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Academic literature on the topic 'Antioncogenes'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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Journal articles on the topic "Antioncogenes"

Knudson, A. G. "Antioncogenes and human cancer." Proceedings of the National Academy of Sciences 90, no. 23 (December 1, 1993): 10914–21. http://dx.doi.org/10.1073/pnas.90.23.10914.

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The antioncogenes, or tumor suppressor genes, as negative regulators of cell division, stand in contrast to oncogenes. For most human cancers, the more frequently mutated genes are the antioncogenes, the principal exception being the leukemias and lymphomas. Persons heterozygous for germ-line mutations in antioncogenes are strongly predisposed to one or more kinds of cancer, and most dominantly inherited cancer is attributable to such heterozygosity. Seven antioncogenes have been cloned through the study of these persons, and several others have been mapped. An eighth one was mapped and cloned through the investigation of tumors and is not yet known in hereditary form. Three dominantly inherited forms of cancer are not attributable to mutations in antioncogenes. The corresponding nonhereditary forms of most cancers generally reveal abnormalities of the same antioncogenes that are found in the hereditary forms but may also show additional ones. Some cancers, especially the embryonal tumors of children, have a small number of antioncogene mutations; some others, such as most sarcomas, have more, and the common carcinomas have the most, reflecting a hierarchy of controls over growth of stem cell populations. Still more members of this gene category remain to be mapped and cloned through the study of cancer families and of tumors. The genes that have been cloned act at diverse points in the signal transduction pathway in cells, from the outer cell membranes to sites of gene transcription, in some cases as negative regulators of oncogene expression.

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Atkin, N. B. "ANTIONCOGENES." Lancet 326, no. 8465 (November 1985): 1189–90. http://dx.doi.org/10.1016/s0140-6736(85)92712-6.

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Goudie, R. B. "What are antioncogenes?" Journal of Pathology 154, no. 4 (April 1988): 297–98. http://dx.doi.org/10.1002/path.1711540402.

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Carbone, David P., and John D. Minna. "Antioncogenes and Human Cancer." Annual Review of Medicine 44, no. 1 (February 1993): 451–64. http://dx.doi.org/10.1146/annurev.me.44.020193.002315.

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Mitchell, C. D. "Recessive oncogenes, antioncogenes and tumour suppression." British Medical Bulletin 47, no. 1 (1991): 136–56. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072452.

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Giaccone, Giuseppe. "Oncogenes and Antioncogenes in Lung Tumorigenesis." Chest 109, no. 5 (May 1996): 130S—134S. http://dx.doi.org/10.1378/chest.109.5_supplement.130s.

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&NA;. "Antioncogenes open new research pathways in cancer therapy." Inpharma Weekly &NA;, no. 733 (April 1990): 3. http://dx.doi.org/10.2165/00128413-199007330-00005.

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Carbone, Michele, and Arthur S. Levine. "Oncogenes, antioncogenes, and the regulation of cell growth." Trends in Endocrinology & Metabolism 1, no. 5 (May 1990): 248–53. http://dx.doi.org/10.1016/1043-2760(90)90005-n.

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Carvajal Yañez, Noelia, and Jorge Marcelo Avedaño. "Manifestaciones neurológicas y cutáneas del complejo de esclerosis tuberosa en adulto. Reporte de un caso." Revista Cientifica Ciencia Medica 24, no. 1 (October 14, 2021): 187–91. http://dx.doi.org/10.51581/rccm.v24i1.346.

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El Complejo de Esclerosis Tuberosa es una enfermedad neurocutánea infrecuente, de característica hereditaria por la mutación de antioncogenes por lo que dentro de sus manifestaciones clínicas están la formación de tumores en diferentes órganos lo que causa una amplia variación de signos y sintomatología. Se presenta el caso clínico de un adulto varón con manifestaciones neurológicas y cutáneas predominantemente.

