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Journal articles on the topic 'Oncogenes'

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Published: 4 June 2021
Last updated: 29 July 2024

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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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2

Martín-Lorenzo, Alberto, Inés Gonzalez-Herrero, Guillermo Rodríguez-Hernández, Idoia García-Ramírez, Carolina Vicente-Dueñas, and Isidro Sánchez-García. "Early epigenetic cancer decisions." Biological Chemistry 395, no. 11 (November 1, 2014): 1315–20. http://dx.doi.org/10.1515/hsz-2014-0185.

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Abstract A cancer dogma states that inactivation of oncogene(s) can cause cancer remission, implying that oncogenes are the Achilles’ heel of cancers. This current model of cancer has kept oncogenes firmly in focus as therapeutic targets and is in agreement with the fact that in human cancers all cancerous cells, with independence of the cellular heterogeneity existing within the tumour, carry the same oncogenic genetic lesions. However, recent studies of the interactions between an oncogene and its target cell have shown that oncogenes contribute to cancer development via developmental reprogramming of the epigenome within the target cell. These results provide the first evidence that carcinogenesis can be initiated by epigenetic stem cell reprogramming, and uncover a new role for oncogenes in the origin of cancer. Here we analyse these evidences and discuss how this vision offers new avenues for developing novel anti-cancer interventions.
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3

Der, C. J. "Cellular oncogenes and human carcinogenesis." Clinical Chemistry 33, no. 5 (May 1, 1987): 641–46. http://dx.doi.org/10.1093/clinchem/33.5.641.

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Abstract Experimental studies over the past decade have identified 30 or so cellular genes as potential oncogenes. The genetic events that lead to cellular oncogene activation may result in the excessive or inappropriate expression of the gene, or the expression of an aberrant gene product. Although the involvement of these putative cellular oncogenes in human oncogenesis has not been proven, the accumulation of considerable experimental evidence strongly implicates some role of these genes in the malignant process. The inactivation of certain genetic loci (suppressor genes) may also contribute to tumor progression.
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4

Vasudevan, D. M. "Oncogenes and oncogenic viruses." Indian Journal of Clinical Biochemistry 11, no. 1 (January 1996): 3–6. http://dx.doi.org/10.1007/bf02868403.

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5

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

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Initially, lymphoid cells transformed by v-abl or BCR/ABL oncogenes are poorly oncogenic but progress to full transformation over time. Although expression of the oncogene is necessary to initiate and maintain transformation, other molecular mechanisms are thought to be required for full transformation. To determine whether tumor progression in ABL oncogene-transformed lymphoid cells has a genetic basis, we examined whether progression of the malignant phenotype of transformed clones correlates with particular cytogenetic abnormalities. A modified in vitro bone marrow transformation model was used to obtain clonal Abelson murine leukemia virus-transformed B lymphoid cells that were poorly oncogenic. Multiple subclones were then derived from each clone and maintained over a marrow-derived stromal cell line for several weeks. Over time, clonally related Abelson murine leukemia virus-transformed subclones progressed asynchronously to full transformation. The data show that tumor progression can occur in the absence of detectable cytogenetic changes but, more importantly, that certain cytogenetic abnormalities appear reproducibly in highly malignant subclones. Therefore, three independent subclones showed deletion in a common region of chromosome 13. Other highly malignant cells carried a common breakpoint in the X chromosome, and, finally, two subclones carried an additional chromosome 5. These results are consistent with the hypothesis that ABL oncogenes are sufficient for the initial transformation of cells but that additional genetic events can drive oncogenic progression. These observations further suggest that diverse genetic mechanisms may be able to drive tumor progression in cells transformed with ABL oncogenes.
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6

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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7

Moore, Patrick S. "KSHV-encoded oncogenes and oncogenesis." Journal of Acquired Immune Deficiency Syndromes & Human Retrovirology 14, no. 4 (April 1997): A14. http://dx.doi.org/10.1097/00042560-199704010-00033.

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8

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

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9

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

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To identify proteins whose production may be altered as a common event in the expression of structurally diverse oncogenes, we compared two-dimensional electropherograms of newly synthesized proteins from NIH/3T3 cell lines transformed by a variety of retroviral oncogenes, from cellular revertant lines, and from a line (433.3) which expresses the v-ras oncogene in response to corticosteroids. Most alterations in the synthesis of specific proteins detected by this approach appeared to be the result of selection during prolonged cultivation and were probably unrelated to the transformation process. However, we detected seven proteins whose synthesis was strongly suppressed in cell lines transformed by each of the six retroviral oncogenes we studied and whose production was fully or partially restored in two cellular revertant lines. Suppression of two of these proteins was also correlated with the initial appearance of morphological alteration during corticosteroid-induced oncogene expression in 433.3 cells. These proteins (p37/4.78 and p41/4.75) were identified as tropomyosins, a group of at least five cytoskeletal proteins. Transformation by the papovaviruses simian virus 40 and polyomavirus caused no suppression of synthesis of these tropomyosins. This indicates that suppression of tropomyosin synthesis is not a nonspecific response by cells to being forced to grow with the transformed phenotype but is specifically associated with oncogenesis by diverse retroviral oncogenes. The results are consistent with the hypothesis that the different biochemical processes initiated by expression of structurally diverse retroviral oncogenes may converge on a limited number of common targets, one of which is the mechanism which regulates the synthesis of tropomyosins.
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10

