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Journal articles on the topic 'Antioncogenes'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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1

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

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

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2

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

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3

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

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4

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

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5

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

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6

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

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7

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

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8

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

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9

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

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

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10

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

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11

Hinds, Philip W. "Commentary on Alfred G. Knudson, Jr.: “Hereditary Cancer, Oncogenes, and Antioncogenes”." Cancer Research 76, no. 10 (May 12, 2016): 2851–53. http://dx.doi.org/10.1158/0008-5472.can-16-1142.

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12

Seizinger, Bernd R. "Antioncogenes and the development of tumors in the human nervous system." Cancer 70, S4 (September 15, 1992): 1782–87. http://dx.doi.org/10.1002/1097-0142(19920915)70:4+<1782::aid-cncr2820701620>3.0.co;2-5.

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13

Imyanitov, E. N., K. M. Pozharissky, and K. P. Hanson. "Molecular genetic approaches to the prevention, diagnosis and treatment of neoplasms." Kazan medical journal 81, no. 4 (February 2, 2022): 322–26. http://dx.doi.org/10.17816/kazmj100076.

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The last 25 years have been marked by truly revolutionary events in fundamental oncology. The rapid development of molecular genetics, in particular, the discovery of oncogenes and antioncogenes, has radically changed the understanding of the mechanisms of the onset of neoplasms [2, 15]. Nevertheless, it is generally accepted that progress in the theoretical field has had little effect on the state of affairs in clinical oncology. The content of this review is intended to demonstrate the groundlessness of such assertions.

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14

Chen, Jie, Lin Lin, Zhaopei Guo, Caina Xu, Huayu Tian, Kinam Park, and Xuesi Chen. "Synergistic treatment of cancer stem cells by combinations of antioncogenes and doxorubicin." Journal of Drug Delivery Science and Technology 30 (December 2015): 417–23. http://dx.doi.org/10.1016/j.jddst.2015.06.004.

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15

Fischer, A., and W. Waldeck. "Selection of cell clones derived from normalized tumorigenic cells for the isolation of antioncogenes." Journal of Cancer Research and Clinical Oncology 121, S1 (January 1995): S14. http://dx.doi.org/10.1007/bf02559808.

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16

Werner, Haim, Michal Shalita-Chesner, Shirley Abramovitch, Gila Idelman, Limor Shaharabani-Gargir, and Tova Glaser. "Regulation of the Insulin-Like Growth Factor-I Receptor Gene by Oncogenes and Antioncogenes: Implications in Human Cancer." Molecular Genetics and Metabolism 71, no. 1-2 (September 2000): 315–20. http://dx.doi.org/10.1006/mgme.2000.3044.

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17

Hatzfeld, J., M. L. Li, E. L. Brown, H. Sookdeo, J. P. Levesque, T. O'Toole, C. Gurney, S. C. Clark, and A. Hatzfeld. "Release of early human hematopoietic progenitors from quiescence by antisense transforming growth factor beta 1 or Rb oligonucleotides." Journal of Experimental Medicine 174, no. 4 (October 1, 1991): 925–29. http://dx.doi.org/10.1084/jem.174.4.925.

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We have used antisense oligonucleotides to study the roles of transforming growth factor beta (TGF-beta) and the two antioncogenes, retinoblastoma susceptibility (Rb) and p53, in the negative regulation of proliferation of early hematopoietic cells in culture. The antisense TGF-beta sequence significantly enhanced the frequency of colony formation by multi-lineage, early erythroid, and granulomonocytic progenitors, but did not affect colony formation by late progenitors. Single cell culture and limiting dilution analysis indicated that autocrine TGF-beta is produced by a subpopulation of early progenitors. Antisense Rb but not antisense p53 yielded similar results in releasing multipotential progenitors (colony-forming unit-granulocyte/erythroid/macrophage/megakaryocyte) from quiescence. Rb antisense could partially reverse the inhibitory effect of exogenous TGF-beta. Anti-TGF-beta blocking antibodies, antisense TGF-beta, or Rb oligonucleotides all had similar effects. No additive effects were observed when these reagents were combined, suggesting a common pathway of action. Our results are consistent with the model that autocrine production of TGF-beta negatively regulates the cycling status of early hematopoietic progenitors through interaction with the Rb gene product.

