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2 edition of Selected abstracts on translocation and amplification of oncogenes found in the catalog.

Selected abstracts on translocation and amplification of oncogenes

Gerald S. Kuncio

Selected abstracts on translocation and amplification of oncogenes

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Published by U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, International Cancer Research Data Bank, National Cancer Institute, For sale by the Supt. of Docs., U.S. G.P.O. in Bethesda, MD, Washington, DC .
Written in English

    Subjects:
  • Oncogenes -- Abstracts.,
  • Translocation (Genetics) -- Abstracts.,
  • Gene amplification -- Abstracts.

  • Edition Notes

    Other titlesTranslocation and amplification of oncogenes.
    StatementPeter C. Nowell, consulting reviewer.
    GenreAbstracts.
    SeriesOncology overview
    ContributionsNowell, Peter C., International Cancer Research Data Bank.
    The Physical Object
    Pagination9, 77, 31, 5 p. ;
    Number of Pages77
    ID Numbers
    Open LibraryOL17570129M

    The introduction of targeted treatments and more recently immune checkpoint inhibitors (ICI) to the treatment of metastatic non-small cell lung cancer (NSCLC) has dramatically changed the prognosis of selected patients. For patients with oncogene-addicted metastatic NSCLC harbouring an epidermal growth factor receptor (EGFR) or v-Raf murine sarcoma viral oncogene homologue B1 (BRAF. To study the pathogenesis of Burkitt lymphoma, we introduced activated c-myc genes into human EBV-infected lymphoblastoid cells derived from in vitro infection of normal cord blood or directly from infected peripheral blood from AIDS patients. In both cell types the constitutive expression of exogenous c-myc caused negative regulation of endogenous c-myc expression, changes in growth. FISH detection of in vivo amplification of the PAX3-FKHR or PAX7-FKHR loci. (A) Tumor cells from case were hybridized with biotindATP-labeled 5′ PAX3 cosmid probe and digoxigenindUTP-la-beled 3′ FKHR cosmid ization signals were detected with FITC-avidin (green signal, 5′ PAX3) and anti-digoxigenin rhodamine (red signal, 3′ FKHR).   Circadian clocks enhance the efficiency and survival of living things by organizing their behavior and body functions. There has been a long history of research seeking a link between circadian clock and tumorigenesis. Studies of animal models and human tumor samples have revealed that the dysregulation of circadian clocks is an important endogenous factor causing mammalian cancer .


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Selected abstracts on translocation and amplification of oncogenes by Gerald S. Kuncio Download PDF EPUB FB2

Get this from a library. Selected abstracts on translocation and amplification of oncogenes. [Gerald S Kuncio; Peter C Nowell; International Cancer Research Data Bank.]. In addition, this probe identifies a novel joint in the amplification unit of one line relative to that of the others.

We suggest that, in the eight lines which have amplified NB–21, the amplification units are overlapping, but not identical, and that transposition of the common sequences may occur prior to by: For patients with oncogene-addicted metastatic NSCLC harbouring an epidermal growth factor receptor (EGFR) or v-Raf murine sarcoma viral oncogene homologue B1 (BRAF) mutation or an anaplastic lymphoma kinase (ALK) or ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) gene alteration (translocation, fusion, amplification) mutation-specific Cited by: Amplification represents one of the major molecular pathways through which the oncogenic potential of proto‐oncogenes is activated during tumorigenesis.

The architecture of amplified genomic structures is simple in some tumor types, involving in the vast majority. Chromosome * Leukemia Translocation Abstract. Eukaryotic cells contain a family of genes termed “cellular oncogenes” or “proto-oncogenes,” thought to regulate normal cell growth and development.

In some cir- cumstances, such as following transduction by retroviruses, activation of these genes causes tumors and leukemias in by: 8. the oncogenes which have been found most frequently to be amplified.

Other genes which have been found to be amplified in some tumor cells include c-Ki-ras, c-myb, c-abl and c-erb B. Oncogene amplification may be associated with tumor progression as seen with N-myc in neuroblastomas and with c-myc in small cell lung carcinomas.

Show abstract Previously, it was reported that the expression of c-Jun is decreased by the adipocyte differentiation signal in 3T3 T cells [26]. Particularly, amplification of the oncogene. Hartl, K. Bister, in Brenner's Encyclopedia of Genetics (Second Edition), Abstract.

Oncogenes are eukaryotic genes that have the potential to become dominant oncogenic determinants in tumorigenesis. They are mutant alleles of normal cellular genes, termed protooncogenes, that are preserved in evolution and have essential physiological functions in normal cells.

Carcinoma ex pleomorphic adenoma (CexPA) is a carcinoma developing within a pre-existing benign pleomorphic adenoma (PA). Here we describe the identification and characterization of a series of genetic events leading to translocation, deletion/amplification, and overexpression of the HMGIC and MDM2 genes in a CexPA at an early stage of Selected abstracts on translocation and amplification of oncogenes book.

