Relevant bibliographies by topics / Oncogenes

Academic literature on the topic 'Oncogenes'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Oncogenes"

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Ito, Reina E., Chitose Oneyama, and Kazuhiro Aoki. "Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction." PLOS ONE 16, no. 4 (April 1, 2021): e0249388. http://dx.doi.org/10.1371/journal.pone.0249388.

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Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity.
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Martín-Lorenzo, Alberto, Inés Gonzalez-Herrero, Guillermo Rodríguez-Hernández, Idoia García-Ramírez, Carolina Vicente-Dueñas, and Isidro Sánchez-García. "Early epigenetic cancer decisions." Biological Chemistry 395, no. 11 (November 1, 2014): 1315–20. http://dx.doi.org/10.1515/hsz-2014-0185.

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Abstract A cancer dogma states that inactivation of oncogene(s) can cause cancer remission, implying that oncogenes are the Achilles’ heel of cancers. This current model of cancer has kept oncogenes firmly in focus as therapeutic targets and is in agreement with the fact that in human cancers all cancerous cells, with independence of the cellular heterogeneity existing within the tumour, carry the same oncogenic genetic lesions. However, recent studies of the interactions between an oncogene and its target cell have shown that oncogenes contribute to cancer development via developmental reprogramming of the epigenome within the target cell. These results provide the first evidence that carcinogenesis can be initiated by epigenetic stem cell reprogramming, and uncover a new role for oncogenes in the origin of cancer. Here we analyse these evidences and discuss how this vision offers new avenues for developing novel anti-cancer interventions.
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Der, C. J. "Cellular oncogenes and human carcinogenesis." Clinical Chemistry 33, no. 5 (May 1, 1987): 641–46. http://dx.doi.org/10.1093/clinchem/33.5.641.

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Abstract Experimental studies over the past decade have identified 30 or so cellular genes as potential oncogenes. The genetic events that lead to cellular oncogene activation may result in the excessive or inappropriate expression of the gene, or the expression of an aberrant gene product. Although the involvement of these putative cellular oncogenes in human oncogenesis has not been proven, the accumulation of considerable experimental evidence strongly implicates some role of these genes in the malignant process. The inactivation of certain genetic loci (suppressor genes) may also contribute to tumor progression.
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Vasudevan, D. M. "Oncogenes and oncogenic viruses." Indian Journal of Clinical Biochemistry 11, no. 1 (January 1996): 3–6. http://dx.doi.org/10.1007/bf02868403.

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Clark, SS, Y. Liang, CK Reedstrom, and SQ Wu. "Nonrandom cytogenetic changes accompany malignant progression in clonal lines abelson virus-infected lymphocytes." Blood 84, no. 12 (December 15, 1994): 4301–9. http://dx.doi.org/10.1182/blood.v84.12.4301.bloodjournal84124301.

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Initially, lymphoid cells transformed by v-abl or BCR/ABL oncogenes are poorly oncogenic but progress to full transformation over time. Although expression of the oncogene is necessary to initiate and maintain transformation, other molecular mechanisms are thought to be required for full transformation. To determine whether tumor progression in ABL oncogene-transformed lymphoid cells has a genetic basis, we examined whether progression of the malignant phenotype of transformed clones correlates with particular cytogenetic abnormalities. A modified in vitro bone marrow transformation model was used to obtain clonal Abelson murine leukemia virus-transformed B lymphoid cells that were poorly oncogenic. Multiple subclones were then derived from each clone and maintained over a marrow-derived stromal cell line for several weeks. Over time, clonally related Abelson murine leukemia virus-transformed subclones progressed asynchronously to full transformation. The data show that tumor progression can occur in the absence of detectable cytogenetic changes but, more importantly, that certain cytogenetic abnormalities appear reproducibly in highly malignant subclones. Therefore, three independent subclones showed deletion in a common region of chromosome 13. Other highly malignant cells carried a common breakpoint in the X chromosome, and, finally, two subclones carried an additional chromosome 5. These results are consistent with the hypothesis that ABL oncogenes are sufficient for the initial transformation of cells but that additional genetic events can drive oncogenic progression. These observations further suggest that diverse genetic mechanisms may be able to drive tumor progression in cells transformed with ABL oncogenes.
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Karlina, I. S., E. S. Gorozhanina, and I. V. Ulasov. "THE PROSPECT OF USING ONCOGENES’ INHA, DLL4 AND MMP2 ROLE IN DIAGNOSIS AND TREATMENT OF ONCOLOGICAL DISEASE." Russian Journal of Biotherapy 20, no. 1 (April 8, 2021): 8–15. http://dx.doi.org/10.17650/1726-9784-2021-20-1-8-15.