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18

Caesar, G. "Oncogenes, antioncogenes, and a hypothesis on cancer therapy, i.e. The origin of cancer, and the prevention of its activity." Medical Hypotheses 40, no. 1 (January 1993): 15–18. http://dx.doi.org/10.1016/0306-9877(93)90190-2.

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19

Long, Jingpei, Zhiwei Ji, Kai Jiang, Zhaoyang Wang, and Guanmin Meng. "miR-193b Modulates Resistance to Doxorubicin in Human Breast Cancer Cells by Downregulating MCL-1." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/373574.

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MicroRNAs (miRNAs) family, which is involved in cancer development, proliferation, apoptosis, and drug resistance, is a group of noncoding RNAs that modulate the expression of oncogenes and antioncogenes. Doxorubicin is an active cytotoxic agent for breast cancer treatment, but the acquisition of doxorubicin resistance is a common and critical limitation to cancer therapy. The aim of this study was to investigate whether miR-193b mediated the resistance of breast cancer cells to doxorubicin by targeting myeloid cell leukemia-1 (MCL-1). In this study, we found that miR-193b levels were significantly lower in doxorubicin-resistant MCF-7 (MCF-7/DOXR) cells than in the parental MCF-7 cells. We observed that exogenous miR-193b significantly suppressed the ability of MCF-7/DOXR cells to resist doxorubicin. It demonstrated that miR-193b directly targeted MCL-1 3′-UTR (3′-Untranslated Regions). Further studies indicated that miR-193b sensitized MCF-7/DOXR cells to doxorubicin through a mechanism involving the downregulation of MCL-1. Together, our findings provide evidence that the modulation of miR-193b may represent a novel therapeutic target for the treatment of breast cancer.

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20

Li, Feng, Bin Wan, and Xiao-qing Li. "Expression Profile and Prognostic Values of CDH Family Members in Lung Adenocarcinoma." Disease Markers 2022 (February 11, 2022): 1–10. http://dx.doi.org/10.1155/2022/9644466.

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Many studies have confirmed that the classical cadherin (CDH) gene family may be involved in the development and progression of various tumors. However, the comprehensive assays of CDH family members in lung adenocarcinoma (LUAD) were rarely reported. In this study, our group analyzed TCGA datasets and identified 18 dysregulated CDH members in LUAD specimens. Several CDH members exhibited an increased level in LUAD specimens, such as CDH1, CDH2, CDH3, CDH4, CDH5, CDH15, CDH16, CDH17, CDH18, CDH24, and CDH26. However, some others exhibited decreased levels in LUAD specimens. Correlation analysis revealed that most CDH members were negatively regulated by the methylation of CDH genes, leading to their low expression in LUAD tissues. Survival assays identified 16 survival-related CDH members in LUAD patients. More importantly, we further performed multivariate analysis to determine the prognostic value of the above CDH family members and found that the expression levels of CDH17, CDH19, and CDH24 were an independent prognostic biomarker of the LUAD outcome. Finally, the results of functional enrichments revealed that CDH members participated in several tumor-related pathways. Collectively, our findings suggest that CDH Family members functioned as oncogenes or antioncogenes in LUAD and may be a potential biomarker for this malignancy.

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21

Kupcho, Kevin, Kevin Hsiao, Bob Bulleit, and Said A. Goueli. "A Homogeneous, Nonradioactive High-Throughput Fluorogenic Protein Phosphatase Assay." Journal of Biomolecular Screening 9, no. 3 (April 2004): 223–31. http://dx.doi.org/10.1177/1087057103262840.

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Protein phosphatases are critical components in cellular regulation; they do not only act as antioncogenes by antagonizing protein kinases, but they also play a positive regulatory role in a variety of cellular processes that require dephosphorylation. Thus, assessing the function of these enzymes necessitates the need for a robust, sensitive assay that accurately measures their activities. The authors present a novel, homogeneous, and nonradioactive assay to measure the enzyme activity of low concentrations of several protein phosphatases (phosphoserine/phosphothreonine phosphatases and phosphotyrosine phosphatases). The assay is based on the use of fluorogenic peptide substrates (rhodamine 110, bis-phosphopeptide amide) that do not fluoresce in their conjugated form, which is resistant to cleavage by aminopeptidases. However, upon dephosphorylation by the phosphatase of interest, the peptides become cleavable by the protease and release the highly fluorescent-free rhodamine 110. The assay is rapid, can be completed in less than 2 h, and can be carried out in multiwell plate formats such as 96-, 384-, and 1536-well plates. The assay has an excellent dynamic range, high signal-to-noise ratio, and a Z′ of more than 0.8, and it is easily adapted to a robotic system for drug discovery programs targeting protein phosphatases.