The tumor had a pseudodiploid stemline. Tumors of the peripheral nervous system include neuroblastomas, pheochromocytomas, and neuroepitheliomas. Neuroblastomas and pheochromocytomas are adrenergic in origin and share certain genetic features, whereas neuroepitheliomas are thought to be cholinergic and are characterized by distinct genetic features.

Neuroblastomas are characterized by deletion of the short arm of. Oncogene amplification, which is selective increase in copy number of the oncogene, provides survival advantages in solid tumors including malignant neuroblastoma. We have decreased expression of N-Myc oncogene using short hairpin RNA (shRNA) plasmid to increase anti-tumor efficacy of the isoflavonoid apigenin (APG) in human malignant.

Title Sources; New York times WWW site, viewed Jan. 11, Selected abstracts on translocation and amplification of oncogenes, van de Vijver M, van de Bersselaar R, Devilee P, Cornelisse C, Peterse J, Nusse R. Amplification of the neu (c-erbB-2) oncogene in human mammmary tumors is relatively frequent and is often accompanied by amplification of the linked c-erbA oncogene.

Mol Cell Biol. May; 7. K.-Y. Jen, in Brenner's Encyclopedia of Genetics (Second Edition), Abstract. Gene amplification is the differential increase in a specific portion of the genome in comparison with the remainder. This process appears to be ubiquitous, occurring in most organisms, and has also been shown to occur in both germline and somatic cells.

Abstract. Oncogenes are activated through well-known chromosomal alterations such as gene fusion, translocation, and focal amplification. In light of recent evidence that the control of key genes depends on chromosome structures called insulated neighborhoods, we investigated whether proto-oncogenes occur within these structures and whether oncogene activation can occur via.

Gene deregulation is a frequent cause of malignant transformation. Alteration of the gene structure and/or expression leading to cellular transformation and tumor growth can be experimentally achieved by insertion of the retroviral genome into the host DNA. Retrovirus-containing host loci found repeatedly in clonal tumors are called common viral integration sites (cVIS).

cVIS are located in. Rearrangement and amplification of c-abl sequences in the human chronic myelogenous leukemia cell line K Proc Natl Acad Sci U S A.

Aug; 80 (15)– [PMC free article] Collins SJ, Kubonishi I, Miyoshi I, Groudine MT. Altered transcription of the c-abl oncogene in K and other chronic myelogenous leukemia cells. Science. AACR International Conference: Molecular Diagnostics in Cancer Therapeutic Development– Sep; Denver, CO Activation of at least one oncogene by mutation, translocation or fusion has been shown to be relatively frequent in adenocarcinomas of the lung.

The types and frequency of these mutations is often related to clinical features including smoking status, ethnicity, gender, age. Importantly, MYC genes are overexpressed, by means of translocation, amplification, increased translation or protein stability, in a wide range of human cancers and are frequently associated to aggressiveness and poor outcome.

Several approaches to interfere with MYC activity have been explored, with so far limited applicability in the clinical. Alterations of receptor-type tyrosine kinases (RTK) are frequent in human cancers.

They can result from translocation, mutation or amplification. The ERBB2 RTK is encoded by a gene that is amplified in about 20% breast cancers. The question is: why is this RTK specifically subjected to this type of alteration.

We propose that ERBB2 gene amplification is used to overcome repression of its. Lymphomas often possess a translocation that juxtaposes the c-myc proto-oncogene and the immunoglobulin heavy chain (IgH) locus. Two hundred kilobases downstream of. The two oncogenes KRas and Myc cooperate to drive tumorigenesis, but the mechanism underlying this remains unclear.

In a mouse lung model of KRasG12D-driven adenomas, we find that co-activation of. Localized and high level amplification of the common kb region is evidence for activation of an oncogene in this region in these MDS and AML cases.

Cases with 20q amplification tended to have a high proportion of erythroblasts in the marrow, with. Transcriptional activation of an unrearranged and untranslocated c-myc oncogene by translocation of a C lambda locus in Burkitt. Proc Natl Acad Sci U S A. Nov; 80 (22)– [PMC free article] Davis M, Malcolm S, Rabbitts TH.

Chromosome translocation can occur on either side of the c-myc oncogene in Burkitt lymphoma cells. Nature. oncogenes derive d from no rmal functional proto-oncogenes are literally the cancer-causing genes. Oncogenes are ac tivated either by viruses or bacteria or o ther environmental factors, e pigenetics.

The human c-myc oncogene: structural consequences of translocation into the IgH locus in Burkitt lymphoma. Cell. Oct; 34 (3)– Bernard O, Cory S, Gerondakis S, Webb E, Adams JM. Sequence of the murine and human cellular myc oncogenes and two modes of myc transcription resulting from chromosome translocation in B lymphoid tumours.