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Crawford, Lionel, and Massimo Tommasino. "Oncogenes and antioncogenes in the development of HPV associated tumors." Clinics in Dermatology 15, no. 2 (March 1997): 207–15. http://dx.doi.org/10.1016/s0738-081x(96)00163-0.

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Dissertations / Theses on the topic "Antioncogenes"

Campbell, Hamish George, and n/a. "The functions of p53 during an adenovirus infection." University of Otago. Dunedin School of Medicine, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080411.115504.

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p53 is a pivotal tumour suppressor in mammalian cells. It protects the integrity of a number of cellular pathways, preventing the malignant transformation of cells. There is however perhaps nothing more efficient at disrupting cellular pathways than a virus. Viruses infiltrate cells commandeering the normal growth and survival pathways for their narcissistic needs. While the association between viral infections and the induction of p53 has long been recognised, there is controversy surrounding the ultimate role of p53 during a virus infection. The classical model of p53 in an adenovirus infection is that p53 is a formidable obstacle which needs to be overcome. Adenoviruses overcome p53 by degrading the protein and removing its ability to transactivate its target genes. However the degradation is not immediate and there is increasing evidence which would suggest p53 is actually beneficial to an adenovirus infection. In the introductory chapter, I review what is known about p53 and virus infections. What emerges from this review is the sheer number of interactions that occur between viruses and p53, indicating its importance in an infection. Additionally it shows that adenoviruses are not the only virus shown to benefit from the presence of p53. What beneficial role p53 may be fulfilling in an adenovirus infection is unclear. The experiments reported in this thesis investigate the functions of p53 in an adenovirus infection. In Chapter Three, immunoblots on a panel of adenovirus infected cells reveal that p53 levels do not correlate with the level of the classical p53 target proteins. This indicates that p53 is disconnected from its target genes during an infection. Promoter/reporter assays carried out on infected cells show that adenovirus can directly regulate p53 target genes independently of p53. In Chapter Five, I show this regulation is dependent on E1a, with transient transfection of E1a resulting in the marked activation of p53 target promoters. E1a mediated transactivation appears to be reliant on the largest splice variant of E1a (E1a-289R) and the presence of pRB. Electrophoresis mobility shift assays reveal that the transcription factor Sp1 is involved. In Chapter Four, p53 transcription in an adenovirus infection was directly assayed by using an artificial p53 consensus response element. The results show that p53 is unable to activate its consensus response element during an infection. However, I show that p53 is transcriptionally competent in an infection, and is able to transactivate a mutant derivative of the p53 consensus sequence. This shows that p53 is not only transcriptional competent but has a gain-of-function in an infection. This gain-of-function requires E1a, and appears not to be due to a change in the DNA binding affinity of p53. The data in this thesis show that adenoviruses not only appear to inhibit and control the normal transcriptional profile of p53 but appear to modify p53, giving it a new transcriptional profile. This provides a possible mechanism by which p53 could aid an adenovirus infection.

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Evdokiou, Andreas. "Tumour-suppressive activity of the growth arrest-specific gene, GAS1 /." Title page, contents and summary only, 1997. http://web4.library.adelaide.edu.au/theses/09ph/09PHE928.pdf.

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Wong, Lok-yee Michelle. "Epigenetic inactivation of RASSF1 candidate tumor suppressor gene on 3p21.3 locus in esophageal cancer." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31971325.

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Ng, Chi-heng David. "Subcellular localisation of growth suppressor protein deleted in liver cancer 2 (DLC2)." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B32028313.

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Yau, Wing Lung. "Investigation of candidate tumor suppressor genes mapped to chromosome 3p21.3 in nasopharyngeal carcinoma /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20YAU.

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Leung, Chi Chung. "Study of a candidate tumor suppressor gene on 9q32, deleted in esophageal cancer 1 (DEC1), in esophageal cancer /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20LEUNG.

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Tsang, Hing-wing. "Analysis of fragile site FRA16D and WWOX gene in non-small cell lung cancer /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34829416.