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22

Law, S. F., J. Estojak, B. Wang, T. Mysliwiec, G. Kruh, and E. A. Golemis. "Human enhancer of filamentation 1, a novel p130cas-like docking protein, associates with focal adhesion kinase and induces pseudohyphal growth in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 7 (July 1996): 3327–37. http://dx.doi.org/10.1128/mcb.16.7.3327.

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Budding in Saccharomyces cerevisiae follows a genetically programmed pattern of cell division which can be regulated by external signals. On the basis of the known functional conservation between a number of mammalian oncogenes and antioncogenes with genes in the yeast budding pathway, we used enhancement of pseudohyphal budding in S. cerevisiae by human proteins expressed from a HeLa cDNA library as a morphological screen to identify candidate genes that coordinate cellular signaling and morphology. In this report, we describe the isolation and characterization of human enhancer of filamentation 1 (HEF1), an SH3-domain-containing protein that is similar in structure to pl30cas, a recently identified docking protein that is a substrate for phosphorylation by a number of oncogenic tyrosine kinases. In contrast to p130cas, the expression of HEF1 appears to be tissue specific. Further, whereas p130cas is localized predominantly at focal adhesions, immunofluorescence indicates that HEF1 localizes to both the cell periphery and the cell nucleus and is differently localized in fibroblasts and epithelial cells, suggesting a more complex role in cell signalling. Through immunoprecipitation and two-hybrid analysis, we demonstrate a direct physical interaction between HEF1 and p130cas, as well as an interaction of the SH3 domain of HEF1 with two discrete proline-rich regions of focal adhesion kinase. Finally, we demonstrate that as with p130cas, transformation with the oncogene v-abl results in an increase in tyrosine phosphorylation on HEF1, mediated by a direct association between HEF1 and v-Abl. We anticipate that HEF1 may prove to be an important linking element between extracellular signalling and regulation of the cytoskeleton.

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23

Royer, Bruno, Dominique Cazals-Hatem, Jean Sibilia, Felix Agbalika, Jean-Michel Cayuela, Thierry Soussi, Frédéric Maloisel, Jean-Pierre Clauvel, Jean-Claude Brouet, and Xavier Mariette. "Lymphomas in Patients With Sjögren's Syndrome Are Marginal Zone B-Cell Neoplasms, Arise in Diverse Extranodal and Nodal Sites, and Are Not Associated With Viruses." Blood 90, no. 2 (July 15, 1997): 766–75. http://dx.doi.org/10.1182/blood.v90.2.766.

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Abstract The occurrence of non-Hodgkin's lymphoma (NHL) is the most serious complication of Sjögren's syndrome (SS). We performed a study of 16 NHLs occurring in patients with an underlying SS. These lymphomas arose not only in salivary glands (7 cases) but also in other mucosal extranodal sites (the stomach [4 cases], the lung [3 cases], the skin [3 cases], the buccal mucosa [1 case], the thymus [1 case]) and in nodal sites (8 cases). Low-grade marginal zone lymphomas (MZL) were diagnosed in 12 of the 16 patients, 9 of mucosa-associated lymphoid tissues (MALT) type in mucosal sites and 3 exclusively nodal. The 4 other patients presented with a high-grade B-cell lymphoma that was probably a histological transformation of an underlying low-grade MZL at least in 3 of the cases involving skin, stomach, and parotid, respectively. A t(14; 18) translocation was detected in 1 of 8 lymphomas tested. We detected serum anti-p53 antibodies in 2 of the 14 studied patients. p53 protein was detected in 1 of 11 lymphomas tested. LMP protein and Eber RNAs of Epstein-Barr virus (EBV) were not detected in the 16 NHL biopsies. Using polymerase chain reaction, EBV was never detected except in 1 of 4 parotid lymphomas. No human T-lymphotropic virus 1 or human herpes virus 8 DNAs were detected in NHL biopsies. None of the patients had hepatitis C virus infection found using serological methods. Chemotherapy was usually efficient. In conclusion, lymphomas occurring in patients with an underlying SS are in most cases MZL. These lymphomas are not associated with viruses known to be present in other types of lymphomas. Some of the translocations or mutations of oncogenes or antioncogenes described in other lymphomas are detected in SS-associated lymphomas.

