers and focal adhesion plaques. We previously have demonstrated that two isoforms, the 600aa EPLIN-alpha and the 759aa EPLIN-beta, are generated from a single gene. In the majority of human breast and prostate cancer cell lines, the expression of EPLIN-alpha is significantly reduced, while the expression of EPLIN-beta is either up-regulated or unchanged. To understand the basis of this differential regulation, we have determined the organization of the human EPLIN gene. The human EPLIN100kb and consists of 11 exons. The EPLIN-beta mRNA requires all 11 exons, while the EPLIN-alpha mRNA requires Exons 4-11. The transcriptional start sites of EPLIN-alpha were mapped within the third intron by 5' RACE and S1 nuclease protection. Similarly, the 5' ends of EPLIN-beta were mapped upstream of Exon 1. The DNA sequences flanking the EPLIN-alpha or EPLIN-beta transcriptional start sites were capable of stimulating the expression of promoter reporter constructs. Interestingly, the endogenous transcription of EPLIN-alpha, but not EPLIN-beta, could be stimulated by serum, indicating that the expression of two EPLIN isoforms can be independently regulated. A consensus serum response element was present within 100bp upstream of the transcriptional start sites of EPLIN-alpha. The activity of 0.7kb EPLIN-alpha promoter reporter construct could be enhanced by activated RhoA, indicating that this serum response element is functional.

3T3 Cells↗
PubMed1994

Immunoglobulin and T-cell receptor gene rearrangement analysis in malignant lymphoid neoplasms.

Gene rearrangement analysis using Southern-blot hybridization technique is a standard method for evaluating clonal receptor gene rearrangement. Both clonality and lineage can be identified in lymphoid neoplasms by the demonstration of one or more rearranged antigen receptor genes of the immunoglobulin supergene family-immunoglobulin and T-cell receptor genes. To evaluate the diagnostic applicability of antigen receptor gene rearrangements in the diagnosis of malignant lymphomas and leukemias, the authors performed a gene rearrangement analysis of 54 cases by southern blot hybridization technique. One or two clonally rearranged bands were detected in the malignant lymphomas and in the lymphoblastic leukemias with a false-negative rate of 13.8%. No clonal, rearranged band was detected in benign reactive hyperplasias, carcinomas or non-lymphocytic leukemias. Rearrangement analysis could resolve the lineage, clonality and stage of differentiation of malignant lymphoid neoplasms.

Gene Rearrangement↗
PubMed1997

High-level DNA amplifications are common genetic aberrations in B-cell neoplasms.

Gene amplification is one of the molecular mechanisms resulting in the up-regulation of gene expression. In non-Hodgkin's lymphomas, such gene amplifications have been identified rarely. Using comparative genomic hybridization, a technique that has proven to be very sensitive for the detection of high-level DNA amplifications, we analyzed 108 cases of B-cell neoplasms (42 chronic B-cell leukemias, 5 mantle cell lymphomas, and 61 aggressive B-cell lymphomas). Twenty-four high-level amplifications were identified in 13% of the patients and mapped to 15 different genomic regions. Regions most frequently amplified were bands Xq26-28, 2p23-24, and 2p14-16 as well as 18q21 (three times each). Amplification of several proto-oncogenes and a cell cycle control gene (N-MYC (two cases), BCL2, CCND2, and GLI) located within the amplified regions was demonstrated by Southern blot analysis or fluorescence in situ hybridization to interphase nuclei of tumor cells. These data demonstrate that gene amplifications in B-cell neoplasms are much more frequent than previously assumed. The identification of highly amplified DNA regions and genes included in the amplicons provides important information for further analyses of genetic events involved in lymphomagenesis.

Cell Cycle Proteins↗
PubMed1995

Loss of expression and loss of heterozygosity in the DCC gene in neoplasms of the human female reproductive tract.

In order to identify the possible role of the DCC gene in neoplasms of the human female reproductive tract, messenger RNA expression of the DCC gene was examined by reverse transcriptase-polymerase chain reaction, and expression of the DCC gene product was detected immunohistochemically. While histologically normal endometrium, cervical epithelium and ovary expressed detectable mRNA of the DCC gene, three of eight (37%) endometrial carcinomas, one of two (50%) cervical carcinomas and 9 of 22 (41%) ovarian malignant tumours had significantly reduced or negligible DCC expression, and another endometrial carcinoma and two other ovarian tumors underexpressed DCC when compared with histologically normal endometrial or ovarian tissues. Impaired DCC mRNA expression was detected more frequently in grade 3 ovarian epithelial tumours than in grade 1 tumours (P = 0.002). Loss of expression of the DCC gene product detected by immunohistochemistry significantly correlated with the loss of mRNA expression in ovarian carcinomas (P = 0.01 by chi-square test) or in both endometrial and ovarian carcinomas combined (P = 0.001). Loss of heterozygosity of the DCC gene was also evaluated by restriction fragment polymorphism analysis of the polymerase chain reaction-amplified DNA fragment. Loss of heterozygosity of the DCC gene was detected in one of seven (14%) informative cases of endometrial carcinomas, 1 of 11 (9%) informative cases of cervical carcinomas and two of six (33%) informative cases of ovarian tumours. These results demonstrate that inactivation of the DCC gene, especially by the loss of expression, plays a significant role in the aetiology of neoplasms of the human reproductive tract.

