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Relevant bibliographies by topics / Oncogene expression

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Academic literature on the topic 'Oncogene expression'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "Oncogene expression"

1

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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Shestakova, E. A. "HOX GENE EXPRESSION IN HUMAN B-CELL PROGENITOR LEUKEMIA CELL LINES EXPRESSING E2A-PBX1 ONCOGENE." Russian Journal of Biotherapy 19, no. 1 (March 22, 2020): 89–95. http://dx.doi.org/10.17650/1726-9784-2019-19-1-89-95.

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Introduction. Acute lymphoblastic leukemia (ALL) is diagnosed mainly in children (2/3 of diseases) making this type of leukemia one of the most common oncological diseases among children. Oncogenes are involved in the development of ALL, in particular the product of chromosomes 1 and 19 translocation, the oncogene E2A-PBX1 that codes for E2A-PBX1 chimeric oncoprotein with strong transcription activation properties as well as oncogenes of HOX family, mainly HOXA and HOXB cluster genes. E2A-PBX1 chimeric oncoprotein and НОХА proteins are associated in vivo with factors participating in epigenetic regulation of gene expression such as chromatin modifying and remodeling enzymes that partially determines their oncogenic properties. In previous studies we obtained data indicating genetic interactions of E2A-PBX1 and НОХ genes participating in leukemia development.The aim of this research was to confirm the role of Е2А – РВХ1 oncogene in the activation of the expression of НОХА cluster genes coding for the proteins with high oncogenic potential.Materials and methods. The objects of the study were four B cell progenitor (pre-B) leukemia cell lines: RCH-ACV, KASUMI-2, 697 and NALM-6. Standard polymerase chain reaction (PCR) was used for the identification of chromosome 1 and 19 translocation product, E2A-PBX1 oncogene and its expression. Method of reverse transcription coupled with quantitative polymerase chain reaction (Q-RT-PCR) was used for the analysis of 11 HOXA cluster genes expression.Results. It is demonstrated that E2A-PBX1 oncogene is present and expressed in three studied human pre-B leukemia cell lines, RCH-ACV, KASUMI-2 and 697, while its expression is absent in NALM-6 cell line. High expression of 7 from 11 HOXА cluster genes is revealed in RCH-ACV, KASUMI-2 and 697 cell lines expressing E2A-PBX1 oncogene, whereas NALM-6 cell line, that does not express E2A-PBX1 oncogene, also does not express HOXA genes except low expression of two genes from this cluster.Conclusions. The data obtained in this study demonstrate that RCH-ACV, KASUMI-2 and 697 human leukemia pre-B cell lines, containing and expressing Е2А-РВХ1 oncogene, also express most of HOXA genes (7 genes of 11 genes) at high level in contrast to control NALM-6 cell line that does not comprise Е2А-РВХ1 oncogene and almost does not express НОХА genes. Therefore, the results of this study suggest the participation of strong transcriptional activator, chimeric oncoprotein Е2А-РВХ1, associated with chromatin modifying and remodeling enzymes, in the expression activation of HOXA cluster genes that also possess high oncogenic potential.

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GOFF, BARBARA A., HOWARD G. MUNTZ, BENJAMIN E. GREER, HISHAM K. TAMIMI, and ALLEN M. GOWN. "Oncogene Expression." Obstetrical & Gynecological Survey 92, no. 1 (July 1998): 88–93. http://dx.doi.org/10.1097/00006250-199807000-00018.

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TIAN, XIAOBING, MOHAN R. ARUVA, PONUGOTI S. RAO, WENYI QIN, PAUL READ, EDWARD R. SAUTER, MATHEW L. THAKUR, and ERIC WICKSTROM. "Imaging Oncogene Expression." Annals of the New York Academy of Sciences 1002, no. 1 (December 2003): 165–88. http://dx.doi.org/10.1196/annals.1281.015.