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24

Royer, Bruno, Dominique Cazals-Hatem, Jean Sibilia, Felix Agbalika, Jean-Michel Cayuela, Thierry Soussi, Frédéric Maloisel, Jean-Pierre Clauvel, Jean-Claude Brouet, and Xavier Mariette. "Lymphomas in Patients With Sjögren's Syndrome Are Marginal Zone B-Cell Neoplasms, Arise in Diverse Extranodal and Nodal Sites, and Are Not Associated With Viruses." Blood 90, no. 2 (July 15, 1997): 766–75. http://dx.doi.org/10.1182/blood.v90.2.766.766_766_775.

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The occurrence of non-Hodgkin's lymphoma (NHL) is the most serious complication of Sjögren's syndrome (SS). We performed a study of 16 NHLs occurring in patients with an underlying SS. These lymphomas arose not only in salivary glands (7 cases) but also in other mucosal extranodal sites (the stomach [4 cases], the lung [3 cases], the skin [3 cases], the buccal mucosa [1 case], the thymus [1 case]) and in nodal sites (8 cases). Low-grade marginal zone lymphomas (MZL) were diagnosed in 12 of the 16 patients, 9 of mucosa-associated lymphoid tissues (MALT) type in mucosal sites and 3 exclusively nodal. The 4 other patients presented with a high-grade B-cell lymphoma that was probably a histological transformation of an underlying low-grade MZL at least in 3 of the cases involving skin, stomach, and parotid, respectively. A t(14; 18) translocation was detected in 1 of 8 lymphomas tested. We detected serum anti-p53 antibodies in 2 of the 14 studied patients. p53 protein was detected in 1 of 11 lymphomas tested. LMP protein and Eber RNAs of Epstein-Barr virus (EBV) were not detected in the 16 NHL biopsies. Using polymerase chain reaction, EBV was never detected except in 1 of 4 parotid lymphomas. No human T-lymphotropic virus 1 or human herpes virus 8 DNAs were detected in NHL biopsies. None of the patients had hepatitis C virus infection found using serological methods. Chemotherapy was usually efficient. In conclusion, lymphomas occurring in patients with an underlying SS are in most cases MZL. These lymphomas are not associated with viruses known to be present in other types of lymphomas. Some of the translocations or mutations of oncogenes or antioncogenes described in other lymphomas are detected in SS-associated lymphomas.

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25

Голубев, А. Г. "Общие принципы взаимоотношений живых организмов с экосистемой и злокачественных клеток с живым организмом." Biosfera 14, no. 2 (July 4, 2022): 1. http://dx.doi.org/10.24855/biosfera.v14i2.674.

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The present review addresses studies based on behavioral similarities between cancer cells in a metazoan organism and unicellular organisms in an ecosystem and between malignant tumors and some primordial colonial forms of life, from which metazoans evolved. Unicellular organisms and their colonies can exist only by compensating for their losses by the proliferation of remaining cells. Therefore, proliferation or readiness to proliferate is a priority for cells. Metazoans evolution was associated with increasing the stringency of the control of this priority. In this perspective, the common set of cancer hallmarks, which emerges in the courses of progression of different cancers, which feature different initial combinations of mutations in oncogenes and antioncogenes and exist under different initial conditions possible in various organs, results not from the convergent evolution but rather from the recapitulation of the evolutionary primordial mode of cell life. The malignant transformation is a manifestation of the disinhibition of a gestalt of traits required for the survival of cell populationin an ecosystem, which is what a tumor host eventually turns to for the tumor. Such ecological attitudes to malignant growth suggest analogies betweenthe therapeutic resistance of cancer with the resistance of pests to pesticides or of bacteria to antibiotics and between metastases and invasive species. An important means used by unicellular organisms to survive in noxious conditions is increasing the rate of mutation to produce different variants, among which some may happen to fit the current situation. This is what occurs upon cancer therapy, which increases the genetic diversity of cancer cells and acts as a factor of the positive selection of cells for resistance to the very same therapy. Because the resulting cell clones compete for body resources, the elimination of the cells that respond to therapy is favorable for the cells that are resistant to it. Therefore, it is unwise to use chemotherapy for tumor elimination. It is more prudent to aim at achieving a balance of cancer cell populations, which makes it possible to turn cancer into a chronic rather than fatal disease. These arguments justify the current efforts to develop regiments of the so-called adaptive therapy for cancer.

