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Relevant bibliographies by topics / Oncogenes – Research

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Academic literature on the topic 'Oncogenes – Research'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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Journal articles on the topic "Oncogenes – Research"

1

Cline, M. J., H. Battifora, and J. Yokota. "Proto-oncogene abnormalities in human breast cancer: correlations with anatomic features and clinical course of disease." Journal of Clinical Oncology 5, no. 7 (July 1987): 999–1006. http://dx.doi.org/10.1200/jco.1987.5.7.999.

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DNAs from fifty-three primary breast cancers were hybridized with 16 different proto-oncogene or oncogene probes. Abnormalities of one or more of five proto-oncogenes were found in fifty-eight percent of tumors at the time of mastectomy. Amplification of c-myc and c-erbB-2, and allelic deletions of c-ras-Ha and c-myb were the most common abnormalities. The presence of altered proto-oncogenes correlated with clinical stage of the cancers. Fifteen of 43 evaluable tumors of stages I to III recurred, and four of five evaluable stage IV tumors progressed within 16 to 24 months of surgery. All but one of the cancers that recurred or progressed had detectably altered proto-oncogenes (P less than .001). Analysis of proto-oncogenes may have prognostic value in breast cancer.

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Higuchi, Akio, Rika Kasajima, Manabu Shiozawa, Masahiro Asari, Masaaki Murakawa, Yusuke Katayama, Koichiro Yamaoku, et al. "Analysis of correlation between oncogene mutation and response to chemotherapy in all RAS wild type metastatic colorectal cancer, using next-generation sequencing technology." Journal of Clinical Oncology 33, no. 3_suppl (January 20, 2015): 553. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.553.

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553 Background: Targeted therapies of monoclonal antibodies have changed the treatment of metastatic colorectal cancer (mCRC). A target therapy with chemotherapy regimen for mCRC was decided by KRAS mutation status (KRAS exon2 [codon12, codon13]). Currently, there are many reports suggesting that in addition to analysis of KRAS mutation status, the evaluation of EGFR gene copy number, levels of EGFR ligands, BRAF, NRAS, PIK3CA mutations could be helpful to have a more accurate selection of patients who may have a benefit from anti-EGFR targeted drugs. Methods: Mutation status of 50 oncogenes were analysed in 35 mCRC patients with all RAS wild type, using next-generation sequencing technology. The response for chemotherapy was classified response group (R group) and non-response group (N group) by RECIST. The relation between mutation status of 50 oncogenes and the response for chemotherapy was assessed. Results: There were 25 oncogene mutations in the 50 genes. Driver mutation associated with oncogenic mutation deeply were 5 oncogenes, which were PIK3CA, AKT1, BRAF, PDGFRA and TP53. Only BRAF mutation was significantly associated with poor chemo response in the 5 oncogenes. A case which had two driver mutations was only in the N group. One of the two driver mutations was tumor suppressor gene, TP53. Conclusions: BRAF mutation and the number of driver mutations are key predictors of chemosensitivity in the mCRC cases with all RAS wild type.

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Benchimol, S. "Oncogenes." Current Opinion in ONCOLOGY 2, no. 1 (February 1990): 138–42. http://dx.doi.org/10.1097/00001622-199002000-00023.

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4

BELL. "Oncogenes." Cancer Letters 36 (July 1987): S5—S6. http://dx.doi.org/10.1016/0304-3835(87)90222-9.

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Bell, John C. "Oncogenes☆." Cancer Letters 40, no. 1 (May 1988): 1–5. http://dx.doi.org/10.1016/0304-3835(88)90255-8.

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Åman, P. "Fusion oncogenes." Seminars in Cancer Biology 15, no. 3 (June 2005): 159–61. http://dx.doi.org/10.1016/j.semcancer.2005.01.001.

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Nurse, Paul. "Oncogenes: Yeast aids cancer research." Nature 313, no. 6004 (February 1985): 631–32. http://dx.doi.org/10.1038/313631a0.

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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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Bookstein, Robert, and D. Craig Allred. "Recessive oncogenes." Cancer 71, S3 (February 1, 1993): 1179–86. http://dx.doi.org/10.1002/1097-0142(19930201)71:3+<1179::aid-cncr2820711442>3.0.co;2-b.

