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Journal articles on the topic 'Oncogenes – Research'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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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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2

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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3

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Oxnard, Geoffrey R., Adam Binder, and Pasi A. Jänne. "New Targetable Oncogenes in Non–Small-Cell Lung Cancer." Journal of Clinical Oncology 31, no. 8 (March 10, 2013): 1097–104. http://dx.doi.org/10.1200/jco.2012.42.9829.

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The identification of oncogenic driver mutations underlying sensitivity to epidermal growth factor receptor and anaplastic lymphoma kinase tyrosine kinase inhibitors has led to a surge of interest in identifying additional targetable oncogenes in non–small-cell lung cancer. A number of new potentially oncogenic gene alterations have been characterized in recent years, including BRAF mutations, HER2 insertions, PIK3CA mutations, FGFR1 amplifications, DDR2 mutations, ROS1 rearrangements, and RET rearrangements. In this review, we will discuss the techniques used to discover each of these candidate oncogenes, the prevalence of each in non–small-cell lung cancer, the preclinical data supporting their role in lung cancer, and data on small molecular inhibitors in development.

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12

Rogounovitch, Tatiana I., Svetlana V. Mankovskaya, Mikhail V. Fridman, Tatiana A. Leonova, Victor A. Kondratovitch, Natalya E. Konoplya, Shunichi Yamashita, Norisato Mitsutake, and Vladimir A. Saenko. "Major Oncogenic Drivers and Their Clinicopathological Correlations in Sporadic Childhood Papillary Thyroid Carcinoma in Belarus." Cancers 13, no. 13 (July 5, 2021): 3374. http://dx.doi.org/10.3390/cancers13133374.

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Childhood papillary thyroid carcinoma (PTC) diagnosed after the Chernobyl accident in Belarus displayed a high frequency of gene rearrangements and low frequency of point mutations. Since 2001, only sporadic thyroid cancer occurs in children aged up to 14 years but its molecular characteristics have not been reported. Here, we determine the major oncogenic events in PTC from non-exposed Belarusian children and assess their clinicopathological correlations. Among the 34 tumors, 23 (67.6%) harbored one of the mutually exclusive oncogenes: 5 (14.7%) BRAFV600E, 4 (11.8%) RET/PTC1, 6 (17.6%) RET/PTC3, 2 (5.9%) rare fusion genes, and 6 (17.6%) ETV6ex4/NTRK3. No mutations in codons 12, 13, and 61 of K-, N- and H-RAS, BRAFK601E, or ETV6ex5/NTRK3 or AKAP9/BRAF were detected. Fusion genes were significantly more frequent than BRAFV600E (p = 0.002). Clinicopathologically, RET/PTC3 was associated with solid growth pattern and higher tumor aggressiveness, BRAFV600E and RET/PTC1 with classic papillary morphology and mild clinical phenotype, and ETV6ex4/NTRK3 with follicular-patterned PTC and reduced aggressiveness. The spectrum of driver mutations in sporadic childhood PTC in Belarus largely parallels that in Chernobyl PTC, yet the frequencies of some oncogenes may likely differ from those in the early-onset Chernobyl PTC; clinicopathological features correlate with the oncogene type.

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13

Williams, Dorothy L. "Cytogenetics and oncogenes." Current Opinion in ONCOLOGY 2, no. 1 (February 1990): 26–33. http://dx.doi.org/10.1097/00001622-199002000-00005.

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14

Goymer, Patrick. "Tiny new oncogenes." Nature Reviews Cancer 6, no. 5 (May 2006): 344. http://dx.doi.org/10.1038/nrc1902.

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15

Cassoni, A. M. "Oncogenes and radiosensitivity." European Journal of Cancer 30, no. 3 (January 1994): 279–81. http://dx.doi.org/10.1016/0959-8049(94)90239-9.

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16

Kamaruzman, Nur Izyani, Noraini Abd Aziz, Chit Laa Poh, and Ezharul Hoque Chowdhury. "Oncogenic Signaling in Tumorigenesis and Applications of siRNA Nanotherapeutics in Breast Cancer." Cancers 11, no. 5 (May 6, 2019): 632. http://dx.doi.org/10.3390/cancers11050632.

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Overexpression of oncogenes and cross-talks of the oncoproteins-regulated signaling cascades with other intracellular pathways in breast cancer could lead to massive abnormal signaling with the consequence of tumorigenesis. The ability to identify the genes having vital roles in cancer development would give a promising therapeutics strategy in combating the disease. Genetic manipulations through siRNAs targeting the complementary sequence of the oncogenic mRNA in breast cancer is one of the promising approaches that can be harnessed to develop more efficient treatments for breast cancer. In this review, we highlighted the effects of major signaling pathways stimulated by oncogene products on breast tumorigenesis and discussed the potential therapeutic strategies for targeted delivery of siRNAs with nanoparticles in suppressing the stimulated signaling pathways.