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26

Trinchieri, Giorgio. "Cytokine receptor gene plays antioncogene." Blood 106, no. 12 (December 1, 2005): 3684–85. http://dx.doi.org/10.1182/blood-2005-09-3678.

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27

Chattaraj, Sourav, Debasis Mitra, Abhishek Chattaraj, Manasi Chattaraj, Meghna Kundu, Arindam Ganguly, and Pradeep K. Das Mohapatra. "Antioncogenic potential of probiotics: Challenges and future prospective." Indian Journal of Microbiology Research 10, no. 1 (May 15, 2023): 1–10. http://dx.doi.org/10.18231/j.ijmr.2023.001.

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Probiotics are beneficial microorganisms that have shown to possess numerous health benefits. Recently, there has been budding interests in the utilization of probiotics as a prospective weapon for cancer deterrence and management. The antioncogenic attributes of probiotics were provided through various mechanisms such as immune modulation, production of anticancer compounds, and regulation of intestinal microbiota. The current study shed light on the antioncogenic probiotic strains and explored their anticancer mechanisms. However, the use of probiotics for cancer prevention and treatment also poses several challenges, including the identification of specific strains with the most potent antioncogenic effects, the optimal dosage and duration of treatment, and the hazards allied with the implementation of live microorganisms. Additionally, the heterogeneity of cancer types and patients' microbiomes further complicate the selection of probiotics for clinical applications. Hence, future study should concentrate on the development of alternative approaches such as the use of microbial-derived components, genetically modified probiotics, and synthetic biology to overcome these challenges and enhance the antioncogenic potential of probiotics.

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28

Horowitz, J., D. Yandell, S. Park, S. Canning, P. Whyte, K. Buchkovich, E. Harlow, R. Weinberg, and T. Dryja. "Point mutational inactivation of the retinoblastoma antioncogene." Science 243, no. 4893 (February 17, 1989): 937–40. http://dx.doi.org/10.1126/science.2521957.

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29

Estes, Myka L., Yuki Ozawa, Ann H. Williams, Alan F. List, and Lubomir Sokol. "Homozygous JAK2 V617P Gain-of-Function Mutation Is Responsible for Constitutive JAK2/STAT5 Activation and Proliferation of HEL.92.1.7. Cell Line." Blood 106, no. 11 (November 16, 2005): 4377. http://dx.doi.org/10.1182/blood.v106.11.4377.4377.

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Abstract HEL (Human erythroleukemia) is a growth factor independent erythroleukemic cell line established from the bone marrow of a patient with relapsed Hodgkin disease after autologous bone marrow transplantation (Martin P & Papayannopoulou T: Science1982;216:1233–1235). HEL cells display a block in differentiation at the level of common erythroid-megakaryocytic progenitor and have been commonly used as a model to study erythroid and megakaryocytic differentiation. Liu RY et al. (Blood1999;93:2369–2379) reported that constitutive activation of JAK2 tyrosine kinase in Dami/HEL cell line correlated with factor independent growth. Recently, several groups of investigators described a point mutation V617P in the autoinhibitory regulatory (JH2) domain of JAK2 tyrosine kinase in patients with myeloproliferative disorders (MPD). This acquired mutation results in constitutive activation of the JAK2/STAT5 pathway in hematopoietic cells. To date, the V617P mutation represents the most common causative genetic defect detected in patients with Philadelphia chromosome negative MPD. Interestingly, rare cases of patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) were found to have the same mutation. We tested several hematopoietic cell lines including HL-60, HEL, KG-1, K-562, TF-1, U937 and UT-7 for the presence of V617P mutation using RFLP and automatic DNA sequencing. We found the homozygous mutation V617P only in HEL cells. This cell line has a very complex karyotype suggesting that a defect of multiple oncogenes or antioncogenes could be responsible for sustained cell proliferation. We employed the JAK2 inhibitor, AG490 at concentrations ranging from 0 to 100 mM and measured proliferation of HEL and control K562 cell lines using MTT assay. We observed dose-dependent inhibition of HEL cell proliferation with low micromolar concentrations of AG490 in contrast to K562 control cell line, harboring bcr-abl fusion tyrosine kinase. IC50 was 13 mM for HEL cells and 65 mM for control K562 cells, respectively. Low concentrations of AG490 significantly decreased phosphorylation of JAK2 and STAT5 in HEL cells but not in control K562 cell line, where bcr-abl activates separately JAK2 and STAT5 pathway. Exposure of HEL cells to AG490 [0–50mM] induced apoptosis as measured by annexin V labeling in a concentration dependent fashion. No significant increase in apoptosis was detected in K562 cells using similar concentrations of the JAK2 inhibitor. Overall, these results suggest that the mechanism of proliferation of the HEL cell line is driven by constitutive activation of JAK2 tyrosine kinase secondary to V617P gain-of-function mutation. Our data provides further evidence that the JAK2/STAT5 intracellular signaling pathway is preserved in this cell line. Thus, HEL cells can serve as a model to test novel JAK2 specific inhibitors in preclinical studies.