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Moore, P. S., and Y. Chang. "Kaposi's Sarcoma-Associated Herpesvirus-Encoded Oncogenes and Oncogenesis." JNCI Monographs 1998, no. 23 (April 1, 1998): 65–71. http://dx.doi.org/10.1093/oxfordjournals.jncimonographs.a024176.

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Dissertations / Theses on the topic "Oncogenes – Research"

1

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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Xie, Dan, and 謝丹. "Application of high-throughput tissue microarray technology in cancer research." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30283619.

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Dong, Suisui, and 董穗穗. "Applications of T-rex tetracycline inducible expression system on identifying downstream targets of oncogenes in HCC research." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45456641.

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Schiavi, Susan C. "MYC and E1A Oncogenes Alter the Response of PC12 Cells to Nerve Growth Factor and Block Differentiation: A Thesis." eScholarship@UMMS, 1988. https://escholarship.umassmed.edu/gsbs_diss/259.

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PC12 rat pheochromocytoma cells respond to nerve growth factor (NGF) by neuronal differentiation and partial growth arrest. Mouse c-myc and adenovirus E1A genes were introduced into PC12 cells to study the influence of these nuclear oncogenes on neuronal differentiation. Expression of myc and E1A blocked morphological differentiation and caused NGF to stimulate rather than inhibit cell proliferation. NGF binding to cell surface receptors, activation of ribosomal S6 kinase, and ornithine decarboxylase induction were similar in myc and E1A expressing clones compared with wild-type PC12 cells, suggesting that changes in the cellular response to NGF were at a post-receptor level. The ability of myc and E1A expression to block the transcription-dependent induction of microtubule associated proteins by NGF further suggested that these genes may inhibit differentiation by interfering with NGP's ability to regulate transcription. These results illustrate that NGF can promote either growth or differentiation of PC12 cells, and that myc or E1A alter the phenotypic responses to growth factors.

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Appleby, Mark William. "Oncogene expression and the modulation of keratinocyte self renewal." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306476.

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Whitelaw, Christopher Bruce Alexander. "An analysis of the transcriptional control domains of the human c-myc proto-oncogene." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306235.

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Lucassen, Emy Marian. "The role of the neu oncogene in the transformation and differentiation of mammary epithelial cells." Thesis, Open University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276089.

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Thomas, Hilary. "A feasibility study of oncogene transgenic mice as therapeutic models in cytokine research." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264165.

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Sumner, Evan T. "Characterizing the Oncogenic Properties of C-terminal Binding Protein." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4153.

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The paralogous C-terminal binding proteins (CtBP) 1 and 2 are evolutionarily conserved transcriptional coregulators that target and disrupt the expression of several genes essential for multiple cellular processes critical to regulating tumor formation. CtBP’s ability to govern the transcription of genes necessary for apoptosis, tumor suppression, invasion/migration and EMT gives rise to its oncogenic activities. Both isoforms of CtBP are found to be overexpressed in cancers including colorectal, pancreatic, ovarian, and breast, with higher levels correlating to lower overall median survival. Although multiple lines of evidence suggest CtBP plays a role in tumorigenesis, it has never been formally characterized as an oncogene. For this reason, the goal of this dissertation was to design a set of experiments to determine the transforming ability of CtBP2 in vitro using both murine and human fibroblast and in vivo using the Apcmin/+ mouse model of cancer. Specifically, we demonstrate that overexpression of CtBP2 alone can drive transformation of NIH3T3 cells leading to loss of contact inhibition, increased x invasion/migration, and anchorage independent growth. In addition, CtBP2 was found to cooperate with the large T-antigen (LT) component of the simian virus 40 (SV40) to lead to transformation of murine embryonic fibroblasts (MEFs) and with both LT and small T-antigen (ST) to induce migration/invasion and anchorage-independent growth in BJ human foreskin fibroblasts. To confirm the role of Ctbp2 in a mouse tumor model with Ctbp overexpression, we bred Apcmin/+ mice to Ctbp2 heterozygous (Ctbp2+/-) mice, which otherwise live normal lifespans. CtBP is a known target of the APC tumor suppressor and is thus stabilized in APC mutated human colon cancers and is found in high levels in Apcmin/+ polyps. Remarkably, removing an allele of Ctbp2 doubled the median survival of Apcmin/+ mice (P <0.001) and reduced polyp formation to near undetectable levels. These data suggest the importance of CtBP2 in driving cellular transformation and identify it as a potential target for prevention or therapy in APC mutant backgrounds.