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17

Rak, Janusz, and Joanne L. Yu. "Oncogenes and tumor angiogenesis." Seminars in Cancer Biology 14, no. 2 (April 2004): 93–104. http://dx.doi.org/10.1016/j.semcancer.2003.09.014.

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18

Felsher, Dean W. "Oncogenes as therapeutic targets." Seminars in Cancer Biology 14, no. 1 (February 2004): 1. http://dx.doi.org/10.1016/j.semcancer.2003.11.001.

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19

Schrier, P. I. "Oncogenes in melanoma." Melanoma Research 3 (September 1993): 4. http://dx.doi.org/10.1097/00008390-199309002-00008.

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20

Klein, Andreas, Nan Li, Joshua M. Nicholson, Amanda A. McCormack, Adolf Graessmann, and Peter Duesberg. "Transgenic oncogenes induce oncogene-independent cancers with individual karyotypes and phenotypes." Cancer Genetics and Cytogenetics 200, no. 2 (July 2010): 79–99. http://dx.doi.org/10.1016/j.cancergencyto.2010.04.008.

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21

Polsky, David, and Carlos Cordon-Cardo. "Oncogenes in melanoma." Oncogene 22, no. 20 (May 2003): 3087–91. http://dx.doi.org/10.1038/sj.onc.1206449.

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22

Fernández-Medarde, Alberto, Javier De Las Rivas, and Eugenio Santos. "40 Years of RAS—A Historic Overview." Genes 12, no. 5 (May 1, 2021): 681. http://dx.doi.org/10.3390/genes12050681.

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It has been over forty years since the isolation of the first human oncogene (HRAS), a crucial milestone in cancer research made possible through the combined efforts of a few selected research groups at the beginning of the 1980s. Those initial discoveries led to a quantitative leap in our understanding of cancer biology and set up the onset of the field of molecular oncology. The following four decades of RAS research have produced a huge pool of new knowledge about the RAS family of small GTPases, including how they regulate signaling pathways controlling many cellular physiological processes, or how oncogenic mutations trigger pathological conditions, including developmental syndromes or many cancer types. However, despite the extensive body of available basic knowledge, specific effective treatments for RAS-driven cancers are still lacking. Hopefully, recent advances involving the discovery of novel pockets on the RAS surface as well as highly specific small-molecule inhibitors able to block its interaction with effectors and/or activators may lead to the development of new, effective treatments for cancer. This review intends to provide a quick, summarized historical overview of the main milestones in RAS research spanning from the initial discovery of the viral RAS oncogenes in rodent tumors to the latest attempts at targeting RAS oncogenes in various human cancers.

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23

Miller, Wilson H., and Ethan Dmitrovsky. "Oncogenes and clinical oncology." Current Opinion in Oncology 3, no. 1 (February 1991): 65–69. http://dx.doi.org/10.1097/00001622-199102000-00010.

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24

Cline, Martin J., and Harish Ahuja. "Oncogenes and Anti-oncogenes in the Evolution of Human Leukemia/Lymphoma." Leukemia & Lymphoma 4, no. 3 (January 1991): 153–58. http://dx.doi.org/10.3109/10428199109068060.

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25

Medina-Martínez, Olga, Verónica Vallejo, Miriam C. Guido, and Alejandro García-Carrancá. "Ha-ras oncogene–induced transcription of human papillomavirus type 18E6 andE7 oncogenes." Molecular Carcinogenesis 19, no. 2 (July 1997): 83–90. http://dx.doi.org/10.1002/(sici)1098-2744(199707)19:2<83::aid-mc3>3.0.co;2-m.

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26

Grzes, Maria, Magdalena Oron, Zuzanna Staszczak, Akanksha Jaiswar, Magdalena Nowak-Niezgoda, and Dawid Walerych. "A Driver Never Works Alone—Interplay Networks of Mutant p53, MYC, RAS, and Other Universal Oncogenic Drivers in Human Cancer." Cancers 12, no. 6 (June 11, 2020): 1532. http://dx.doi.org/10.3390/cancers12061532.

