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PubMed1993

Induction of T cells specific for the mutated segment of oncogenic P21ras protein by immunization in vivo with the oncogenic protein.

Many malignancies harbor mutated ras proto-oncogenes encoding 21 kDa proteins with single amino acid substitutions. Previous studies have shown that the aberrant p21ras proteins are potential tumor-specific antigens in that CD4+ class II major histocompatibility complex-restricted T cells specific for the mutated segment of various oncogenic p21ras proteins can be elicited by immunization in vivo with synthetic peptides corresponding to the mutated segment. T-cell recognition of an antigenic peptide within a protein may be influenced substantially, either positively or negatively, by flanking amino acid sequences as well as by more distal immunogenic or tolerogenic epitopes within the same protein. This study examined whether T cells specific for the mutated segment of an oncogenic p21ras protein can be elicited by immunization in vivo with the protein. The results showed that p21ras protein bearing the transforming single amino acid substitution of leucine for glutamine at residue 61 could elicit T cells specifically reactive to the mutated region of the protein in C3H/HeN mice. Thus, an abnormal p21ras protein specifically associated with malignant transformation can be immunogenic in vivo. These results predict that in some circumstances, mutated p21ras proteins expressed by malignancies might elicit detectable mutation-specific T-cell responses.

Amino Acid Sequence↗
PubMed1986

Characterization of murine A-raf, a new oncogene related to the v-raf oncogene.

A 1.6-kilobase cDNA (A-raf) has been isolated from a murine spleen cDNA library which encodes part of a protein related to the raf oncogene. Its amino acid sequence has 85% homology to raf in a central portion of 100 amino acids. In contrast to raf, A-raf shows a highly restricted tissue distribution of expression, with highest levels observed in epididymis, followed by intestine. When incorporated into a retrovirus, the resulting gag-A-raf fusion gene causes transformation in vitro and induces tumors in newborn mice. Thus, A-raf represents a new proto-oncogene. Transformation by A-raf is independent of ras gene function, as is the case for raf and mos but not other oncogenes.

Amino Acid Sequence↗
PubMed2002

Detection of oncogenes in the diagnosis of cancers with active oncogenic signaling.

Releasing individuals from susceptibility to and anxiety about the development of cancer is an eventual goal of cancer research. This owes much to rapid progress in molecular oncology that is supported by advances in technology. Cancers of the colon and rectum, pancreas and lung that share certain clinical and molecular oncological characteristics represent timely and important target of this field. Of the genes altered in these types of cancers, the best documented is K-ras. Currently highlighted along with this oncogene is beta-catenin, which has roles in both cell adhesion and transformation. Molecular diagnosis and susceptibility assessment targeting of such oncogenes will be promising for improvement in treatment and prevention of cancer, thereby contributing to human healthcare. Here we review recent knowledge on molecular diagnosis of sporadic cancers, with focus on K-ras and beta-catenin oncogenes.

Adenocarcinoma↗
PubMed1990

[Expression of cellular oncogenes in human hepatocellular carcinoma cell line BEL 7402 and the effect of sodium butyrate on the expression of cellular oncogenes].

With dot blot and cytoplasmic hybridization techniques we found that the c-Ha-ras, c-Ki-ras, c-N-ras, c-myc and c-fos oncogenes were over-expressed in human hepatocellular carcinoma cell line BEL 7402 cells. The mRNA expression of c-Ha-ras, c-Ki-ras, c-N-ras and c-myc oncogenes could be inhibited by 2 mmol/L sodium butyrate treatment, but this had no effect on the expression of c-fos. However, the mRNA expression of c-Ha-ras, c-N-Ras and c-myc oncogenes was enhanced by 4 mmol/L sodium butyrate treatment, while the expression of c-Ki-ras and c-fos remained unchanged. No significant effect on the expression of carbamyl phosphate synthetase I, a tissue-specific enzyme associated with the differentiation of liver cells, was observed by 2 mmol/L or 4 mmol/L sodium butyrate treatment of the hepatoma cells.

Butyrates↗
PubMed1995

[Inheritable phenotypic normalization of rodent cells transformed by simian adenovirus SA7 E1 oncogenes by singled-stranded oligonucleotides complementary to a long region of integrated oncogenes].