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

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To identify proteins whose production may be altered as a common event in the expression of structurally diverse oncogenes, we compared two-dimensional electropherograms of newly synthesized proteins from NIH/3T3 cell lines transformed by a variety of retroviral oncogenes, from cellular revertant lines, and from a line (433.3) which expresses the v-ras oncogene in response to corticosteroids. Most alterations in the synthesis of specific proteins detected by this approach appeared to be the result of selection during prolonged cultivation and were probably unrelated to the transformation process. However, we detected seven proteins whose synthesis was strongly suppressed in cell lines transformed by each of the six retroviral oncogenes we studied and whose production was fully or partially restored in two cellular revertant lines. Suppression of two of these proteins was also correlated with the initial appearance of morphological alteration during corticosteroid-induced oncogene expression in 433.3 cells. These proteins (p37/4.78 and p41/4.75) were identified as tropomyosins, a group of at least five cytoskeletal proteins. Transformation by the papovaviruses simian virus 40 and polyomavirus caused no suppression of synthesis of these tropomyosins. This indicates that suppression of tropomyosin synthesis is not a nonspecific response by cells to being forced to grow with the transformed phenotype but is specifically associated with oncogenesis by diverse retroviral oncogenes. The results are consistent with the hypothesis that the different biochemical processes initiated by expression of structurally diverse retroviral oncogenes may converge on a limited number of common targets, one of which is the mechanism which regulates the synthesis of tropomyosins.
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11

Rey, Federica, Letizia Messa, Cecilia Pandini, Rossella Launi, Bianca Barzaghini, Giancarlo Micheletto, Manuela Teresa Raimondi, et al. "Transcriptome Analysis of Subcutaneous Adipose Tissue from Severely Obese Patients Highlights Deregulation Profiles in Coding and Non-Coding Oncogenes." International Journal of Molecular Sciences 22, no. 4 (February 17, 2021): 1989. http://dx.doi.org/10.3390/ijms22041989.

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Obesity is a major risk factor for a large number of secondary diseases, including cancer. Specific insights into the role of gender differences and secondary comorbidities, such as type 2 diabetes (T2D) and cancer risk, are yet to be fully identified. The aim of this study is thus to find a correlation between the transcriptional deregulation present in the subcutaneous adipose tissue of obese patients and the oncogenic signature present in multiple cancers, in the presence of T2D, and considering gender differences. The subcutaneous adipose tissue (SAT) of five healthy, normal-weight women, five obese women, five obese women with T2D and five obese men were subjected to RNA-sequencing, leading to the identification of deregulated coding and non-coding RNAs, classified for their oncogenic score. A panel of DE RNAs was validated via Real-Time PCR and oncogene expression levels correlated the oncogenes with anthropometrical parameters, highlighting significant trends. For each analyzed condition, we identified the deregulated pathways associated with cancer, the prediction of possible prognosis for different cancer types and the lncRNAs involved in oncogenic networks and tissues. Our results provided a comprehensive characterization of oncogenesis correlation in SAT, providing specific insights into the possible molecular targets implicated in this process. Indeed, the identification of deregulated oncogenes also in SAT highlights hypothetical targets implicated in the increased oncogenic risk in highly obese subjects. These results could shed light on new molecular targets to be specifically modulated in obesity and highlight which cancers should receive the most attention in terms of better prevention in obesity-affected patients.
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12

Deng, Davy, Frank Dubois, Alexander Crane, Ashot Harutyunyan, Rameen Beroukhim, and Pratiti Bandopadhayay. "EPCO-21. CORE REGULATORY CIRCUIT TRANSCRIPTION FACTORS DRIVE EXPRESSION FROM HIGH LEVEL AMPLICONS IN PEDIATRIC HIGH-GRADE GLIOMAS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi6. http://dx.doi.org/10.1093/neuonc/noab196.020.

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Abstract BACKGROUND Pediatric High-Grade Gliomas (pHGGs) show recurrent high-level amplifications around the oncogenes MET, MYCN and EGFR. However what drives expression of the oncogenes from these amplicons remains unclear. We aim to discover enhancers on these amplicons that are responsible for oncogene expressions and the core regulatory transcription factors (TFs) they bind. METHOD Using RNA-seq from 12 pHGG cell lines, we identified groups of high and low-expressing pHGG lines for MET, MYCN and EGFR. We then compared the H3K27Ac ChIP-seq between the two groups using diffbind. This allowed us to identify statistically significant peaks that are differentially activated in the oncogene-high v.s. oncogene-low expressing groups. Additionally, we overlapped the positions of these candidate oncogene enhancers with the regions that are recurrently incorporated into high-level amplicons based on published whole genome sequencing data. Using a previously defined set of core regulatory TFs we determined which TF binds the amplified oncogene enhancers and could be driving oncogenic expressions of MET, MYCN and EGFR in pHGGs. RESULTS We identify 3 cell lines for both the high- and low-expressing groups for each oncogene. Cell lines with high expression of the oncogene showed distinct enhancers with significant enrichment in H3K27Ac compared to the cell lines with low expression for each oncogene. Of all enhancers with enrichment high oncogene expression groups those with binding sites for known pHGG core regulatory circuit TF were preferentially incorporated into the high-level amplicons of the oncogene. We also identified core TFs that bind enhancers for MYCN, EGFR and MET as well as core TFs that are unique to a single oncogene. CONCLUSION We identified candidate core transcription factor that drives expression of multiple oncogenes in pHGG. These could serve as a potential novel therapeutic target for pHGGs with addiction to MYCN or RTK signaling.
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13

Moskalev, Aleksandr V., Boris Yu Gumilevsky, Aleksandr V. Zhestkov, and Maksim O. Zolotov. "The effect of virus-induced cellular transformation on oncogenesis." Science and Innovations in Medicine 8, no. 2 (May 7, 2023): 108–15. http://dx.doi.org/10.35693/2500-1388-2023-8-2-108-115.