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Knarr, Matthew J. "The Monkey in the Wrench: MiR-181a's Role in Promoting Adipogenesis and Ovarian Cancer Transformation." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1554481048956007.

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Books on the topic "Oncogenes – Research"

1

G, Knudson Alfred, ed. Genetic basis for carcinogenesis: Tumor suppressor genes, and oncogenes : proceedings of the 20th International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, 1989. Tokyo: Japan Scientific Societies Press, 1990.

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2

Perrey, Christophe. Un ethnologue chez les chasseurs de virus. Paris: L'Harmattan, 2012.

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3

Gaines, Ann. Robert A. Weinberg and the search for the cause of cancer. Bear, Del: Mitchell Lane, 2002.

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4

Symposium, Takamatsu no Miya Hi Gan Kenkyū Kikin International. Multistage carcinogenesis: Proceedings of the 22nd International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, 1991. Tokyo: Japan Scientific Societies Press, 1992.

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1943-, Harris Curtis C., ed. Multistage carcinogenesis: Proceedings of the 22nd International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, ₉91. Tokyo: Japan Scientific Societies Press, 1993.

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Curing cancer: The story of the men and women unlocking the secrets of our deadliest illness. New York, NY: Simon & Schuster, 1997.

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Takamatsu no Miya Hi Gan Kenkyū Kikin. International Symposium. Oncogenes and cancer: Proceedings of the 17th International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, 1986. Tokyo: Japan Scientific Societies Press, 1987.

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8

Angier, Natalie. Natural obsessions: The search for the oncogene. Boston: Houghton Mifflin, 1988.

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9

Crafting science: A sociohistory of the quest for the genetics of cancer. Cambridge, Mass: Harvard University Press, 1996.

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10

Catalog of human cancer genes: McKusick's Mendelian inheritance in man for clinical and research oncologists (onco-MIM). Baltimore: Johns Hopkins University Press, 1999.

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Book chapters on the topic "Oncogenes – Research"

1

Dang, Chi V. "Oncogenes and proto-oncogenes: General concepts." In Cancer Treatment and Research, 3–24. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5_1.

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2

Larrick, James W., and Edison Liu. "Therapeutic applications of oncogenes." In Cancer Treatment and Research, 319–30. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5_14.

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3

Kirschenbaum, Alexander, and Michael J. Droller. "Oncogenes and genitourinary neoplasia." In Cancer Treatment and Research, 101–19. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2033-3_11.

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4

Ratner, Lee, Robert C. Gallo, and Flossie Wong-Staal. "Cloning of Human Oncogenes." In Recombinant DNA Research and Viruses, 15–35. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2565-9_2.

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Der, Channing J. "The ras family of oncogenes." In Cancer Treatment and Research, 73–119. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5_4.

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Rochlitz, Christoph F., and Christopher C. Benz. "Oncogenes in human solid tumors." In Cancer Treatment and Research, 199–240. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5_9.

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Liu, Edison. "Oncogenes in human leukemias and lymphomas." In Cancer Treatment and Research, 241–65. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5_10.

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Lee, William M. F. "The myc family of nuclear proto-oncogenes." In Cancer Treatment and Research, 37–71. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1599-5_3.

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Sandberg, Avery A., and Surabhi Kakati. "Chromosome Alterations and Oncogenes in Human Neoplasia." In Trends in Chromosome Research, 190–203. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-10621-1_13.

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Ghigna, Claudia, Silvano Riva, and Giuseppe Biamonti. "Alternative Splicing of Tumor Suppressors and Oncogenes." In Cancer Treatment and Research, 95–117. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-31659-3_4.

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Conference papers on the topic "Oncogenes – Research"

1

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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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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Dupain, C., L. Massaad-Massade, AC Harttrampf, and C. Gracia. "PO-508 Detection and role of novel fusion oncogenes in paediatric cancers." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.523.