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A large role in the development of malignant tumors is played by a genetic predisposition. Risk factors for cancer include the presence of mutations in oncogenes‑genes that cause the development of tumors. They were first found in the genome of viruses, and their analogs, called proto‑oncogenes, were found in humans. The study of the work of oncogenes is a promising direction in the development of new methods for the diagnosis and treatment of oncological diseases. The discovery and research of oncogenes of all classes are necessary not only to understand the mechanisms of neoplasm development but also to develop new methods of cancer treatment. Oncogenes are responsible for the synthesis of growth factors, and also control the course of the cell cycle. With an excess or violation of the functions of gene products, the processes of cell growth and division are disrupted, which leads to cell degeneration, their uncontrolled division, and, as a result, to the formation of a tumor. Based on the above, we can say that by studying the mechanisms of oncogenes at the molecular level, the functions of their products, and their influence on the vital processes of cells and the whole organism, it is possible to develop ways to treat cancer by inhibiting or correcting the work of a particular oncogene or its product. The process of oncogene activation is multifaceted and can be caused by the persistence of oncogenic viruses, the integration of retroviruses into the cell genome, the presence of point mutations or deletions in genomic DNA, chromosome translocation, or protein‑protein interaction. That is why the total number of oncogenes and possible ways of their activation at different stages of tumor progression are not fully known. In this regard, we decided in this review to analyze the available information about the relatively new and poorly studied oncogenes INHA, DLL4, and MMP2, which control important functions, including metastasis and tumor growth.
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Moore, Patrick S. "KSHV-encoded oncogenes and oncogenesis." Journal of Acquired Immune Deficiency Syndromes & Human Retrovirology 14, no. 4 (April 1997): A14. http://dx.doi.org/10.1097/00042560-199704010-00033.

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Wilson, Joanna. "Oncogenes. Oncogenes." Cell 63, no. 2 (October 1990): 249–50. http://dx.doi.org/10.1016/0092-8674(90)90156-9.

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Cooper, H. L., N. Feuerstein, M. Noda, and R. H. Bassin. "Suppression of tropomyosin synthesis, a common biochemical feature of oncogenesis by structurally diverse retroviral oncogenes." Molecular and Cellular Biology 5, no. 5 (May 1985): 972–83. http://dx.doi.org/10.1128/mcb.5.5.972-983.1985.

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To identify proteins whose production may be altered as a common event in the expression of structurally diverse oncogenes, we compared two-dimensional electropherograms of newly synthesized proteins from NIH/3T3 cell lines transformed by a variety of retroviral oncogenes, from cellular revertant lines, and from a line (433.3) which expresses the v-ras oncogene in response to corticosteroids. Most alterations in the synthesis of specific proteins detected by this approach appeared to be the result of selection during prolonged cultivation and were probably unrelated to the transformation process. However, we detected seven proteins whose synthesis was strongly suppressed in cell lines transformed by each of the six retroviral oncogenes we studied and whose production was fully or partially restored in two cellular revertant lines. Suppression of two of these proteins was also correlated with the initial appearance of morphological alteration during corticosteroid-induced oncogene expression in 433.3 cells. These proteins (p37/4.78 and p41/4.75) were identified as tropomyosins, a group of at least five cytoskeletal proteins. Transformation by the papovaviruses simian virus 40 and polyomavirus caused no suppression of synthesis of these tropomyosins. This indicates that suppression of tropomyosin synthesis is not a nonspecific response by cells to being forced to grow with the transformed phenotype but is specifically associated with oncogenesis by diverse retroviral oncogenes. The results are consistent with the hypothesis that the different biochemical processes initiated by expression of structurally diverse retroviral oncogenes may converge on a limited number of common targets, one of which is the mechanism which regulates the synthesis of tropomyosins.
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Cooper, H. L., N. Feuerstein, M. Noda, and R. H. Bassin. "Suppression of tropomyosin synthesis, a common biochemical feature of oncogenesis by structurally diverse retroviral oncogenes." Molecular and Cellular Biology 5, no. 5 (May 1985): 972–83. http://dx.doi.org/10.1128/mcb.5.5.972.