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Aim to summarize the scientific data presented in the recent publications on tumor-associated processes induced by viruses. We analyzed 23 international publications devoted to the development and course of tumor-related processes associated with oncogenic viruses. The tumor-associated mechanisms are based on the processes of cell transformation, which largely depend on the state of telomeres. No less important are viral and cellular oncogenes, molecular circuits that control cell proliferation. Viral oncogenes encode proteins that increase the concentration of telomerase in the infected cells, and thereby increase the number of cell division cycles. The immune homeostasis, maintaining the integrity of body tissues, is regulated by activating and inhibiting metabolic pathways. The errors in the functioning of these signaling pathways caused by oncogenic viruses can lead to cell transformation and oncogenesis. Guaninenucleotide-binding protein RAS and protein kinase AKT are important components of signaling pathways that contribute to the production of D-type cyclins that control the cell cycle and regulate the activity of metabolic enzymes. Cyclin-dependent kinase is an important factor controlling cell cycles, damage and problems with nucleic acid replication, as well as proper assembly of the mitotic spindle. These processes can be disrupted by the transformation caused by oncogenic viruses. In most cases, viral oncogenes undergo additional changes that contribute to their transformation potential. The transformative activity of viral gene products correlates with binding to specific cellular proteins. In the immunopathogenesis of oncogenesis, an important role belongs to the inactivation of tumor suppressors, and the processes of phosphorylation.
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14

Stasevich, Ekaterina Mikhailovna, Aksinya Nicolaevna Uvarova, Matvey Mikhailovich Murashko, Elmira Ramilevna Khabusheva, Saveliy Andreevich Sheetikov, Vladimir Sergeyevich Prassolov, Dmitriy Vladimirovich Kuprash, Denis Eriksonovich Demin, and Anton Markovich Schwartz. "Enhancer RNA AL928768.3 from the IGH Locus Regulates MYC Expression and Controls the Proliferation and Chemoresistance of Burkitt Lymphoma Cells with IGH/MYC Translocation." International Journal of Molecular Sciences 23, no. 9 (April 21, 2022): 4624. http://dx.doi.org/10.3390/ijms23094624.

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Chromosomal rearrangements leading to the relocation of proto-oncogenes into transcription-active regions are found in various types of tumors. In particular, the transfer of proto-oncogenes to the locus of heavy chains of immunoglobulins (IGH) is frequently observed in B-lymphomas. The increased expression of the MYC proto-oncogene due to IGH/MYC translocation is detected in approximately 85% of Burkitt lymphoma cases. The regulatory mechanisms affecting the oncogenes upon translocation include non-coding enhancer RNAs (eRNAs). We conducted a search for the eRNAs that may affect MYC transcription in the case of IGH/MYC translocation in Burkitt lymphoma, looking for potentially oncogenic eRNAs located at the IGH locus and predominantly expressed in B cells. Overexpression and knockdown of our primary candidate eRNA AL928768.3 led to the corresponding changes in the expression of MYC proto-oncogene in Burkitt lymphoma cells. Furthermore, we demonstrated that AL928768.3 knockdown decreased lymphoma cell proliferation and resistance to chemotherapy. Significant effects were observed only in cell lines bearing IGH/MYC abnormality but not in B-cell lines without this translocation nor primary B-cells. Our results indicate that AL928768.3 plays an important role in the development of Burkitt’s lymphoma and suggest it and similar, yet undiscovered eRNAs as potential tissue-specific targets for cancer treatment.
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15

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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16

Melnick, A. "Targeting aggressive B-cell lymphomas with cell-penetrating peptides." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 802–6. http://dx.doi.org/10.1042/bst0350802.

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DLBCL (diffuse large B-cell lymphoma) is the most common subtype of non-Hodgkin's lymphoma. Current therapy for patients includes chemotherapy and monoclonal antibodies. Although oncogene-targeted therapy is dramatically successful for patients with certain kinds of leukaemias, there are no such agents yet for DLBCL. One reason for this is that several key oncogenes involved in DLBCL pathogenesis are transcription factors, which are difficult to therapeutically target with small molecules. Recent advances in the structural and functional characterization of DLBCL oncogenes have facilitated design of CPPs (cellpenetrating peptides) with potent inhibitory effects on DLBCL and other aggressive lymphomas. CPPs targeting the Bcl (B-cell lymphoma)-6, Bcl-2, Myc and NF-κB (nuclear factor κB) oncogenic pathways, among others, could improve efficacy and reduce toxicity of anti-lymphoma therapy. Another barrier towards effective therapy in DLBCL is its profound molecular heterogeneity. Combinatorial administration of oncogene-targeted CPPs based on the molecular profiles of individual patient tumours could allow individualized targeted therapy regimens to be developed.
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17

Brown, Geoffrey. "Oncogenes, Proto-Oncogenes, and Lineage Restriction of Cancer Stem Cells." International Journal of Molecular Sciences 22, no. 18 (September 7, 2021): 9667. http://dx.doi.org/10.3390/ijms22189667.