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The knowledge accumulating on the occurrence and mechanisms of the activation of oncogenes in human neoplasia necessitates an increasingly detailed understanding of their systemic interactions. None of the known oncogenic drivers work in isolation from the other oncogenic pathways. The cooperation between these pathways is an indispensable element of a multistep carcinogenesis, which apart from inactivation of tumor suppressors, always includes the activation of two or more proto-oncogenes. In this review we focus on representative examples of the interaction of major oncogenic drivers with one another. The drivers are selected according to the following criteria: (1) the highest frequency of known activation in human neoplasia (by mutations or otherwise), (2) activation in a wide range of neoplasia types (universality) and (3) as a part of a distinguishable pathway, (4) being a known cause of phenotypic addiction of neoplastic cells and thus a promising therapeutic target. Each of these universal oncogenic factors—mutant p53, KRAS and CMYC proteins, telomerase ribonucleoprotein, proteasome machinery, HSP molecular chaperones, NF-κB and WNT pathways, AP-1 and YAP/TAZ transcription factors and non-coding RNAs—has a vast network of molecular interrelations and common partners. Understanding this network allows for the hunt for novel therapeutic targets and protocols to counteract drug resistance in a clinical neoplasia treatment.

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27

Åman, Pierre. "Fusion oncogenes in tumor development." Seminars in Cancer Biology 15, no. 3 (June 2005): 236–43. http://dx.doi.org/10.1016/j.semcancer.2005.01.009.

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28

Hamblin, Terry. "Oncogenes in Cancer diagnosis." Leukemia Research 15, no. 5 (January 1991): 403. http://dx.doi.org/10.1016/0145-2126(91)90018-o.

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29

Compere, Sally J., Patricia Baldacci, and Rudolf Jaenisch. "Oncogenes in transgenic mice." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 948, no. 2 (November 1988): 129–49. http://dx.doi.org/10.1016/0304-419x(88)90008-x.

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30

Anania, Maria Chiara, Tiziana Di Marco, Mara Mazzoni, and Angela Greco. "Targeting Non-Oncogene Addiction: Focus on Thyroid Cancer." Cancers 12, no. 1 (January 4, 2020): 129. http://dx.doi.org/10.3390/cancers12010129.

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Thyroid carcinoma (TC) is the most common malignancy of endocrine organs with an increasing incidence in industrialized countries. The majority of TC are characterized by a good prognosis, even though cases with aggressive forms not cured by standard therapies are also present. Moreover, target therapies have led to low rates of partial response and prompted the emergence of resistance, indicating that new therapies are needed. In this review, we summarize current literature about the non-oncogene addiction (NOA) concept, which indicates that cancer cells, at variance with normal cells, rely on the activity of genes, usually not mutated or aberrantly expressed, essential for coping with the transformed phenotype. We highlight the potential of non-oncogenes as a point of intervention for cancer therapy in general, and present evidence for new putative non-oncogenes that are essential for TC survival and that may constitute attractive new therapeutic targets.

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31

Weiss, Robin A. "A perspective on the early days of RAS research." Cancer and Metastasis Reviews 39, no. 4 (July 29, 2020): 1023–28. http://dx.doi.org/10.1007/s10555-020-09919-1.

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AbstractThe name of the oncogene, ras, has its origin in studies of murine leukemia viruses in the 1960s by Jenny Harvey (H-ras) and by Werner Kirsten (K-ras) which, at high doses, produced sarcomas in rats. Transforming retroviruses were isolated, and its oncogene was named ras after rat sarcoma. From 1979, cellular ras sequences with transforming properties were identified by transfection of tumor DNA initially by Robert Weinberg from rodent tumors, and the isolation of homologous oncogenes from human tumors soon followed, including HRAS and KRAS, and a new member of the family named NRAS. I review these discoveries, placing emphasis on the pioneering research of Christopher Marshall and Alan Hall, who subsequently made immense contributions to our understanding of the functions of RAS and related small GTPases to signal transduction pathways, cell structure, and the behavior of normal and malignant cells.

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32

Sasaki, Rumi, Mako Narisawa-Saito, Takashi Yugawa, Masatoshi Fujita, Hironori Tashiro, Hidetaka Katabuchi, and Tohru Kiyono. "Oncogenic transformation of human ovarian surface epithelial cells with defined cellular oncogenes." Carcinogenesis 30, no. 3 (January 6, 2009): 423–31. http://dx.doi.org/10.1093/carcin/bgp007.

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33

Butturini, Anna, Emma Sthivelman, Eli Canaani, and Robert Peter Gale. "Oncogenes in Human Leukemias." Cancer Investigation 6, no. 3 (January 1988): 305–16. http://dx.doi.org/10.3109/07357908809080653.

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34

Pimentel, Enrique. "Oncogenes and human cancer." Cancer Genetics and Cytogenetics 14, no. 3-4 (January 1985): 347–68. http://dx.doi.org/10.1016/0165-4608(85)90201-8.

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35

Vogt, Peter K. "Retroviral oncogenes: a historical primer." Nature Reviews Cancer 12, no. 9 (August 17, 2012): 639–48. http://dx.doi.org/10.1038/nrc3320.