G11 mouse cells and SH2 rat cells transformed with simian adenovirus SA7 DNA showed inheritable oncogen-specific phenotypic normalization when treated with sense and antisense oligonucleotides complementary to long RNA sequences, plus or minus strands of the integrated adenovirus oncogenes E1A and E1B. Transitory treatment of the cells with the oligonucleotides in the absence of serum was shown to cause the appearance of normalized cell lines with fibroblastlike morphology, slower cell proliferation, and lack of ability to form colonies in soft agar. Proliferative activity and adhesion of the normalized cells that established cell lines were found to depend on the concentration of growth factors in the cultural medium. In some of the cell lines, an inhibition of transcription of the E1 oncogenes was observed. The normalization also produced cells that divided 2 - 5 times and died and cells that reverted to a transformed phenotype in 2 - 10 days. The latter appeared predominantly upon the action of the antisense oligonucleotides.

3T3 Cells↗
PubMed1988

Expression of c-myc oncogene product and ras family oncogene products in various human malignant lymphomas defined by immunohistochemical techniques.

The authors studied the expression of c-myc and ras family oncogene products in 43 cases of malignant lymphoma (ML) using the immunoperoxidase method. Unfixed frozen sections of lymph nodes from four patients with Hodgkin's disease and 39 with non-Hodgkin's lymphoma, together with normal lymph nodes, were studied by the avidin-biotin-peroxidase complex (ABC) technique. Two monoclonal antibodies, MYC-2 raised against recombinant human c-myc protein (reacting specifically with the c-myc products P62 and P67) and RASK-4 (raised against recombinant P21 and reacting specifically with ras-family product P21) were used. The c-myc product was detected in nuclei of ML cells and some normal, mainly germinal center, lymphocytes. When the staining intensity shown by normal germinal-center lymphocytes was graded as positive (+) or weakly positive (+/-), a very intensely positive reaction ( to ++) was observed in 37 cases (86%) of ML, a positive reaction (+) in four cases (9.3%), and a weakly positive reaction (+/-) in two cases (4.7%). The ras family oncogene product reaction was intensely positive (++) in two cases (4.7%), positive (+) in 16 cases (37.2%), weakly positive (+/-) in 13 cases (30.2%), and negative in 12 cases (27.9%). Western blot analysis confirmed an elevated level of c-myc products in two cases, which showed intense MYC-2 staining, and of ras family products in one case, which demonstrated intense RASK-4 staining. The enhanced expression of these gene products may play an important role in lymphomagenesis of such cases.

Antibodies, Monoclonal↗
PubMed1995

Mouse Elk oncogene maps to chromosome X and a novel Elk oncogene (Elk3) maps to chromosome 10.

The Elk protein is a member of the Ets family found in both vertebrates and invertebrates. Human ELK1 encoded by ELK1 binds alone or together with serum response factor to DNA and regulates gene expression in a variety of biological processes. Using a panel of interspecific backcross mice, we have mapped the Elk oncogene (Elk) and a novel type Elk oncogene (Elk3), closely related to ELK1. Elk maps to Chr X, and Elk3 maps to the proximal region of Chr 10.

Animals↗
PubMed1989

[Oncogenes and anti-oncogenes in breast cancer].

Recent developments in molecular oncology have permitted the definition of alterations in proto-oncogenes (ras, myc, neu and hst/int.2) and anti-oncogenes (Rb.1) in human breast carcinomas. Detection of these abnormalities could be of prognostic interest. However, this remains controversial.

Breast Neoplasms↗
PubMed1996

V-myb oncogene and c-myb proto-oncogene expression in avian cells: morphological changes of the cells and topographic localization of myb proteins.

Morphological changes of avian cells expressing the v-myb oncogene or c-myb proto-oncogene were studied by means of electron microscopy. Expression of both genes lead to distinct morphological changes of these cells. The nucleus of LSCC-BM2 cells espressing v-myb gene was of normal size but usually of irregular shape. It contained large unravelled nucleoli with typical interstices in some cells. Small nucleolar structures were also localized in the periphery of nuclear membrane. Nuclear envelope revealed reduced perinuclear space between two membranes. LSCC-BK3 cells expressing the c-myb gene were characterized by distinctly enlarged nucleus, in most cases of irregular shape. It contained only one nucleolus markedly enlarged, often unravelled, with apparent interstitial area. Nucleoli with nucleolonemas were observed in some cells. Nuclear envelope formed by two obscure membranes showed reduced perinuclear space. Topographic localization of v-Myb and c-Myb protein products was not basically different, both being detected in the nucleus of avian cells. v-Myb and c-Myb markers were distributed mostly in clusters, usually associated with interchromatin granules, but some marker was associated also with the nuclear membrane. Both Myb products were never detected in nucleolar structures of avian cells. Morphological changes of avian cells expressing myb genes and topographic localization of Myb proteins in these cells were different from those found in the insect cells expressing myb genes. The observed differences are discussed.