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In principle, an oncogene is a cellular gene (proto-oncogene) that is dysfunctional, due to mutation and fusion with another gene or overexpression. Generally, oncogenes are viewed as deregulating cell proliferation or suppressing apoptosis in driving cancer. The cancer stem cell theory states that most, if not all, cancers are a hierarchy of cells that arises from a transformed tissue-specific stem cell. These normal counterparts generate various cell types of a tissue, which adds a new dimension to how oncogenes might lead to the anarchic behavior of cancer cells. It is that stem cells, such as hematopoietic stem cells, replenish mature cell types to meet the demands of an organism. Some oncogenes appear to deregulate this homeostatic process by restricting leukemia stem cells to a single cell lineage. This review examines whether cancer is a legacy of stem cells that lose their inherent versatility, the extent that proto-oncogenes play a role in cell lineage determination, and the role that epigenetic events play in regulating cell fate and tumorigenesis.
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18

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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19

Alema, S., F. Tato, and D. Boettiger. "myc and src oncogenes have complementary effects on cell proliferation and expression of specific extracellular matrix components in definitive chondroblasts." Molecular and Cellular Biology 5, no. 3 (March 1985): 538–44. http://dx.doi.org/10.1128/mcb.5.3.538-544.1985.

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The effects of the avian viral oncogenes src and myc were compared for their ability to alter the differentiated phenotype and the proliferative capacity of definitive chondroblasts. As previously demonstrated, viruses carrying the src oncogene suppressed the synthesis of the chondroblast-specific products, type II collagen and cartilage-specific sulfated proteoglycan. In contrast, infection with MC29 and HB1 viruses, which carry the myc oncogene, did not suppress the synthesis of these normal differentiated cell products, but the infected cells exhibited an increased proliferative potential. The MH2 virus, which carries both the myc and mil oncogenes, both induced the suppression of these chondroblast-specific products and increased cell proliferation. The implications of these results for cooperation between oncogenes and the multi-oncogene models for neoplastic transformation are discussed.
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20

Alema, S., F. Tato, and D. Boettiger. "myc and src oncogenes have complementary effects on cell proliferation and expression of specific extracellular matrix components in definitive chondroblasts." Molecular and Cellular Biology 5, no. 3 (March 1985): 538–44. http://dx.doi.org/10.1128/mcb.5.3.538.

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The effects of the avian viral oncogenes src and myc were compared for their ability to alter the differentiated phenotype and the proliferative capacity of definitive chondroblasts. As previously demonstrated, viruses carrying the src oncogene suppressed the synthesis of the chondroblast-specific products, type II collagen and cartilage-specific sulfated proteoglycan. In contrast, infection with MC29 and HB1 viruses, which carry the myc oncogene, did not suppress the synthesis of these normal differentiated cell products, but the infected cells exhibited an increased proliferative potential. The MH2 virus, which carries both the myc and mil oncogenes, both induced the suppression of these chondroblast-specific products and increased cell proliferation. The implications of these results for cooperation between oncogenes and the multi-oncogene models for neoplastic transformation are discussed.
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21

Bootsma, Dirk. "ONCOGENES AND ANTI-ONCOGENES." Pediatric Research 20, no. 10 (October 1986): 1031–32. http://dx.doi.org/10.1203/00006450-198610000-00051.

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22

Cooper, J. A. "Oncogenes and anti-oncogenes." Current Opinion in Cell Biology 2, no. 2 (April 1990): 285–95. http://dx.doi.org/10.1016/0955-0674(90)90021-6.

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23

Bishop, J. Michael. "Oncogenes and proto-oncogenes." Journal of Cellular Physiology 129, S4 (1986): 1–5. http://dx.doi.org/10.1002/jcp.1041290403.

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24

Scarzello, Anthony, Jim Stauffer, Tim Back, Jeff Subleski, Jonathan Weiss, John Ortaldo, and Robert Wiltrout. "Immunological characterization of oncogene-driven models of hepatocellular carcinoma. (100.19)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 100.19. http://dx.doi.org/10.4049/jimmunol.184.supp.100.19.

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Abstract Constitutively active AKT, MET, and beta-catenin (CAT) are initiating oncogenes that efficiently induce hepatic primary tumors when co-delivered; but not as single agents. Using a qPCR assay, we have begun to detail the early events of oncogene integration and to correlate the amount of integrated oncogene with developing tumor size. Furthermore, we found that the serum from mice injected with MET/CAT have elevated levels of alpha fetoprotein, a biomarker which has been similarly observed in advanced cases of HCC. Correlating the influx of infiltrating leukocytes and serum biomarker levels with the quantity of integrated oncogenes is critical to characterize their relative contributions to tumor progression. The profile of liver leukocytes in both MET/CAT and AKT/CAT murine models display phenotypes similar to those in HCC patients. By day 14, increased frequency and numbers of Tregs, MDSCs, as well as an up-regulation of PD-1 on CD4+ and CD8+ T cells was observed. The oncogene-driven tumor models described in this study exhibit many of the molecular and cellular events underlying HCC progression in humans. This molecularly defined approach to hepatocellular oncogenesis should enable us to characterize the contributions of inflammation in a primary tumor model with a defined oncogene signaling pathway.
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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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Land, H., A. C. Chen, J. P. Morgenstern, L. F. Parada, and R. A. Weinberg. "Behavior of myc and ras oncogenes in transformation of rat embryo fibroblasts." Molecular and Cellular Biology 6, no. 6 (June 1986): 1917–25. http://dx.doi.org/10.1128/mcb.6.6.1917-1925.1986.