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Mukherjee, Archana, Eric Wickstrom, and Mathew L. Thakur. "Imaging oncogene expression." European Journal of Radiology 70, no. 2 (May 2009): 265–73. http://dx.doi.org/10.1016/j.ejrad.2009.01.043.

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Luna, Adrian J., Rosa T. Sterk, Anastacia M. Griego-Fisher, Joon-Yong Chung, Kiersten L. Berggren, Virginie Bondu, Pamela Barraza-Flores, et al. "MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors." PLOS Pathogens 17, no. 1 (January 22, 2021): e1009216. http://dx.doi.org/10.1371/journal.ppat.1009216.

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Intracellular pathogens have evolved to utilize normal cellular processes to complete their replicative cycles. Pathogens that interface with proliferative cell signaling pathways risk infections that can lead to cancers, but the factors that influence malignant outcomes are incompletely understood. Human papillomaviruses (HPVs) predominantly cause benign hyperplasia in stratifying epithelial tissues. However, a subset of carcinogenic or “high-risk” HPV (hr-HPV) genotypes are etiologically linked to nearly 5% of all human cancers. Progression of hr-HPV-induced lesions to malignancies is characterized by increased expression of the E6 and E7 oncogenes and the oncogenic functions of these viral proteins have been widely studied. Yet, the mechanisms that regulate hr-HPV oncogene transcription and suppress their expression in benign lesions remain poorly understood. Here, we demonstrate that EGFR/MEK/ERK signaling, influenced by epithelial contact inhibition and tissue differentiation cues, regulates hr-HPV oncogene expression. Using monolayer cells, epithelial organotypic tissue models, and neoplastic tissue biopsy materials, we show that cell-extrinsic activation of ERK overrides cellular control to promote HPV oncogene expression and the neoplastic phenotype. Our data suggest that HPVs are adapted to use the EGFR/MEK/ERK signaling pathway to regulate their productive replicative cycles. Mechanistic studies show that EGFR/MEK/ERK signaling influences AP-1 transcription factor activity and AP-1 factor knockdown reduces oncogene transcription. Furthermore, pharmacological inhibitors of EGFR, MEK, and ERK signaling quash HPV oncogene expression and the neoplastic phenotype, revealing a potential clinical strategy to suppress uncontrolled cell proliferation, reduce oncogene expression and treat HPV neoplasia.

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Byun, Eunyoung, Joo Weon Lim, Jung Mogg Kim, and Hyeyoung Kim. "α-Lipoic Acid InhibitsHelicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells." Mediators of Inflammation 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/380830.

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Hyperproliferation and oncogene expression are observed in the mucosa ofHelicobacter pylori- (H. pylori-)infected patients with gastritis or adenocarcinoma. Expression of oncogenes such asβ-catenin and c-myc is related to oxidative stress.α-Lipoic acid (α-LA), a naturally occurring thiol compound, acts as an antioxidant and has an anticancer effect. The aim of this study is to investigate the effect ofα-LA onH. pylori-induced hyperproliferation and oncogene expression in gastric epithelial AGS cells by determining cell proliferation (viable cell numbers, thymidine incorporation), levels of reactive oxygen species (ROS), NADPH oxidase activation (enzyme activity, subcellular levels of NADPH oxidase subunits), activation of redox-sensitive transcription factors (NF-κB, AP-1), expression of oncogenes (β-catenin, c-myc), and nuclear localization ofβ-catenin. Furthermore, we examined whether NADPH oxidase mediates oncogene expression and hyperproliferation inH. pylori-infected AGS cells using treatment of diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase. As a result,α-LA inhibited the activation of NADPH oxidase and, thus, reduced ROS production, resulting in inhibition on activation of NF-κB and AP-1, induction of oncogenes, nuclear translocation ofβ-catenin, and hyperproliferation inH. pylori-infected AGS cells. DPI inhibitedH. pylori-induced activation of NF-κB and AP-1, oncogene expression and hyperproliferation by reducing ROS levels in AGS cells. In conclusion, we propose that inhibiting NADPH oxidase byα-LA could prevent oncogene expression and hyperproliferation occurring inH. pylori-infected gastric epithelial cells.