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Leung, Ho-yin Thomas. "Identification and characterization of a novel tumor suppressor gene, delected in liver cancer 2, (DLC2)." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36445058.

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Zhu, Cailei. "Characterization of tumor suppressing function of PCAF in esophageal squamous cell carcinoma." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557480.

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Wong, Lai-ting. "Study of the role of the tumor suppressor phosphatase and tensin homolog (PTEN) in hepatocellular carcinoma." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290495.

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Books on the topic "Antioncogenes"

Lees, Jaqueline. Absracts of papers presented at the 2004 meeting on cancer genetics & tumor suppressor genes: August 18-August 22, 2004. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2004.

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G, Vile Richard, ed. Introduction to the molecular genetics of cancer. Chichester: Wiley, 1992.

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M, Glover David, Hall A, and Hastie Nicholas, eds. Cell biology of cancer. Cambridge, Eng: Company of Biologists Ltd., 1994.

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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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The oncogene and tumour suppressor gene factsbook. 2nd ed. San Diego, Calif: Academic Press, 1997.

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Enrico, Mihich, Housman David E, and Pezcoller Symposium on Cancer Genes: Functional Aspects (7th. : 1995 : Trento, Italy), eds. Cancer genes: Functional aspects. New York: Plenum Press, 1996.

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Macdonald, F. Oncogenes and tumor suppressor genes. Oxford: BIOS, 1990.

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Macdonald, F. Oncogenes and tumor suppressor genes. Oxford: Bios Scientific Publishers, 1991.

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Laboratory, Cold Spring Harbor, ed. Abstracts of papers presented at the 2002 meeting on cancer genetics & tumor suppressor genes, August 14-August 18, 2002. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2002.

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Hendrix, Mary. Maspin. Georgetown, Tex: Landes Bioscience, 2001.

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Book chapters on the topic "Antioncogenes"

Knudson, Alfred G. "Two-Event Carcinogenesis: Roles of Oncogenes and Antioncogenes." In Scientific Issues in Quantitative Cancer Risk Assessment, 32–48. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-9218-7_3.

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Perucho, Manuel. "PCR and Cancer Diagnostics: Detection and Characterization of Single Point Mutations in Oncogenes and Antioncogenes." In The Polymerase Chain Reaction, 369–94. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4612-0257-8_31.

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Ladik, Janos, and Wolfgang Förner. "Mechanism of Oncogene Activation or Antioncogene Inactivation by External Factors." In The Beginnings of Cancer in the Cell, 103–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78984-7_7.

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Ladik, Janos, and Wolfgang Förner. "The Disturbance of Cell-Self-Regulation Due to Oncogene Activation and Antioncogene Inactivation." In The Beginnings of Cancer in the Cell, 141–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78984-7_8.

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"Antioncogenes." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 120. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_956.

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Rosenfeld, Myrna R., Jan J. Verschuuren, and Josep Dalmau. "Transfer and Expression of Antioncogenes and Paraneoplastic Genes in Normal and Neoplastic Cells in Vitro and in Vivo." In Viral Vectors, 275—VIII. Elsevier, 1995. http://dx.doi.org/10.1016/b978-012397570-6/50018-6.

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Cardarelli, Nate F. "Towards a New Theory of Antioncogenesis." In Tin as a Vital Nutrient:, 263–88. CRC Press, 2019. http://dx.doi.org/10.1201/9780429280511-27.

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Gupta, Megha. "Parvovirus Vectors: The Future of Gene Therapy." In Veterinary Medicine and Science. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105085.