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The requirements for transformation of rat embryo fibroblasts (REFs) by transfected ras and myc oncogenes were explored. Under conditions of dense monolayer culture, neither oncogene was able to transform REFs on its own. However, the introduction of a ras oncogene together with a selectable neomycin resistance marker into REFs allowed killing of the normal nontransfected cells and the outgrowth of colonies of ras transformants, 10% of which survived crisis and became tumorigenic. These cells expressed greater than 10-fold-higher levels of ras p21 than tumorigenic cells cotransfected with ras and myc oncogenes. The myc oncogene similarly was unable to induce tumorigenic conversion of REFs unless especially refractile colonies of oncogene-bearing cells, produced by use of a cotransfected selectable marker, were picked and subcultured. Tumorigenic conversion of REFs by single transfected oncogenes appears to require special culture conditions and high levels of gene expression.
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Land, H., A. C. Chen, J. P. Morgenstern, L. F. Parada, and R. A. Weinberg. "Behavior of myc and ras oncogenes in transformation of rat embryo fibroblasts." Molecular and Cellular Biology 6, no. 6 (June 1986): 1917–25. http://dx.doi.org/10.1128/mcb.6.6.1917.

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The requirements for transformation of rat embryo fibroblasts (REFs) by transfected ras and myc oncogenes were explored. Under conditions of dense monolayer culture, neither oncogene was able to transform REFs on its own. However, the introduction of a ras oncogene together with a selectable neomycin resistance marker into REFs allowed killing of the normal nontransfected cells and the outgrowth of colonies of ras transformants, 10% of which survived crisis and became tumorigenic. These cells expressed greater than 10-fold-higher levels of ras p21 than tumorigenic cells cotransfected with ras and myc oncogenes. The myc oncogene similarly was unable to induce tumorigenic conversion of REFs unless especially refractile colonies of oncogene-bearing cells, produced by use of a cotransfected selectable marker, were picked and subcultured. Tumorigenic conversion of REFs by single transfected oncogenes appears to require special culture conditions and high levels of gene expression.
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Tian, Shuangmei, Jing Wang, Fangyuan Zhang, and Degeng Wang. "Comparative Analysis of microRNA Binding Site Distribution and microRNA-Mediated Gene Expression Repression of Oncogenes and Tumor Suppressor Genes." Genes 13, no. 3 (March 9, 2022): 481. http://dx.doi.org/10.3390/genes13030481.

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MicroRNAs (miRNAs) are a family of short, noncoding RNAs that can regulate gene expression levels of over half of the human genome. Previous studies on the role of miRNAs in cancer showed overall widespread downregulation of miRNAs as a hallmark of human cancer, though individual miRNAs can be both tumor suppressive and oncogenic, and cancer genes are speculated to be more targeted by miRNA. However, the extents to which oncogenes and tumor suppressor genes (TSG) are controlled by miRNA have not been compared. To achieve this goal, we constructed lists of oncogenes and TSGs and compared them with each other, and with the whole protein-coding gene population, in terms of miRNA binding sites distribution and expression level changes upon genetic disruption of miRNA production. As expected, the results show that cancer gene mRNAs anchor more miRNA binding sites, and are under a higher degree of miRNA-mediated repression at both mRNA abundance and translation efficiency levels than the whole protein-coding gene population. Importantly, on average, TSG mRNAs are more highly targeted and regulated by miRNA than oncogene mRNAs. To the best of our knowledge, this is the first comparison of miRNA regulation of oncogenes and TSGs.
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Nowell, Peter C., and Carlo M. Croce. "Chromosomal approaches to oncogenes and oncogenesis 1." FASEB Journal 2, no. 15 (December 1988): 3054–60. http://dx.doi.org/10.1096/fasebj.2.15.3056765.

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30

Scheerger and Zempleni. "Expression of Oncogenes Depends on Biotin in Human Small Cell Lung Cancer Cells NCI-H69." International Journal for Vitamin and Nutrition Research 73, no. 6 (December 1, 2003): 461–67. http://dx.doi.org/10.1024/0300-9831.73.6.461.

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Oncogenes play important roles in cell proliferation and biotin status correlates with gene expression and proliferation rates in human cells. In this study we determined whether biotin supply affects biotin homeostasis, expression of oncogenes, and proliferation rates in NCI-H69 small cell lung cancer cells. NCI-H69 cells were cultured in media containing deficient (0.025 nmol/L), physiologic (0.25 nmol/L), or pharmacologic (10 nmol/L) concentrations of biotin for 3 weeks. Biotin concentrations in culture media correlated negatively with biotin transport rates, suggesting that cells responded to marginal biotin supply with increased expression of biotin transporters. Increased biotin uptake was not sufficient to prevent depletion of intracellular biotin in cells cultured in biotin-deficient medium, as judged by decreased activity of biotin-dependent propionyl-CoA carboxylase and decreased biotinylation of histones. The expression of oncogenes N-myc, c-myb, N-ras, and raf correlated with biotin supply in media: oncogene expression increased by up to 20% in cells cultured in pharmacologic medium compared to physiologic controls; oncogene expression decreased by up to 47% in cells cultured in deficient medium. This observation is consistent with a role for biotin in oncogene-dependent metabolic pathways. Cellular uptake of thymidine (marker for proliferation) was not affected by biotin supply, suggesting that effects of biotin-dependent expression of oncogenes on the growth of tumor cells are quantitatively minor. The clinical significance of effects of biotin supply on expression of oncogenes remains to be elaborated.
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31

Monier, R. "PROTO-ONCOGENES ET ANTI-ONCOGENES." Reproduction Nutrition Développement 29, Suppl. 1 (1989): 49. http://dx.doi.org/10.1051/rnd:19890785.

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32

Zhao, Ran, Bin Hu, Lei Chen, and Bo Zhou. "Identification of Latent Oncogenes with a Network Embedding Method and Random Forest." BioMed Research International 2020 (September 23, 2020): 1–11. http://dx.doi.org/10.1155/2020/5160396.