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Chernov, A. N. "The impact of the nerve growth factor on the number of MYCC, MYCN oncogene copies in human medulloblastoma cells." Malignant tumours 9, no. 1 (April 10, 2019): 22–28. http://dx.doi.org/10.18027/2224-5057-2019-9-1-22-28.

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Introduction: The search for new molecular targets for chemotherapy of malignancies, particularly pediatric brain tumors, is a relevant issue of modern oncology. MYC expression and amplification is often observed in brain tumors, which is an unfavorable prognostic factor. Many oncogenic processes are regulated by some growth factors including the nerve growth factor (NGF).Purpose: To study the changes in the number of MYCCand MYCN‑gene copies in MB cells exposed to the NGF.Material and methods: The impact of the NGF on the number of MYCC‑, MYCN oncogene copies in the primary human medulloblastoma cell culture was assessed using the method of fluorescence in situ hybridization.Results: Exposure to the NGF was shown to decrease the number of MB cells containing 6, 8 copies of MYCN oncogenes and 3, 8 copies of MYCC oncogene. The NGF was also shown to increase the number of tumor cells that contain a double set of copies of both oncogenes. There was a statistically significant (p<0.0001) negative correlation (r=–0.65) between the average number of MYCC oncogene copies and the NGF cytotoxicity index.Conclusion: The increased number of oncogene copies reduces the susceptibility of MB cells to the growth factor.

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Rowley, Peter T., and Gary R. Skuse. "Oncogene expression in myelopoiesis." International Journal of Cell Cloning 5, no. 4 (1987): 255–66. http://dx.doi.org/10.1002/stem.5530050402.

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ROWLEY, PETER T., BARBARA KOSCIOLEK, and JUDITH L. BADER. "Oncogene Expression in Neurofibromatosis." Annals of the New York Academy of Sciences 486, no. 1 Neurofibromat (December 1986): 327–32. http://dx.doi.org/10.1111/j.1749-6632.1986.tb48085.x.

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Dissertations / Theses on the topic "Oncogene expression"

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Ellis, D. K. "Cellular oncogene expression during retinal transdifferentiation." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371121.

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Chan, Yuk Fai. "Manipulation of EWS oncogene expression using RNAi /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20CHAN.

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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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Watson, Dorothy M. A. "Cyclic nucleotide binding and oncogene expression in breast cancer." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/19398.

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Radhakrishnan, Vijayababu, Charles Putnam, Wenqing Qi, and Jesse Martinez. "P53 suppresses expression of the 14-3-3gamma oncogene." BioMed Central, 2011. http://hdl.handle.net/10150/610345.

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BACKGROUND:14-3-3 proteins are a family of highly conserved proteins that are involved in a wide range of cellular processes. Recent evidence indicates that some of these proteins have oncogenic activity and that they may promote tumorigenesis. We previously showed that one of the 14-3-3 family members, 14-3-3gamma, is over expressed in human lung cancers and that it can induce transformation of rodent cells in vitro.METHODS:qRTPCR and Western blot analysis were performed to examine 14-3-3gamma expression in non-small cell lung cancers (NSCLC). Gene copy number was analyzed by qPCR. P53 mutations were detected by direct sequencing and also by western blot. CHIP and yeast one hybrid assays were used to detect p53 binding to 14-3-3gamma promoter.RESULTS:Quantitative rtPCR results showed that the expression level of 14-3-3gamma was elevated in the majority of NSCLC that we examined which was also consistent with protein expression. Further analysis of the expression pattern of 14-3-3gamma in lung tumors showed a correlation with p53 mutations suggesting that p53 might suppress 14-3-3 gamma expression. Analysis of the gamma promoter sequence revealed the presence of a p53 consensus binding motif and in vitro assays demonstrated that wild-type p53 bound to this motif when activated by ionizing radiation. Deletion of the p53 binding motif eliminated p53's ability to suppress 14-3-3gamma expression.CONCLUSION:Increased expression of 14-3-3gamma in lung cancer coincides with loss of functional p53. Hence, we propose that 14-3-3gamma's oncogenic activities cooperate with loss of p53 to promote lung tumorigenesis.