Animals↗
PubMed1990

Oncogenic activation of the human trk proto-oncogene by recombination with the ribosomal large subunit protein L7a.

The trk-2h oncogene, isolated from the human breast carcinoma cell line MDA-MB 231 by genomic DNA-transfection into NIH3T3 cells, consists of the trk proto-oncogene receptor kinase domain fused to a N-terminal 41 amino acid activating sequence (Kozma, S.C., Redmond, S.M.S., Xiao-Chang, F., Saurer, S.M., Groner, B. and Hynes, N.E. (1988) EMBO J., 7, 147-154). Antibodies raised against a bacterially produced beta gal-trk receptor kinase fusion protein recognized a 44 kd phosphoprotein phosphorylated on serine, threonine and tyrosine in extracts of trk-2h transformed NIH3T3 cells. In vitro, in the presence of Mn2+/gamma ATP, this protein became phosphorylated extensively on tyrosine. Cells transformed by trk-2h did not, however, show an elevation in total phosphotyrosine. We have cloned and sequenced the cDNA encoding the amino terminal activating sequences of trk-2h (Kozma et al., 1988). The encoded protein has a high basic amino acid content and the gene is expressed as an abundant 1.2 kb mRNA in human, rat and mouse cells. Antipeptide antibodies raised against a C-terminal peptide recognized specifically a 30 kd protein on Western blots of human, rat and mouse cell extracts. Immunofluorescence revealed, in addition to granular cytoplasmic fluorescence, intense nucleolar staining. The high basic amino acid content and nucleolar staining prompted us to investigate whether the 30 kd protein could be a ribosomal protein. Western immunoblotting analysis of 2D-electrophoretically resolved ribosomal proteins indicated that the 30 kd protein is the ribosomal large subunit protein L7a.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1990

[Oncogenes and oncogene products--possibilities and significance of their detection].

Diagnosis- and/or prognosis-related alterations of (proto) oncogenes may be detected in neuroblastoma (N-myc), carcinoma of breast and ovary (HER2/neu), NHL (c-myc, bcl-2), CML (c-abl/bcr), and some other neoplasias. A wide variety of methods for the detection of gene alterations can be applied. The methods of detection have to be chosen according to the expected mechanisms of oncogene activation, the availability of adequately prepared tissue, and the technical standard of the laboratory. The sensitivity, specificity, and quantitation of morphological techniques (immunohistochemistry and in situ hybridization) is restricted and their results have to be interpreted most carefully. Whenever possible, at least two different techniques should be used, preferably on two different levels, i.e. RNA/DNA and protein. Furthermore, the combination of morphological and non morphological methods should be aspired.

Animals↗
PubMedDate not supplied

[Microcalorimetric study of the oncogene EJ and proto-oncogene EC in the plasmid pBR 322].

Thermodynamic parameters were obtained of melting of the linear form of plasmids pBR 322 and plasmids pBR 322 with incorporated oncogene EC. The melting temperature of the main stage of heat absorption of the oncogene EJ was shown to be 1.6 degrees C lower than in the norm (EC). It is suggested that the thermostability change observed is related not only with point mutations of high-melting GC-pairs of bases for more low melting AT-pairs, but evidently with the structural changes in the DNA double helix as well.

Base Sequence↗
PubMed1985

Inhibition of DNA and RNA synthesis in rat liver nuclei by oncogenic and non-oncogenic beta-blockers.

The beta-blocker DL-1-(2-nitro-3-methylphenoxy)-3-tert-butylaminopropan-2-ol (ZAMI 1305), hepatocarcinogenic to the female rat, and the non-oncogenic beta-blockers DL-1-(2-nitro-5-methylphenoxy)-3-tert-butylaminopropan-2-ol (ZAMI 1327), DL-propranolol, and DL-atenolol were studied for their capacity to interfere with hepatic DNA and RNA synthesis. These moieties inhibit DNA and RNA synthesis, in a dose-dependent fashion, when added in vitro to nuclei isolated from the liver of male or female rats. The inhibition is due to a decrease of the initial rate of synthesis and of the total amount of labeled precursor incorporated into the growing chains. When administered in vivo both the oncogenic ZAMI 1305 and its non-oncogenic isomer ZAMI 1327 inhibit hepatic DNA and RNA synthesis in female rats, as evaluated by the determination of nucleic acids synthesis in liver nuclei isolated from female rats 5 and 15 min after the injection of the drug. No influence on hepatic DNA and RNA synthesis is observed when the molecules are administered to male rats. The in vivo administration of DL-propranolol causes an increase of hepatic DNA and RNA synthesis in male rats, while it is uneffective in female rats.