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Oncogene is a special type of genes, which can promote the tumor initiation. Good study on oncogenes is helpful for understanding the cause of cancers. Experimental techniques in early time are quite popular in detecting oncogenes. However, their defects become more and more evident in recent years, such as high cost and long time. The newly proposed computational methods provide an alternative way to study oncogenes, which can provide useful clues for further investigations on candidate genes. Considering the limitations of some previous computational methods, such as lack of learning procedures and terming genes as individual subjects, a novel computational method was proposed in this study. The method adopted the features derived from multiple protein networks, viewing proteins in a system level. A classic machine learning algorithm, random forest, was applied on these features to capture the essential characteristic of oncogenes, thereby building the prediction model. All genes except validated oncogenes were ranked with a measurement yielded by the prediction model. Top genes were quite different from potential oncogenes discovered by previous methods, and they can be confirmed to become novel oncogenes. It was indicated that the newly identified genes can be essential supplements for previous results.
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33

Bitler, Benjamin G., Lauren S. Fink, Zhi Wei, Jeffrey R. Peterson, and Rugang Zhang. "A High-Content Screening Assay for Small-Molecule Modulators of Oncogene-Induced Senescence." Journal of Biomolecular Screening 18, no. 9 (June 3, 2013): 1054–61. http://dx.doi.org/10.1177/1087057113491827.

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Cellular senescence is a state of stable cell growth arrest. Activation of oncogenes such as RAS in mammalian cells typically triggers cellular senescence. Oncogene-induced senescence (OIS) is an important tumor suppression mechanism, and suppression of OIS contributes to cell transformation. Oncogenes trigger senescence through a multitude of incompletely understood downstream signaling events that frequently involve protein kinases. To identify target proteins required for RAS-induced senescence, we developed a small-molecule screen in primary human fibroblasts undergoing senescence induced by oncogenic RAS (H-RasG12V). Using a high-content imaging system to monitor two hallmarks of senescence, senescence-associated β-galactosidase activity expression and inhibition of proliferation, we screened a library of known small-molecule kinase inhibitors for those that suppressed OIS. Identified compounds were subsequently validated and confirmed using a third marker of senescence, senescence-associated heterochromatin foci. In summary, we have established a novel high-content screening platform that may be useful for elucidating signaling pathways mediating OIS by targeting critical pathway components.
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34

Hamilton, Zac, Noor Naffakh, Natalie Marie Reizine, Frank Weinberg, Shikha Jain, Vijayakrishna K. Gadi, Christopher Bun, and Ryan Huu-Tuan Nguyen. "Relevance and accuracy of ChatGPT-generated NGS reports with treatment recommendations for oncogene-driven NSCLC." Journal of Clinical Oncology 41, no. 16_suppl (June 1, 2023): 1555. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.1555.

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1555 Background: Next-generation sequencing (NGS) is a routine clinical practice in advanced NSCLC. NGS reports are information-dense and clinical interpretation remains a challenge. ChatGPT is a large language model (LLM) AI chatbot that can generate text in response to user-generated prompts. We sought to assess the clinical relevance and accuracy of ChatGPT-generated NGS reports with first-line (1L) treatment recommendations for NSCLC patients with targetable driver oncogenes. Methods: Eight driver oncogenes with FDA-approved targeted treatment for 1L stage IV NSCLC were identified in the latest NCCN Clinical Practice Guidelines available to the AI model (version 5, September 2021). The prompt, “Create a next-generation sequencing report with a list of first-line treatment options for a patient with stage IV non-small cell lung cancer with an [oncogenic driver].” was run in a separate “new chat” 10 times for each driver oncogene (n=80). Each ChatGPT output was recorded and scored. The Relevance Score (RS) awarded 1 point for every NCCN preferred option and 0.5 points for each “other recommended” treatment listed in the AI-generated output, divided by the maximum possible score for the driver oncogene. Spurious recommendations were awarded 0 points. The Accuracy Score (AS) represents reported treatment options listed in NCCN over the total number of treatments in a report. Percentage of reports listing an NCCN-preferred 1L therapy, a clinical trial as an option, and character and word count were also captured. Results: The average length of the AI-generated NGS reports was 117 words (range: 44 – 232). The median number of treatments recommended was 5 (range: 3 – 8). An oncogenic driver-specific preferred 1L treatment was included in 55 reports (68.8%), and a recommendation to explore clinical trials was listed in 43 reports (53.8%). The RS for the total sample was 0.59 (95% CI: 0.52 – 0.65), and the AS was 46.0% (95% CI: 40.2% – 51.8%). Conclusions: ChatGPT can rapidly generate concise NGS reports with treatment options for NSCLC with driver oncogenes. Recommendation relevance was moderate, and accuracy was limited with high variability across oncogenes. Overall, ChatGPT recommendations were promising given the complexity of the task with no prompting or training provided to the AI. As LLM AI platforms mature, they may generate more relevant and accurate NGS reports, offering a potentially valuable tool for NGS report annotation for clinicians, and increased accessibility for patients.[Table: see text]
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35

Wojtyś, Weronika, and Magdalena Oroń. "How Driver Oncogenes Shape and Are Shaped by Alternative Splicing Mechanisms in Tumors." Cancers 15, no. 11 (May 26, 2023): 2918. http://dx.doi.org/10.3390/cancers15112918.