Adenocarcinoma↗
PubMed1985

NIH conference. Molecular genetic analysis of human lymphoid neoplasms. Immunoglobulin genes and the c-myc oncogene.

Immunoglobulin genes responsible for individual antibodies are organized as discontinuous DNA segments in their germline form. As an uncommitted stem cell develops into an antibody-synthesizing plasma cell, rearrangements of these immunoglobulin gene segments serve to activate the genes and to generate the virtually unlimited capacity to synthesize antibodies that recognize potential antigens. The analysis of immunoglobulin gene structure and arrangement has been of immense value in the study of human lymphoid neoplasms. Recombinant DNA technology involving analysis of immunoglobulin gene arrangement has been used to classify neoplasms of previously uncertain lineage, aid in the diagnosis of neoplasms of the B-cell series, and define the state of differentiation of neoplastic B-cell precursors. Furthermore, the demonstration of translocation of a particular transforming gene, the c-myc oncogene, into the immunoglobulin gene locus in Burkitt's lymphoma has provided a major insight into the cause of malignant transformation of these lymphoid cells.

Alleles↗
PubMed1988

B-lymphoid neoplasms: immunoglobulin genes as molecular determinants of clonality, lineage, differentiation, and translocation.

The basic rules of Ig gene recombination that were learned from examining clonal proliferations of B cells have paid enormous dividends in improving our understanding of B-cell malignancy. The DNA rearrangements of Ig genes creates a tumor-specific marker capable of establishing the clonality, cellular lineage, and stage of development of a lymphoid tumor. Most importantly, the Ig genes have proved to be the sites of interchromosomal translocations that contribute directly to the malignant phenotype. These genetic tools hold the promise of improving our classification schemes, providing sensitive and specific approaches to following the clinical course, and providing insights into pathogenesis that will prompt improved therapies.

B-Lymphocytes↗
PubMed1980

Transforming genes of neoplasms induced by avian lymphoid leukosis viruses.

Oncogenic avian retroviruses can be classified into three groups: sarcoma viruses, acute leukaemia viruses and lymphoid leukosis viruses (LLVs). Sarcoma and acute leukaemia viruses transform fibroblasts and/or haematopoietic cells in culture and induce tumours with short latent periods in infected birds. In contrast, LLVs do not transform cells in vitro and require long latent periods before formation of neoplasms in vivo. The most frequent neoplasm induced by LLVs is malignant lymphoma of the bursa of Fabricius, but LLVs also induce other neoplasms, including sarcomas, nephroblastomas and erythroblastosis. The genomes of both sarcoma and acute leukaemai viruses contain specific genes responsible for viral oncogenicity, whereas the genome of LLVs apparently includes only genes required for virus replication. The genetic basis for the low oncogenic potential of LLVs is therefore obscure. The present experiments indicate that LLV-induced tumours contain transforming genes that can be detected by transfection of NH 3T3 mouse cells. These transforming genes are not linked to LLV DNA sequences, suggesting that oncogenesis by LLVs may result from indirect activation of cellular transforming genes.

Alpharetrovirus↗
PubMed1992

[Mutations of the p53 gene in hematologic neoplasms].

The p53 gene encodes a nuclear phosphoprotein and is now considered as a tumor suppressor gene. Mutations of the p53 gene have frequently been observed in several types of solid tumors and are believed to be implicated in the development of these tumors. Recent studies have shown that the p53 gene is altered in chronic myelogenous leukemia (CML) in blast crisis. In CML, alterations of the p53 gene may play an important role in the development of blast crisis. More recently, p53 mutations have been reported in other types of hematologic neoplasms, such as acute leukemia, adult T-cell leukemia, and malignant lymphoma. These observations suggest that inactivation of the p53 gene is involved in the tumorigenesis of various types of hematologic neoplasms.

Blast Crisis↗
PubMed1993

Mutations of the p53 tumor suppressor gene in neoplasms of the human nervous system.