Adrenergic beta-Antagonists↗
PubMed2002

The N-ras proto-oncogene can suppress the malignant phenotype in the presence or absence of its oncogene.

ras proto-oncogenes have traditionally been associated with the regulation and promotion of cell growth. We have induced thymic lymphomas in N-ras(-/-) mice and in transgenic mice that overexpress wild-type N-ras and found that the lack of wild-type N-ras alleles favors the development of thymic lymphomas,whereas overexpression of wild-type N-ras protects against thymic lymphomagenesis in the presence or absence of its oncogene. To investigate the inhibitory role of wild-type N-ras in in vitro transformation, we introduced wild-type N-ras in N-ras-deficient tumor cells that lack ras activating mutations and found decreased growth in both low serum and soft agar. Taken together, our results indicate that wild-type N-ras has "tumor suppressor" activity, even in the absence of its oncogenic allele.

Alleles↗
PubMedDate not supplied

Study of oncogenic potentialities of human melanoma: identification of N-ras oncogene after DNA transfer and tumour induction.

The oncogenic potentialities of human melanoma cells derived from two different patients were studied using DNA-mediated gene transfer into NIH 3T3 cells followed by tumor induction into athymic nude nice. 64% of the mice injected subcutaneously with selected cells which had been co-transfected with human melanoma DNA and the selective marker NeoR developed tumors within 3-4 weeks, while up to 100% of those injected with cells transfected three days before with melanoma DNA developed tumors within 4-6 weeks. Southern blots analysis of the tumors indicated that almost all of them contained human sequences. Hybridization with different oncogene probes showed the presence of an human Eco RI N-ras-hybridizing fragment in the primary and secondary derived tumors, indicating that a transforming N-ras oncogene in human melanoma had been transferred to recipient cells and that transformed cells induced tumors in nude mice.

Animals↗
PubMed1995

[Characteristics of mutants induced by the c-Ha-ras1 oncogene and the nature of the oncogene's mutagenic action].

Chinese hamster cell clones of independent origin, which were resistant to purine base analogs and induced by the activated c-Ha-ras1 oncogene, were isolated. It was shown that the isolated clones stably retained resistance after cultivation on a medium without an analog, confirming mutational nature of the resistance. Most of the clones are able to grow on the HAT medium, retaining partial activity of the hypoxanthine phosphoribosyltransferase enzyme (HPRT); i.e., they are leaky mutants. Analysis by blot-hybridization did not reveal the presence of human ras-sequences in any of the mutants studied. Evidently, the mutagenic action of the oncogene is not insertional, and resistance is not linked to the stably integrated oncogene. The mutagenic effect of c-Ha-ras1 is likely to be of the "hit-and-run" type.

Animals↗
PubMed1993

Different expression patterns of oncogenes and proto-oncogenes in hereditary and carcinogen-induced tumors of Xiphophorus.

Hereditary melanoma in Xiphophorus hybrids carrying the melanoma-inducing Tu-Sd locus is caused by transcriptional activation of the Xmrk gene that resides at the Tu-Sd locus and encodes a novel member of receptor tyrosine kinases (RTK). In this study, a total of 27 hereditary melanomas from various hybrid genotypes harbouring 7 different Tu alleles were also found to over-express the corresponding Xmrk alleles. The level of over-expression correlated with the degree of malignancy of the melanoma. In addition, Xsrc expression was high in many malignant melanomas. Expression patterns and levels of the Xiphophorus EGF-receptor gene (Xerb B), the c-myc (Xmyc), and the PDGF (Xsis) gene(s) were not intriguing. Transcription of the ras gene(s) may be correlated to secondary events of melanoma progression. Expression patterns of Xfms, the Xiphophorus CSF-I receptor homologue, can be explained by different contents of infiltrating macrophages in the tumors. In carcinogen-induced tumors including one melanoma no significant expression of the Xmrk oncogene could be detected. Xsrc expression, however, was strikingly high. This indicates that activation of oncogenes other than Xmrk is instrumental in tumorigenesis of neoplasia of non-hereditary origin.

Animals↗