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The development of RNA sequencing methods has allowed us to study and better understand the landscape of aberrant pre-mRNA splicing in tumors. Altered splicing patterns are observed in many different tumors and affect all hallmarks of cancer: growth signal independence, avoidance of apoptosis, unlimited proliferation, invasiveness, angiogenesis, and metabolism. In this review, we focus on the interplay between driver oncogenes and alternative splicing in cancer. On one hand, oncogenic proteins—mutant p53, CMYC, KRAS, or PI3K—modify the alternative splicing landscape by regulating expression, phosphorylation, and interaction of splicing factors with spliceosome components. Some splicing factors—SRSF1 and hnRNPA1—are also driver oncogenes. At the same time, aberrant splicing activates key oncogenes and oncogenic pathways: p53 oncogenic isoforms, the RAS-RAF-MAPK pathway, the PI3K-mTOR pathway, the EGF and FGF receptor families, and SRSF1 splicing factor. The ultimate goal of cancer research is a better diagnosis and treatment of cancer patients. In the final part of this review, we discuss present therapeutic opportunities and possible directions of further studies aiming to design therapies targeting alternative splicing mechanisms in the context of driver oncogenes.
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36

Needleman, SW, MH Kraus, SK Srivastava, PH Levine, and SA Aaronson. "High frequency of N-ras activation in acute myelogenous leukemia." Blood 67, no. 3 (March 1, 1986): 753–57. http://dx.doi.org/10.1182/blood.v67.3.753.753.

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Abstract Using the NIH/3T3 cell transfection assay, activated cellular oncogenes have been detected in around 10% to 20% of human tumors. From a series of DNA preparations from tissues infiltrated with acute myelogenous leukemia (AML), 50% (3/6) caused transformation of NIH/3T3 cells. Thus AML appears to be the human tumor with the highest frequency of oncogenes detected by DNA transfection. In each case the oncogene involved was N-ras, a member of the ras gene family. Biologic and clinical parameters of AML patients with and without N-ras oncogenes in their tumors are discussed.
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37

Needleman, SW, MH Kraus, SK Srivastava, PH Levine, and SA Aaronson. "High frequency of N-ras activation in acute myelogenous leukemia." Blood 67, no. 3 (March 1, 1986): 753–57. http://dx.doi.org/10.1182/blood.v67.3.753.bloodjournal673753.

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Using the NIH/3T3 cell transfection assay, activated cellular oncogenes have been detected in around 10% to 20% of human tumors. From a series of DNA preparations from tissues infiltrated with acute myelogenous leukemia (AML), 50% (3/6) caused transformation of NIH/3T3 cells. Thus AML appears to be the human tumor with the highest frequency of oncogenes detected by DNA transfection. In each case the oncogene involved was N-ras, a member of the ras gene family. Biologic and clinical parameters of AML patients with and without N-ras oncogenes in their tumors are discussed.
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38

Fan, Alice C., Debabrita Deb-Basu, Melissa Horoschak, Amy Shirer, David Voehringer, Roger O’Neill, and Dean W. Felsher. "Nano-Fluidic Detection of Oncoprotein Signaling in Preclinical and Patient Lymphoma Samples." Blood 108, no. 11 (November 16, 2006): 2527. http://dx.doi.org/10.1182/blood.v108.11.2527.2527.

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Abstract Inactivation of oncogenes can be an effective cancer therapy. Determining precise levels of oncogene expression is important in the development of drugs to target oncogenes. We have developed a novel automated nano-fluidic Western-blot-like technology to detect and quantify oncogene expression in small numbers of mouse and human hematopoietic tumor cells. To detect different levels of oncogene expression, we generated transgenic mice in which the MYC or BCL2 oncogenes are regulated conditionally via the Tetracycline Regulatory System (Tet-system). Using lymphoma- derived cell lines from these mice, we titrated the level of oncogene expression by adding different concentrations of doxycycline in vitro. We were able to distinguish among different levels of oncogene expression in cell lysates, with high sensitivity in as few as 400 cells by nano-fluidic detection. Next, lymphoma derived cell lines were injected subcutaneously into syngeneic mice. Upon tumor development, MYC or BCL2 oncogenes were inactivated in vivo. Both MYC and BCL2 levels decreased in serial fine needle aspirations (FNAs) of tumor nodules upon parallel analysis with nano-fluidic detection and Western blot. Finally, we used nano-fluidic detection to determine levels of MYC, BCL2, AKT and ERK in lymph node samples from patients with follicular, transformed DLBC, Burkitt’s, and mantle cell lymphomas. BCL2 was overexpressed in mantle cell and follicular lymphoma patients, confirmed by Western analysis, whereas MYC was found to be overexpressed in Burkitt’s lymphoma. These results demonstrate that nano-fluidic detection technology may be used both as a preclinical tool for the assessment of changes in oncoprotein signaling and as a clinical diagnostic modality on microscopic clinical specimens.
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39

Coulier, F., R. Kumar, M. Ernst, R. Klein, D. Martin-Zanca, and M. Barbacid. "Human trk oncogenes activated by point mutation, in-frame deletion, and duplication of the tyrosine kinase domain." Molecular and Cellular Biology 10, no. 8 (August 1990): 4202–10. http://dx.doi.org/10.1128/mcb.10.8.4202-4210.1990.