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The unique diversity of parvoviral vectors with innate antioncogenic properties, autonomous replication, ease of recombinant vector production and stable transgene expression in target cells makes them an attractive choice as viral vectors for gene therapy protocols. Amongst various parvoviruses that have been identified so far, recombinant vectors originating from adeno-associated virus, minute virus of mice (MVM), LuIII and parvovirus H1 have shown promising results in many preclinical models of human diseases including cancer. The adeno-associated virus (AAV), a non-pathogenic human parvovirus, has gained attention as a potentially useful vector. The improved understanding of the metabolism of vector genomes and the mechanism of transduction by AAV vectors is leading to advancement in the development of more sophisticated AAV vectors. The in-depth studies of AAV vector biology is opening avenues for more robust design of AAV vectors that have potentially increased transduction efficiency, increased specificity in cellular targeting, and an increased payload capacity. This chapter gives an overview of the application of autonomous parvoviral vectors and AAV vectors, based on our current understanding of viral biology and the state of the platform.

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Jain, Aakanchha, Shiv Kumar Prajapati Prajapati, Dolly Jain, Richa Jain, Amrita Kumari Panda, Satpal Singh Bisht, and Santosh Kumar Behera. "Cancer Biology." In Therapeutic Nanocarriers in Cancer Treatment: Challenges and Future Perspective, 1–30. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815080506123010004.

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As stated by Globocan, there were around 82 lakh cancer-related deaths and 141 lakh new cancer diagnoses worldwide in 2012. Normal genes that are expressed improperly or exhibit aberrant expression may cause neoplasia, often known as cancer. Oncogenes are mutated forms of normal cellular genes that contribute to the development of cancer. Typically, oncogenes govern cell development and differentiation. Proapoptotic genes initiate cell death and decrease the number of cells. Antioncogens, or tumour suppressor genes, regulate cell division negatively. Tumours are caused by genes that directly or indirectly control cellular proliferation or inhibition, or that govern apoptosis or any sort of cell death. As a target for the development of novel cancer treatments, tumour cell metabolism has gained substantial attention. Identification of cancer has always been a crucial aspect of diagnosis and therapy. Markers for cancer are one of the most effective approaches for recognising, diagnosing, treating, monitoring progressions, and evaluating chemical resistance. A biomarker is “a distinctive biochemical, genetic, or molecular characteristic or material that signals a particular biological state or treatment.” Tumour biomarkers are often seen in moderation in the absence of a tumour. The activation of CDKs (protein kinases) aids in the progression of cells from one phase of the cell cycle to the next. Various isoforms of CDK/cyclin complexes are capable of binding with a regulating cyclin protein. Aloisine is a potent inhibitor of CDK1, CDK 2, and CDK 5, and it has been observed that GSK3 (Glycogen synthase kinase 3) terminates cell division. Antimicrotubule medicines cause the mitotic Chk to halt the cell cycle by inhibiting microtubules. The presence of cancer cells results in enhanced cell proliferation and expansion. They can result in an absence of apoptosis and excessive cell proliferation. DNA damage or significant cellular stress might result in cell death. In cancer cells, proapoptosis is often missing or inhibited. iPSCs and cancer cells have comparable transcriptome profiles, including surface antigen markers identified by the immune system. MSCs producing IFN- accelerate the killing of tumour cells, augment NK cell activity, and decrease angiogenesis. This chapter provides an introduction of the fundamentals of cancer biology, including its characteristics, metabolic processes, and biomarkers.

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Conference papers on the topic "Antioncogenes"

Rusconi, Paolo, Federica Polato, Alberto Musi, and Massimo Broggini. "Abstract 792: DRAGO (KIAA0247), a new p53-regulated antioncogene." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-792.

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Tripathi, Veenu, Drazen B. Zimonjic, and Nicholas C. Popescu. "Abstract 4017: DLC1 and α-catenin protein interaction enhances DLC1 antioncogenic activity by stabilizing adherens junctions and suppressing NFκB signaling." 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.am2011-4017.

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Reports on the topic "Antioncogenes"

Avruch, Joseph. The Rap-1 Antioncogene in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada303668.

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Kute, Timothy E. Role of a Novel Antioncogene that Prevents Metastatic Spread of Disease. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada358048.

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