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Artykuły w czasopismach na temat „Oncogenes”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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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 (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 in

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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 (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 reprog

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Der, C. J. "Cellular oncogenes and human carcinogenesis." Clinical Chemistry 33, no. 5 (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 contribut

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4

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

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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 (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

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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 (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

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7

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 (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 proce

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8

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 (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 proce

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9

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

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Rey, Federica, Letizia Messa, Cecilia Pandini, 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 (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,

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11

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

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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 (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

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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 (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

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14

Stasevich, Ekaterina Mikhailovna, Aksinya Nicolaevna Uvarova, Matvey Mikhailovich Murashko, et al. "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 (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 transcrip

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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 (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 medulloblast

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16

Melnick, A. "Targeting aggressive B-cell lymphomas with cell-penetrating peptides." Biochemical Society Transactions 35, no. 4 (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 des

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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 (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 o

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Brown, Geoffrey. "Oncogenes, Proto-Oncogenes, and Lineage Restriction of Cancer Stem Cells." International Journal of Molecular Sciences 22, no. 18 (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

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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 (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.

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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 (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.

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Scarzello, Anthony, Jim Stauffer, Tim Back, et al. "Immunological characterization of oncogene-driven models of hepatocellular carcinoma. (100.19)." Journal of Immunology 184, no. 1_Supplement (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 l

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Higuchi, Akio, Rika Kasajima, Manabu Shiozawa, 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 (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 w

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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 (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

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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 (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

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Hall, Lisa, Madison Kouche, Emma Harrison, Kareesma Parbhoo, Elaine Mardis, and Genevieve Kendall. "Abstract A023: Zebrafish personalized medicine models of fusion-driven rhabdomyosarcoma." Cancer Research 85, no. 5_Supplement (2025): A023. https://doi.org/10.1158/1538-7445.genfunc25-a023.

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Abstract Clinical sequencing efforts have revolutionized our approaches to categorizing pediatric cancers in real time. This has dramatically improved our ability to profile pediatric tumors and in some circumstances to identify actionable vulnerabilities and personalize clinical care. Unfortunately, many of the fusion positive pediatric sarcomas are driven by oncogenic fusions that have unclear mechanisms of transformation and lack therapeutic targets. Many of these fusion-oncogenes have no cell, patient derived xenograft (PDX), or animal model to understand the biology of the human disease.

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Igarashi, Taichi, Kimiyoshi Yano, Syoju Endo, and Bunsyo Shiotani. "Tolerance of Oncogene-Induced Replication Stress: A Fuel for Genomic Instability." Cancers 16, no. 20 (2024): 3507. http://dx.doi.org/10.3390/cancers16203507.

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Activation of oncogenes disturbs a wide variety of cellular processes and induces physiological dysregulation of DNA replication, widely referred to as replication stress (RS). Oncogene-induced RS can cause replication forks to stall or collapse, thereby leading to DNA damage. While the DNA damage response (DDR) can provoke an anti-tumor barrier to prevent the development of cancer, a small subset of cells triggers replication stress tolerance (RST), allowing precancerous cells to survive, thereby promoting clonal expansion and genomic instability (GIN). Genomic instability (GIN) is a hallmark

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

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

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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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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 (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 w

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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 (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

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Nowell, Peter C., and Carlo M. Croce. "Chromosomal approaches to oncogenes and oncogenesis 1." FASEB Journal 2, no. 15 (1988): 3054–60. http://dx.doi.org/10.1096/fasebj.2.15.3056765.

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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 procedu

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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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Kendall, Genevieve. "Abstract IA015: Comprehensive in vivo phenotyping of fusion-driven pediatric sarcomas." Cancer Research 85, no. 5_Supplement (2025): IA015. https://doi.org/10.1158/1538-7445.genfunc25-ia015.

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Abstract Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma that has molecular features of immature skeletal muscle. The most aggressive forms of rhabdomyosarcoma are driven by two genes that are inappropriately juxtaposed to form a fusion-oncogene. These fusion-oncogenes consists of transcription factors, various chromatin regulators, and kinases that obtain gain-of-function activities. Fusion-positive rhabdomyosarcomas have no targeted therapies. Patients are treated general chemotherapy, surgery, and radiation and survivors of childhood cancer have an increased risk of

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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 (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

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Wojtyś, Weronika, and Magdalena Oroń. "How Driver Oncogenes Shape and Are Shaped by Alternative Splicing Mechanisms in Tumors." Cancers 15, no. 11 (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, p

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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 (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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39

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 (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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40

Fan, Alice C., Debabrita Deb-Basu, Melissa Horoschak, et al. "Nano-Fluidic Detection of Oncoprotein Signaling in Preclinical and Patient Lymphoma Samples." Blood 108, no. 11 (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 fr

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Hamilton, Zac, Noor Naffakh, Natalie Marie Reizine, et al. "Relevance and accuracy of ChatGPT-generated NGS reports with treatment recommendations for oncogene-driven NSCLC." Journal of Clinical Oncology 41, no. 16_suppl (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 l

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42

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 (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

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43

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 (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

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44

Yousefi, Maryam, Gábor Boross, Carly Weiss, et al. "Combinatorial Inactivation of Tumor Suppressors Efficiently Initiates Lung Adenocarcinoma with Therapeutic Vulnerabilities." Cancer Research 82, no. 8 (2022): 1589–602. http://dx.doi.org/10.1158/0008-5472.can-22-0059.

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Abstract Lung cancer is the leading cause of cancer death worldwide, with lung adenocarcinoma being the most common subtype. Many oncogenes and tumor suppressor genes are altered in this cancer type, and the discovery of oncogene mutations has led to the development of targeted therapies that have improved clinical outcomes. However, a large fraction of lung adenocarcinomas lacks mutations in known oncogenes, and the genesis and treatment of these oncogene-negative tumors remain enigmatic. Here, we perform iterative in vivo functional screens using quantitative autochthonous mouse model system

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Hughes, Stephen H. "The RCAS Vector System." Folia Biologica 50, no. 3-4 (2004): 107–19. https://doi.org/10.14712/fb2004050030107.

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Retroviruses have long been studied in animal models and cell culture. Initially, the primary reason to study retroviruses was that certain retroviruses efficiently induced tumours in animals and transformed cells in culture. Experiments with one of these rapidly oncogenic retroviruses, Rous sarcoma virus (RSV), led to the discovery of cellular oncogenes, a discovery that provides the foundation for our current understanding of cancer. The discovery of pathogenic human retroviruses, in particular the identification about 25 years ago of human immunodeficiency virus (HIV)-1 as the causative age

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

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

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

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

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