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Malignant activation of the human trk proto-oncogene, a member of the tyrosine protein kinase receptor family, has been implicated in the development of certain human cancers, including colon and thyroid papillary carcinomas. trk oncogenes have also been identified in cultured cells transfected with various DNAs. In this study, we report the characterization of three in vitro-generated trk oncogenes, trk2, trk4, and trk5 (R. Oskam, F. Coulier, M. Ernst, D. Martin-Zanca, and M. Barbacid, Proc. Natl. Acad. Sci. USA 85:2964-2968, 1988), in an effort to understand the spectrum of mutational events that can activate the human trk gene. Nucleotide sequence analysis of cDNA clones of trk2 and trk4 revealed that these oncogenes were generated by a head-to-tail arrangement of two trk tyrosine protein kinase domains connected by a purine-rich region. These oncogenes code for cytoplasmic molecules of 67,000 (p67trk2) and 69,000 (p69trk4) daltons. In contrast, the product of the trk5 oncogene, gp95trk5, is a cell surface glycoprotein of 95,000 daltons. This oncogene was generated by a 153-base-pair in-frame deletion within sequences coding for the extracellular domain of the trk receptor. This activating deletion encompasses a triplet coding for one of the nine cysteine residues that the trk receptor shares with the product of the highly related trkB tyrosine protein kinase gene. Introduction of a single point mutation (TGT----AGT) in this codon resulted in a novel trk oncogene whose product, gp140S345, differs from the nontransforming trk proto-oncogene receptor in a single amino acid residue, Ser-345 instead of Cys-345. These results illustrate that multiple molecular mechanisms, including point mutation, internal deletion, and kinase domain duplication, can result in the malignant activation of the human trk proto-oncogene.
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40

Coulier, F., R. Kumar, M. Ernst, R. Klein, D. Martin-Zanca, and M. Barbacid. "Human trk oncogenes activated by point mutation, in-frame deletion, and duplication of the tyrosine kinase domain." Molecular and Cellular Biology 10, no. 8 (August 1990): 4202–10. http://dx.doi.org/10.1128/mcb.10.8.4202.

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Malignant activation of the human trk proto-oncogene, a member of the tyrosine protein kinase receptor family, has been implicated in the development of certain human cancers, including colon and thyroid papillary carcinomas. trk oncogenes have also been identified in cultured cells transfected with various DNAs. In this study, we report the characterization of three in vitro-generated trk oncogenes, trk2, trk4, and trk5 (R. Oskam, F. Coulier, M. Ernst, D. Martin-Zanca, and M. Barbacid, Proc. Natl. Acad. Sci. USA 85:2964-2968, 1988), in an effort to understand the spectrum of mutational events that can activate the human trk gene. Nucleotide sequence analysis of cDNA clones of trk2 and trk4 revealed that these oncogenes were generated by a head-to-tail arrangement of two trk tyrosine protein kinase domains connected by a purine-rich region. These oncogenes code for cytoplasmic molecules of 67,000 (p67trk2) and 69,000 (p69trk4) daltons. In contrast, the product of the trk5 oncogene, gp95trk5, is a cell surface glycoprotein of 95,000 daltons. This oncogene was generated by a 153-base-pair in-frame deletion within sequences coding for the extracellular domain of the trk receptor. This activating deletion encompasses a triplet coding for one of the nine cysteine residues that the trk receptor shares with the product of the highly related trkB tyrosine protein kinase gene. Introduction of a single point mutation (TGT----AGT) in this codon resulted in a novel trk oncogene whose product, gp140S345, differs from the nontransforming trk proto-oncogene receptor in a single amino acid residue, Ser-345 instead of Cys-345. These results illustrate that multiple molecular mechanisms, including point mutation, internal deletion, and kinase domain duplication, can result in the malignant activation of the human trk proto-oncogene.
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41

Tsuchida, Nobuo. "Oncogenes." JOURNAL OF THE STOMATOLOGICAL SOCIETY,JAPAN 52, no. 4 (1985): 607–16. http://dx.doi.org/10.5357/koubyou.52.607.

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42

Sikora, Karol. "Oncogenes." Scandinavian Journal of Gastroenterology 20, sup117 (January 1985): 1–8. http://dx.doi.org/10.3109/00365528509092223.

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43

Haber, Michelle, and Bernard W. Stewart. "Oncogenes." Medical Journal of Australia 142, no. 7 (April 1985): 402–6. http://dx.doi.org/10.5694/j.1326-5377.1985.tb133155.x.

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44

Chang, Hyuck-Soon. "Oncogenes." Journal of Clinical Otolaryngology Head and Neck Surgery 7, no. 1 (May 1996): 1–9. http://dx.doi.org/10.35420/jcohns.1996.7.1.1.

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45

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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46

FRIEDMAN, WILLIAM H., BARRY N. ROSENBLUM, PAUL LOEWENSTEIN, HELEN THORNTON, GEORGE KATSANTONIS, and MAURICE GREEN. "ONCOGENES." Laryngoscope 95, no. 3 (March 1985): 315???318. http://dx.doi.org/10.1288/00005537-198503000-00015.

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47

Krontiris, Theodore G. "Oncogenes." New England Journal of Medicine 333, no. 5 (August 3, 1995): 303–6. http://dx.doi.org/10.1056/nejm199508033330508.

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48

MARSHALL, C. J. "Oncogenes." Journal of Cell Science 1986, Supplement 4 (January 1, 1986): 417–30. http://dx.doi.org/10.1242/jcs.1986.supplement_4.22.

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49

GORDON, HYMIE. "Oncogenes." Mayo Clinic Proceedings 60, no. 10 (October 1985): 697–713. http://dx.doi.org/10.1016/s0025-6196(12)60746-0.

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50

TAYLOR, DOLORES L. "ONCOGENES." Nursing 25, no. 6 (June 1995): 55–57. http://dx.doi.org/10.1097/00152193-199506000-00022.

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