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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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Amouyel, Philippe. "Expression des proto-oncogenes ets dans les astrocytes et dans les tumeurs astrocytaires." Lille 2, 1988. http://www.theses.fr/1988LIL2M054.

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Ritchie, Andrew John. "Endocrinology, oncogene expression and outcome in carcinoma of the lung." Thesis, Queen's University Belfast, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357457.

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9

Richards, Sally. "Inhibition of oncogene expression by the formation of Triplex DNA." Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368703.

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Faulkner, Lee. "Expression of the c-fgr proto-oncogene in monoblastoid cells." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309109.

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Books on the topic "Oncogene expression"

1

Travers, Helen. Oncogene regulation of gene expression. Manchester: University of Manchester, 1996.

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2

Morgan, James I. Proto-Oncogene expression in the nervous /system. Amsterdam: Published by Elsevier for the Foundation for the study of the Nervous System (FESN), 1991.

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3

Rowley, S. Nuclear oncogene expression in the prognosis of colorectal cancer. Birmingham: University of Birmingham, 1990.

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4

Detta, Allah. Proliferative potential and proto-oncogene expression in human meningioma. Birmingham: Universityof Birmingham, 1993.

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5

Darley, Richard Lawrence. Modulation of major histocompatibility antigen expression by the ras oncogene in murine fibroblast cells. [s.l.]: typescript, 1992.

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6

Jordan, Richard. A study of c-erbB-2 oncogene expression in salivary gland neoplasms by in situ hybridisation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Jordan, Richard. A study of c-erb B-2 oncogene expression in salivary gland neoplasms by in situ hybridisation. [Toronto: Faculty of Dentistry, University of Toronto], 1992.

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8

Chapman, Rachel Susan. Investigation into the relationship between expression of the activated Abelson oncogene, drug sensitivity and suppression of apoptosis in chronic myeloid Leukaemia. Manchester: University of Manchester, 1995.

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9

rdh-Nilsson, Anna Hultga. Oncogenes and second messengers in the regulation of smooth muscle cell growth and differentiation. Stockholm: Kongl. Carolinska Medico Chirurgiska Institutet, 1991.

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10

David, Puett, ed. Advances in gene technology: Molecular biology of the endocrine system : proceedings of the Eighteenth Miami Winter Symposium, Miami, Florida, U.S.A., February 3-7, 1986. Cambridge: Cambridge University Press, 1986.

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Book chapters on the topic "Oncogene expression"

1

Klement, V. "Radiation-Enhanced Oncogene Expression." In Realm of Tolerance, 180–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74712-0_21.

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2

Höfler, H. "Oncogene and Receptor Expression." In Current Topics in Pathology, 435–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75515-6_12.

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Ichimura, Koichi, Kimiyoshi Hirakawa, Atsushi Komatsuzaki, and Yasuhito Yuasa. "Oncogene Expression in Acoustic Neurinomas." In Biological Aspects of Brain Tumors, 337–42. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_45.

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Symonds, R. P., T. Habeshaw, J. Paul, D. J. Kerr, A. Darling, R. A. Burnett, F. Sotsiou, S. Linardopoulos, and D. A. Spandidos. "Oncogene Expression and Cervical Cancer." In The Superfamily of ras-Related Genes, 277–83. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6018-6_30.

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Baker, Vicki V. "Oncogene expression in cervical cancer." In Gynecologic Oncology, 43–51. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2598-1_4.

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Sasaki, Yutaka, Norio Hayashi, Masayoshi Horimoto, Toshifumi Ito, Hideyuki Fusamoto, and Takenobu Kamada. "Oncogene Expression in Liver Injury." In Liver and Environmental Xenobiotics, 151–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-12385-0_12.