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To identify proteins whose production may be altered as a common event in the expression of structurally diverse oncogenes, we compared two-dimensional electropherograms of newly synthesized proteins from NIH/3T3 cell lines transformed by a variety of retroviral oncogenes, from cellular revertant lines, and from a line (433.3) which expresses the v-ras oncogene in response to corticosteroids. Most alterations in the synthesis of specific proteins detected by this approach appeared to be the result of selection during prolonged cultivation and were probably unrelated to the transformation process. However, we detected seven proteins whose synthesis was strongly suppressed in cell lines transformed by each of the six retroviral oncogenes we studied and whose production was fully or partially restored in two cellular revertant lines. Suppression of two of these proteins was also correlated with the initial appearance of morphological alteration during corticosteroid-induced oncogene expression in 433.3 cells. These proteins (p37/4.78 and p41/4.75) were identified as tropomyosins, a group of at least five cytoskeletal proteins. Transformation by the papovaviruses simian virus 40 and polyomavirus caused no suppression of synthesis of these tropomyosins. This indicates that suppression of tropomyosin synthesis is not a nonspecific response by cells to being forced to grow with the transformed phenotype but is specifically associated with oncogenesis by diverse retroviral oncogenes. The results are consistent with the hypothesis that the different biochemical processes initiated by expression of structurally diverse retroviral oncogenes may converge on a limited number of common targets, one of which is the mechanism which regulates the synthesis of tropomyosins.
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Dissertations / Theses on the topic "Oncogenes"

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SCHAFFHAUSER, CHRISTOPHE. "Les oncogenes viraux." Strasbourg 1, 1987. http://www.theses.fr/1987STR10692.

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Pandey, Vijay. "Secreted oncogenes in endometrial carcinoma." Thesis, University of Auckland, 2010. http://hdl.handle.net/2292/8195.

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Endometrial carcinoma is the most common malignancy of the female reproductive tract and the incidence in developed countries is rising. Poor survival of late stage and recurrent endometrial carcinoma patients, particularly with an aggressive histologic subtype, necessitate the development of new therapeutic modalities for advanced stage and recurrent endometrial carcinoma. Recent published data have demonstrated elevated levels of human growth hormone (hGH) in endometriosis and endometrial adenocarcinoma. Herein, I demonstrate that autocrine production of hGH can enhance the in vitro and in vivo oncogenic potential of endometrial carcinoma cells. Forced expression of hGH in endometrial carcinoma cell lines RL95-2 and AN3 resulted in an increased total cell number through enhanced cell cycle progression and decreased apoptotic cell death. In addition, autocrine hGH expression in endometrial carcinoma cells promoted anchorage-independent growth and increased cell migration/invasion in vitro. In a xenograft model of human endometrial carcinoma, autocrine hGH enhanced tumor size and progression. Changes in endometrial carcinoma cell gene expression stimulated by autocrine hGH was consistent with the altered in vitro and in vivo behavior. Functional antagonism of hGH in wild-type RL95-2 cells significantly reduced cell proliferation, cell survival, and anchorage- independent cell growth. These studies demonstrate a functional role for autocrine hGH in the development and progression of endometrial carcinoma and indicate potential therapeutic relevance of hGH antagonism in the treatment of endometrial carcinoma. I further provided evidence for the functional role of the neurotrophic factor artemin (ARTN) in progression of endometrial carcinoma. Increased ARTN protein expression was observed in endometrial carcinoma and ARTN protein expression in endometrial carcinoma was significantly associated with higher tumor grade and invasiveness. Forced expression of ARTN in endometrial carcinoma cells significantly increased total cell number as a result of enhanced cell cycle progression and cell survival. In addition, forced expression of ARTN significantly enhanced anchorage-independent growth and invasiveness of endometrial carcinoma cells. Moreover, forced expression of ARTN increased tumor size in xenograft models and produced highly proliferative, poorly differentiated and invasive tumors. The ARTN stimulated increases in oncogenicity and invasion were mediated by increased expression and activity of AKT1. siRNA mediated depletion or antibody inhibition of ARTN significantly reduced oncogenicity and invasion of endometrial carcinoma cells. Thus, inhibition of ARTN may be considered as a potential therapeutic strategy to retard progression of endometrial carcinoma. Furthermore, I demonstrated that ARTN stimulates the oncogenicity and invasiveness of endometrial carcinoma cells. Herein, I demonstrate that ARTN modulates the sensitivity of endometrial carcinoma cells to agents used to treat latestage endometrial carcinoma. Forced expression of ARTN in endometrial carcinoma cells decreased sensitivity to doxorubicin and paclitaxel. Accordingly, depletion of ARTN by small interfering RNA or functional inhibition of ARTN with antibodies significantly increased sensitivity of endometrial carcinoma cells to doxorubicin and paclitaxel. Forced expression of ARTN in endometrial carcinoma cells abrogated doxorubicininduced G2-M arrest and paclitaxel-induced apoptosis. ARTN increased CD24 expression in endometrial carcinoma cells by transcriptional up-regulation, and CD24 was partially correlated to ARTN expression in endometrial carcinoma. Forced expression of CD24 in endometrial carcinoma cells stimulated cell proliferation and oncogenicity, enhanced cell invasion, and decreased sensitivity to doxorubicin and paclitaxel. Depletion of CD24 in endometrial carcinoma cells abrogated ARTNstimulated resistance to doxorubicin and paclitaxel. ARTN-stimulated resistance to doxorubicin and paclitaxel in endometrial carcinoma cells is therefore mediated by the specific regulation of CD24. Functional inhibition of ARTN may therefore be considered as an adjuvant therapeutic approach to improve the response of endometrial carcinoma to specific chemotherapeutic agents.
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Scully, Jaqueline Susan. "Insertion of oncogenes into mouse mammary epithelium." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315287.