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36

Baer, Maria R., and Clara D. Bloomfield. "Cytogenetics and oncogenes in leukemia." Current Opinion in Oncology 4, no. 1 (February 1992): 24–32. http://dx.doi.org/10.1097/00001622-199202000-00005.

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37

Hogge, Donna E. "Cytogenetics and oncogenes in leukemia." Current Opinion in Oncology 6, no. 1 (January 1994): 3–13. http://dx.doi.org/10.1097/00001622-199401000-00002.

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38

Idelevich, Efraim, Marta Mozes, Noa Ben-Baruch, Monica Huszar, Anna Kruglikova, Rivka Katsnelson, and Adi Shani. "Oncogenes in Male Breast Cancer." American Journal of Clinical Oncology 26, no. 3 (June 2003): 259–61. http://dx.doi.org/10.1097/01.coc.0000020582.25017.5d.

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39

Børresen, A.-L. "Mutant Oncogenes. Targets for Therapy." British Journal of Cancer 68, no. 2 (August 1993): 446–47. http://dx.doi.org/10.1038/bjc.1993.360.

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40

Hausen, Harald zur. "Viral oncogenes causing human cancers." European Journal of Cancer Supplements 4, no. 6 (June 2006): 17. http://dx.doi.org/10.1016/j.ejcsup.2006.04.037.

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41

Mercatelli, Neri, Ramona Palombo, and Maria Paola Paronetto. "Emerging Contribution of PancRNAs in Cancer." Cancers 12, no. 8 (July 24, 2020): 2035. http://dx.doi.org/10.3390/cancers12082035.

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“Cancer” includes a heterogeneous group of diseases characterized by abnormal growth beyond natural boundaries. Neoplastic transformation of cells is orchestrated by multiple molecular players, including oncogenic transcription factors, epigenetic modifiers, RNA binding proteins, and coding and noncoding transcripts. The use of computational methods for global and quantitative analysis of RNA processing regulation provides new insights into the genomic and epigenomic features of the cancer transcriptome. In particular, noncoding RNAs are emerging as key molecular players in oncogenesis. Among them, the promoter-associated noncoding RNAs (pancRNAs) are noncoding transcripts acting in cis to regulate their host genes, including tumor suppressors and oncogenes. In this review, we will illustrate the role played by pancRNAs in cancer biology and will discuss the latest findings that connect pancRNAs with cancer risk and progression. The molecular mechanisms involved in the function of pancRNAs may open the path to novel therapeutic opportunities, thus expanding the repertoire of targets to be tested as anticancer agents in the near future.

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42

Bai, Wen-Xia, Wei Liu, and Rui-Hua Shi. "Advances in research of esophageal carcinoma-related oncogenes." World Chinese Journal of Digestology 18, no. 35 (2010): 3752. http://dx.doi.org/10.11569/wcjd.v18.i35.3752.

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43

Butturini, Anna, and Robert Peter Gale. "Oncogenes in chronic lymphocytic leukemia." Leukemia Research 12, no. 1 (January 1988): 89–92. http://dx.doi.org/10.1016/s0145-2126(98)80013-1.

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44

Dipple, Anthony, Colin Garner, and Curtis Harris. "Forum on oncogenes in carcinogenesis." Carcinogenesis 9, no. 5 (1988): 689. http://dx.doi.org/10.1093/carcin/9.5.689.

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45

Muschel, Ruth, and Lance A. Liotta. "Role of oncogenes in metastases." Carcinogenesis 9, no. 5 (1988): 705–10. http://dx.doi.org/10.1093/carcin/9.5.705.

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46

Alitalo, Kari, Päivi Koskinen, Tomi P. Mäkelä, Kalle Saksela, Lea Sistonen, and Robert Winqvist. "myc oncogenes: activation and amplification." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 907, no. 1 (April 1987): 1–32. http://dx.doi.org/10.1016/0304-419x(87)90016-3.

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47

Balmain, A. "Transforming ras oncogenes and multistage carcinogenesis." British Journal of Cancer 51, no. 1 (January 1985): 1–7. http://dx.doi.org/10.1038/bjc.1985.1.

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48

Peehl, Donna M. "Oncogenes in prostate cancer. An update." Cancer 71, S3 (February 1, 1993): 1159–64. http://dx.doi.org/10.1002/1097-0142(19930201)71:3+<1159::aid-cncr2820711439>3.0.co;2-u.

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49

Felsher, Dean W. "Cancer revoked: oncogenes as therapeutic targets." Nature Reviews Cancer 3, no. 5 (May 2003): 375–79. http://dx.doi.org/10.1038/nrc1070.

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50

Malumbres, Marcos, and Mariano Barbacid. "RAS oncogenes: the first 30 years." Nature Reviews Cancer 3, no. 6 (June 1, 2003): 459–65. http://dx.doi.org/10.1038/nrc1097.

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