A variety of neoplasms of the human nervous system were analyzed for the presence of mutations in the p53 tumor suppressor gene. DNA was extracted from frozen or formalin-fixed, paraffin-embedded material. Single-strand conformation polymorphism (SSCP) analysis for exons 5-8 was followed by direct DNA sequencing. Mutations leading to an amino acid change were found in three of 11 (27%) low-grade (World Health Organization (WHO) Grade II) astrocytomas. They were located in codon 183 (TCA-->TGA) of exon 5, codon 237 (ATG-->ATA) of exon 7, and codon 273 (CGT-->CAT) of exon 8. In one of these cases, the sequence indicated loss of the wild-type allele. Of 12 juvenile pilocytic astrocytomas (WHO Grade I), none contained a p53 mutation, suggesting a different molecular basis for this childhood neoplasm. Except for a mutation in one of seven (14%) meningeal hemangiopericytomas (codon 238; TGT-->TTT, Cys-->Phe), no mutations were observed in exons 5-8 of the p53 gene in any of the following tumors of the nervous system and its coverings: 13 schwannomas, 12 central neurocytomas, 22 meningiomas, 10 choroid plexus papillomas and carcinomas, and 30 neuroblastomas of the sympathetic nervous system. These and published data support the view that p53 mutations are frequently involved both in low-grade and progressive (anaplastic) astrocytomas, including glioblastomas multiforme. Oligodendrogliomas, medulloblastomas, meningiomas, and hemangiopericytomas rarely (< 15%) show p53 mutations in exons 5-8, whereas none of the remaining nervous system neoplasms revealed evidence of an involvement of the p53 gene in their development.

Adolescent↗
PubMed2006

[Expression of adhesive molecules, angiogenesis markers and protein products of suppressor genes in neoplasms of oral cavity and maxillary sinus].

INTRODUCTION: Adhesion molecules, angiogenesis markers and protein products of suppressor genes are potential prognostic indicators in different type of tumours. The purpose of this study was to analyze relations between expression of these markers and clinical as well as histological features of oral cavity and maxillary sinus tumours. MATERIAL AND METHODS: Measurements of expression of CD44, TP53, Nm23 oncoproteins and angiogenesis markers were performed. Forty-three patients treated in years 1985-2000 in the Department of Maxillofacial Surgery of the University Hospital in Wroclaw entered our study. Thirty-two of them were treated for oral cavity cancers. Remaining eleven patients were treated for maxillary sinus cancers. RESULTS: We have shown, there was a positive correlation between the number of the vessels and presence of the nodal metastases; between histological grading and VCAM expression; between CD44 expression and total surface area of the blood vessels. There was also correlation between total surface area of the blood vessels and patients' survival time.

Biomarkers, Tumor↗
PubMed1984

The 1984 Walter Hubert lecture. Activation of transforming genes in neoplasms.

Cellular oncogenes have been identified by the biological activity of tumour DNAs in transfection assays and/or by homology to the transforming genes of retroviruses. In some tumours, the biological activity, organization or expression of these genes is altered, suggesting that such alterations contribute to the development of neoplastic disease. Experiments leading to the identification of cellular oncogenes are reviewed and our current understanding of the mechanisms by which they induce transformation of cells in culture and may contribute to the pathogenesis of neoplasms in vivo is discussed.

Animals↗
PubMed2004

Molecular analysis of Hurthle cell neoplasms by gene profiling.

BACKGROUND: Though Hurthle cell tumors are considered a variant of follicular lesions, recent data have suggested that Hurthle cell carcinomas may be more closely related to papillary thyroid carcinomas (PTCs). These studies were conducted to determine if molecular profiling can enhance our understanding of Hurthle cell neoplasms. METHODS: Thirteen Hurthle cell tumors (9 adenomas, 4 carcinomas) were analyzed with the Affymetrix HU-95 gene chips. Molecular profiles obtained were compared to 14 follicular adenomas (FAs), 7 follicular carcinomas (FCs), 10 PTCs, 11 follicular variant PTCs, and 9 hyperplastic nodules. Hierarchical cluster analysis defined potential groupings and differences among samples. RESULTS: Hurthle cell carcinomas grouped with FCs 100% of the time. Surprisingly, Hurthle cell adenomas clustered with FCs when compared to FAs and FCs in 8/9 (88%) cases. All 13 Hurthle cell lesions migrated as a distinct group separate from PTCs and FVPTCs. Finally, all Hurthle cell lesions clustered with FCs, rather than PTCs, when compared to both groups. CONCLUSIONS: Molecular profiles of Hurthle cell adenomas and carcinomas are more similar to FCs than benign lesions or PTCs. Although Hurthle cell adenomas generally behave in a benign fashion, the molecular signature of these lesions suggests a more malignant phenotype.

Adenocarcinoma, Follicular↗