Cancer - Cancer - Chromosomal translocation: Chromosomal translocation has been linked to several types of human leukemias and lymphomas and, through comprehensive sequencing studies of the genomes of cancers, to epithelial tumours such as prostate cancer.

Through chromosomal translocation one segment of a chromosome breaks off and is joined to another chromosome. Amplification of chromosomal band 11q13 is a common event in human cancer.

It has been reported in about 45% of head and neck carcinomas and in other cancers including esophageal, breast, liver, lung, and bladder cancer. To understand the mechanism of 11q13 amplification and to identify the potential oncogene(s) driving it, we have fine-mapped the structure of the amplicon in oral.

Evidence for Replicative Repair of DNA Double-Strand Breaks Leading to Oncogenic Translocation and Gene Amplification September Journal of Experimental Medicine (4) In human carcinomas, especially breast cancer, chromosome arm 8p is frequently involved in complex chromosomal rearrangements that combine amplification at 8p, break in the 8p region, and loss of 8pter.

Several studies have identified putative oncogenes in the 8p amplicon. However, discrepancies and the lack of knowledge on the structure of this amplification lead us to think.

Cytogenetic and molecular analyses have demonstrated that alteration of 3q27, BCL6, or both is one of the most common genetic abnormalities in B-cell tumors. The BCL6 gene was first identified at the breakpoints on 3q27 involved in t(3;14)(q27; q32) and t(3;22)(q27;q11) translocations in diffuse aggressive large B-cell lymphoma.

Initial studies suggested that 3q27 translocation or. We modified reporters recently developed to study rearrangements at Alu elements 9 ().Central to the translocation reporters is a neomycin phosphotransferase gene (neo) split by an intron to form neoSD and SAneo, each of which contains an I-SceI endonuclease cleavage site and is targeted to chromosomes 17 or 14, respectively, in mouse embryonic stem (ES) cells.

Resorting to Polymerase Chain Reaction (PCR) translocation t (14;18) was assessed by means of short nucleotides hybridizing with 14 and 18 chromosome sequences restricting this translocation.

The amplification product was subsequently studied by Southern's method with probe bcl Translocation Cdk Amplification, increased expression Cdk Point mutation Cyclin D: Amplification, translocation Cyclin E: Amplification HPV-E7: Viral Infection p Point mutation p Point mutation p Point mutation Rb: Point mutation.

The cancer clonal fraction of the 63 driver genes was in general higher in oncogenes than tumor suppressor genes (P oncogene activation either being an earlier event in progression to MM or asserting a greater selection pressure than tumor suppressor gene inactivation.

This seems to be a novel finding, but. A 'read' is counted each time someone views a publication summary (such as the title, abstract, and list of authors), clicks on a figure, or views or downloads the full-text.

Learn more DOI:   Common recurrent translocation partner genes of IgH account for 40–50% of cases and these rearrangements result in the transcriptional dysregulation of various proto-oncogenes such as CCND1, CCND3, FGFR3/MMSET, c-MAF, MAFB, MUM 1(IRF-4), c-MYC and it is becoming clear that these dysregulated genes play important roles in the pathogenesis and.

The p64 and p67 proteins were found to be highly related by partial V8 proteolytic mapping, and both were demonstrated to be encoded by the c-myc oncogene, using hybrid-selected translation of myc-specific RNA.

In addition, the p64 protein was specifically precipitated from cells transfected with a translocated c-myc gene. Gene amplification of oncogenes could be detected by several methods, including DNA-based techniques (PCR or Southern blot), molecular cytogenetic techniques (FISH, fluorescence in situ hybridization) with gene-specific probes, and comparative genomic hybridization (CGH) (38).

PCR, Southern blot and FISH are mostly restricted to the analysis of. The Linked Data Service provides access to commonly found standards and vocabularies promulgated by the Library of Congress.

This includes data values and the controlled vocabularies that house them. Datasets available include LCSH, BIBFRAME, LC Name Authorities, LC Classification, MARC codes, PREMIS vocabularies, ISO language codes, and more.

Gene amplification is one of the common mechanisms that activate oncogenes. In this study, we used single nucleotide polymorphism array to analyze genome-wide DNA copy number alterations in 31 high-grade ovarian serous carcinomas, the most lethal gynecologic neoplastic disease in women.

We identified an amplicon at 19p in 6 of 31 (%) ovarian high-grade serous carcinomas.The t(4;14) translocation occurs frequently in multiple myeloma (MM) and results in the simultaneous dysregulated expression of 2 potential oncogenes, FGFR3 (fibroblast growth factor receptor 3) from der(14) and multiple myeloma SET domain protein/Wolf-Hirschhorn syndrome candidate gene 1 .Proto-oncogene amplification is usually associated with late stages of tumor progression; however, amplified HER2/neu has been observed in early clinical stages of mammary neoplasia.

Activation of proto-oncogenes by chromosomal translocation has been detected at a high frequency in several hematopoietic tumors.