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Williams, Alistair Robert William. "Expression of oncogenes in human colorectal neoplasms." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/19415.

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Imler, Jean-Luc. "Identification d'une cible transcriptionnelle pour les oncogenes." Université Louis Pasteur (Strasbourg) (1971-2008), 1988. http://www.theses.fr/1988STR13193.

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Gerlinger, Emmanuel. "Proto-oncogenes et developpement embryonnaire : etude bibliographique." Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR1M202.

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Jaggi, Rolf. "Interaction of oncogenes with the glucocorticoid receptor /." Bern, 1989. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Kemble, David J. "A biochemical study on the regulation of the SRC and FGFR family of protein tyrosine kinases /." View online ; access limited to URI, 2009. http://0-digitalcommons.uri.edu.helin.uri.edu/dissertations/AAI3367994.

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Jenkins, Brendan John. "Activating point mutations in the common ?gb?s[beta]-subunit of the human GM-CSF, IL-3 and IL-5 receptors : implications for receptor function and role in disease / by Brendan John Jenkins." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phj518.pdf.

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Bartel, Courtney A. "Novel Roles for FAM83 Oncogenes in Breast Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1512682785418426.

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Books on the topic "Oncogenes"

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. Oncogenes. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1.

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Benz, Christopher, and Edison Liu, eds. Oncogenes. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5.

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Vogt, Peter K., ed. Oncogenes. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74697-0.

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M, Glover David, and Hames B. D, eds. Oncogenes. Oxford: IRL Press, 1989.

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S, Papas Takis, and Vande Woude George F, eds. Oncogenes. New York: Elsevier, 1986.

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Christopher, Benz, and Liu Edison T, eds. Oncogenes. Boston: Kluwer Academic Publishers, 1989.

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Cancer, Research Workshop (8th 1989 Grenoble France). Growth factors and oncogenes =: Facteurs de croissance et oncogènes. London: J. Libbey Eurotext ; Paris : Editions INSERM, 1989.

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Spandidos, Demetrios, ed. ras Oncogenes. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3.

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NATO Advanced Research Workshop on Ras Oncogenes (1988 Athens, Greece). Ras oncogenes. New York: Plenum Press, 1989.

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W, Alt Frederick, Harlow Edward, Ziff Edward, and Cold Spring Harbor Laboratory, eds. Nuclear oncogenes. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1987.

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Book chapters on the topic "Oncogenes"

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Introduction." In Oncogenes, 1–3. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_1.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "myc and Other Nuclear Oncogenes." In Oncogenes, 198–221. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_10.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Additional Oncogenes." In Oncogenes, 222–33. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_11.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Transgenic Mice: Direct In Vivo Assay for Oncogenes." In Oncogenes, 234–40. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_12.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Potential Diagnostic Uses of Oncogenes." In Oncogenes, 241–61. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_13.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Potential Therapeutic Applications of Oncogenes." In Oncogenes, 262–78. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_14.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Oncogene Paradigm: Contribution to a Fundamental Understanding of Malignancy." In Oncogenes, 279–80. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_15.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Assays: Tools of the New Biology." In Oncogenes, 4–37. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_2.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Viruses and Oncogenes." In Oncogenes, 38–66. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_3.