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Baum, Ellen Z., Geraldine A. Bebernitz, and Philip M. Sass. "Expression of ras Oncogene in Xenopus laevis." In ras Oncogenes, 269–74. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_35.

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Hawley, P., and I. Gibson. "Suppression of ras Oncogene Expression Using Sequence Specific Oligodeoxynucleotides." In ras Oncogenes, 165–74. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_23.

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Collins, Steven J. "Oncogene Expression and Arrangement in Human Leukemia." In Biology and Therapy of Acute Leukemia, 65–76. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2609-0_5.

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McGeady, Mary Lou, Thomas G. Wood, Donald G. Blair, Arun Seth, Friedrich Propst, Marianne Oskarsson, Martin Schmidt, and George Vande Woude. "Cis Regulatory Control of mos Oncogene Expression." In Molecular Biology of the Arterial Wall, 76–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83118-8_24.

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Conference papers on the topic "Oncogene expression"

1

Feng, Gong, Patricia Hicks, Charles W. Prince, Candece Gladson, and Pi-Ling Chang. "OSTEOPONTIN ENHANCES PROTO-ONCOGENE (Junb) EXPRESSION IN PRENEOPLASTIC MOUSE CELLS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.253.

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Ge, Lin, Lin Ge, Wenxia Meng, Hongmei Zhou, and Neil Bhowmick. "Abstract 1015: Head and neck cancer expression of YAP65: A novel oncogene." 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.am10-1015.

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Dachineni, Rakesh, Goqiang Ai, and Jayarama B. Gunaje. "Abstract 3501: Aspirin modulates oncogene expression in hct 116 colon cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3501.

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Koch, Daniel, Stacey Adams, Andrew Gentles, Benedict Anchang, Delaney Sullivan, Sylvia Plevritis, and Dean Felsher. "Abstract A48: Gene expression signatures associated with MYC oncogene addiction in lymphoma." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-a48.

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Wormser, L., A. Gaza, V. Fritz, C. Hellerbrand, AK Bosserhoff, and P. Dietrich. "Expression and function of neuroblastoma RAS viral oncogene homolog (NRAS) in hepatocellular carcinoma." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677241.

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Guerrero, Sergi, Rudolf Fehrmann, and Marcel ATM van Vugt. "Abstract 1406: Towards an RNA expression-based signature for oncogene-induced replication stress." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1406.

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Saidi, J., AM Kaufmann, K. Bendahhou, R. Bekkali, Y. Chami, A. Belakhal, IK Ahmadaye, Z. Lakehayli, A. Benider, and J. Sehouli. "Cervical cancer screening feasibility study MorocOncoE6 comparing VIA with molecular HPV oncogene expression testing." In 62. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe – DGGG'18. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1671379.

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Benitez, Jorge A., Webster K. Cavenee, and Frank F. Furnari. "Abstract 5253: PTEN represses oncogene expression by regulating Daxx-H3.3 deposition in the chromatin." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5253.

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Bollig-Fischer, Aliccia B., and Stephen P. Ethier. "Abstract 114: Identification of HER2 oncogene-regulated genes and pathways from dynamic gene expression data." 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.am10-114.

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Ding, Yali, Jonathon L. Payne, Shriya Kane, Elanora Dovat, Mario Soliman, Chunhua Song, and Sinisa Dovat. "Abstract 2537: Regulation of LMO2 oncogene expression in high-risk B-cell acute lymphoblastic leukemia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2537.

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Reports on the topic "Oncogene expression"

1

Anderson, A., and G. E. Woloschak. Cellular oncogene expression following exposure of mice to {gamma}-rays. Office of Scientific and Technical Information (OSTI), June 1991. http://dx.doi.org/10.2172/10148918.

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McGuffie, Eileen M., and Carlo V. Catapano. Development of Triplex-Forming Oligonucleotides to Inhibit Expression of the c-myc Oncogene in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416148.

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Imbalzano, Anthony N. In Vivo and In Vitro Analysis of the Regulation of c-myc Proto-Oncogene Expression in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada305616.

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