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Mudassir, M., MA Kassab, S. Ansari, M. Bhagat, and P. Chattopadhyay. "PO-002 Single siRNA mediated post transcriptional and transcriptional gene silencing of HPV18 oncogenes." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.540.

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Sodi, Valerie L., Shane W. O'Brien, Chao Wu, Roland L. Dunbrack, Tiffiney R. Hartman, Alana M. O'Reilly, and Denise C. Connolly. "Abstract A24: Cell adhesion molecule (CAM)-related downregulated by oncogenes (CDON) promotes ovarian cancer adhesion and survival." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a24.

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Souchelnytskyi, Serhiy. "Systemic properties of Carcinogenesis: Lessons from studies on the Earth and in the Space." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0118.

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proteins and genes act in coordinated ways, and their relations are visualized as networks. Networks are more accurate descriptions of cancer regulatory mechanisms, in comparison to lists of oncogenes and tumor suppressors. To extract essential regulators (nodes) and connections (edges), interrogations of these networks are performed, e.g. cancer cells are subjected to different treatments. Interrogations force cancer cells to engage nodes and edges essential for maintaining cancer properties, i.e. drivers, and nonessential followers. The challenge is to discriminate which of the mechanisms drive tumorigenesis, and which are followers. Interrogation of cancer cells under variable g-forces is the treatment to which cancer cells are not normally exposed. Therefore, low (weightlessness) and high (acceleration) g-forces may trigger responses, which may differ in part of followers from responses on the Earth, but still engage carcinogenesis-essential drivers nodes and edges. Methodology: Experimental interrogation of human cancer cells to generate carcinogenesis-related regulatory networks was performed by using proteomics, cell biology, biochemistry, immunohistochemistry and bioinformatics tools. We used also reported datasets deposited in various databases. These networks were analyzed with algorithms to extract drivers of carcinogenesis. Results: Systemic analysis of human breast carcinogenesis has shown mechanisms of engagement of all known cancer hallmarks. Moreover, novel hallmarks have emerged, e.g. involvement of mechanisms of virus-cell interaction and RNA/miR processing. The breast cancer networks are rich, with >6,000 involved proteins and genes. The richness of the networks may explain many clinical observations, e.g. personalized response to treatments. Systemic analysis highlighted novel opportunities for treatment of cancer, by identifying key nodes of known and novel hallmark mechanisms. Systemic properties of the cancer network provides an opportunity to study compensatory mechanisms. These compensatory mechanisms frequently contribute to development of resistance to treatment. These mechanisms will be discussed. Cancer cells are not “wired” to function in weightlessness. The cells would have to adapt. This adaptation will include preserving mechanisms driving carcinogenesis, in addition to the space-only-related adaptation. Key carcinogenesis regulators in the space would be the same as on the Earth, while “passenger”-mechanisms would differ. Systems biology allows integration of a space- and the Earth-data, and would extract key regulators, and, subsequently lead to better diagnostic. Conclusion: Systemic analysis of carcinogenesis studies with different ways of interrogation delivered better diagnostic and novel modalities of treatment.

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Levine, Beth C. "Abstract IA18: Oncogene regulation of the autophagy machinery." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-ia18.

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Tang, Hua, Tao Liu, Yuanyuan Lang, Min Liu, Yixuan Li, and Xin Li. "Abstract A30: MicroRNA-27a functions as an oncogene in gastric adenocarcinoma by targeting prohibitin." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a30.

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Liu, Xi, Lorenzo Sempere, Fabrizio Galimberti, Sarah Freemantle, Candice Black, Steven Fiering, Charles Cole, et al. "Abstract A135: Uncovering tumor suppressive and oncogenic microRNAs in lung cancer." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a135.

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Rorie, C. J., and B. E. Weissman. "Ews/Fli-1 Chimeric Oncogene: Role in Neuronal Differentiation and Abrogation of p53 A Two-Year Study." In Minority Trainee Research Forum, 2004. TheScientificWorld Ltd, 2004. http://dx.doi.org/10.1100/tsw.2004.147.

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