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Burck, Kathy B., Edison T. Liu, and James W. Larrick. "Human T Cell Lymphotropic/Leukemia Viruses." In Oncogenes, 67–77. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_4.

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Conference papers on the topic "Oncogenes"

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Young, Richard A. "Abstract IA01: Transcriptional and epigenetic control of oncogenes." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-ia01.

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Shrestha, Yashaswi, Eric J. Schafer, Barbara Weir, Jesse Boehm, Sapana Thomas, and William C. Hahn. "Abstract A38: Human kinase screen for breast cancer oncogenes." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-a38.

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Yue, Xiao, Lei Han, Fengming Lan, Yang Yang, Zhendong Shi, Jian Zou, Peiyu Pu, and Chunsheng Kang. "Abstract 5003: β-catenin regulates multiple oncogenes in glioma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5003.

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Slotkin, Emily, Elisa de Stanchina, Luca Cartegni, Marc Ladanyi, and Lee Spraggon. "Abstract B26: Therapeutic targeting of sarcomas driven by EWSR1 fusion oncogenes by modulation of the fusion oncogene pre-mRNA." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-b26.

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Huang, Bin, Weijia Zhang, Winfried Edelmann, and Yuxun Wang. "Abstract 2219: Identification of oncogenes in mutant Rpa1 associated tumorigenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2219.

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Salcedo, Adriana, John D. Watson, Hilary Racher, Diane Rushlow, Shadrielle Melijah G. Espiritu, Doroto H. Sendorek, Stephenie D. Prokopec, et al. "Abstract 3771: Oncogenes and tumour-suppressors drive differential retinoblastoma evolution." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3771.

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Salcedo, Adriana, John D. Watson, Hilary Racher, Diane Rushlow, Shadrielle Melijah G. Espiritu, Doroto H. Sendorek, Stephenie D. Prokopec, et al. "Abstract 3771: Oncogenes and tumour-suppressors drive differential retinoblastoma evolution." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3771.

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Abraham, Brian J., Nicholas Kwiatkowski, Abraham S. Weintraub, Denes Hnisz, Nancy Hannett, and Richard A. Young. "Abstract PR14: Nucleation of transcriptional super-enhancers at tumor oncogenes." In Abstracts: AACR Special Conference: Translation of the Cancer Genome; February 7-9, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.transcagen-pr14.

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Abraham, Brian J., Nicholas Kwiatkowski, Abraham S. Weintraub, Denes Hnisz, Nancy Hannett, and Richard A. Young. "Abstract PR06: Nucleation of transcriptional super-enhancers at tumor oncogenes." In Abstracts: AACR Special Conference: Computational and Systems Biology of Cancer; February 8-11, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.compsysbio-pr06.

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Guest, Stephen, Ramsi Haddad, Joe Gray, and Stephen Ethier. "Abstract 5125: Functional genomic strategies to identify oncogenes in breast cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5125.

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Reports on the topic "Oncogenes"

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Shrestha, Yashaswi. Identifying Breast Cancer Oncogenes. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada545002.

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Shrestha, Yashaswi. Identifying Breast Cancer Oncogenes. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada555898.

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Fiordalisi, James J., and Channing Der. Novel Oncogenes in Breast Cancer Development. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada403648.

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Shields, Janiel, and Der Channing. Novel Oncogenes in Breast Cancer Development. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390710.

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Lopez-Diego, Rocio S., and Gregory M. Shackleford. Identification of Oncogenes Cooperating in Murine Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada396673.

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Kao, Jessica Y. Characterizing Candidate Oncogenes at 8q21 in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada485724.

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Lopez-Diego, Rocio S., and Gregory M. Shackleford. Identification of Oncogenes Cooperating in Murine Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada409479.

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Kao, Jessica. Characterizing Candidate Oncogenes at 8q21 in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada469206.

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Der, Channing J. Cloning of Novel Oncogenes Involved in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada406359.

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Der, Channing J. Cloning of Novel Oncogenes Involved in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada418063.

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