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30

Tong, Alex W., Yu-An Zhang, Casey Cunningham, Phillip Maples, and John Nemunaitis. "Potential Clinical Application of Antioncogene Ribozymes for Human Lung Cancer." Clinical Lung Cancer 2, no. 3 (February 2001): 220–26. http://dx.doi.org/10.3816/clc.2001.n.007.

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31

Chen, Jingnan, Yan Wei, Xinyu Chen, Jingjing Jiao, and Yu Zhang. "Polyunsaturated fatty acids ameliorate aging via redox-telomere-antioncogene axis." Oncotarget 8, no. 5 (December 26, 2016): 7301–14. http://dx.doi.org/10.18632/oncotarget.14236.

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32

Ahuja, HG, PS Jat, A. Foti, M. Bar-Eli, and MJ Cline. "Abnormalities of the retinoblastoma gene in the pathogenesis of acute leukemia." Blood 78, no. 12 (December 15, 1991): 3259–68. http://dx.doi.org/10.1182/blood.v78.12.3259.3259.

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Abstract The retinoblastoma-susceptibility (Rb) gene is an antioncogene that is frequently altered in retinoblastomas, sarcomas, and some epithelial tumors. We examined the structure of the Rb gene by Southern blotting in 215 cases of leukemias and lymphomas of diverse phenotype and in 15 leukemic cell lines. In selected cases Rb protein expression was examined with specific monoclonal antibodies. Structural abnormalities of the Rb gene with absent protein expression were frequent in all types of human acute leukemia, but were particularly common (27% incidence) in M4 and M5 myeloid leukemia with monocytic differentiation and in Philadelphia chromosome (Ph1)-positive leukemia of lymphoid phenotype (11% to 29% incidence). Changes in Rb were observed early in the transition to acute leukemia in cases of myelodysplastic syndrome and in the accelerated phase of chronic myelocytic leukemia in transition to blast crisis. In one case, molecular changes in Rb could be correlated with leukemia remission and relapse. We conclude that the Rb antioncogene is commonly involved in the evolution of human acute leukemias, particularly in those of a monocytic phenotype and in lymphoid leukemia in which there is an antecedent alteration of the Ph1 chromosome.

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Ahuja, HG, PS Jat, A. Foti, M. Bar-Eli, and MJ Cline. "Abnormalities of the retinoblastoma gene in the pathogenesis of acute leukemia." Blood 78, no. 12 (December 15, 1991): 3259–68. http://dx.doi.org/10.1182/blood.v78.12.3259.bloodjournal78123259.

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The retinoblastoma-susceptibility (Rb) gene is an antioncogene that is frequently altered in retinoblastomas, sarcomas, and some epithelial tumors. We examined the structure of the Rb gene by Southern blotting in 215 cases of leukemias and lymphomas of diverse phenotype and in 15 leukemic cell lines. In selected cases Rb protein expression was examined with specific monoclonal antibodies. Structural abnormalities of the Rb gene with absent protein expression were frequent in all types of human acute leukemia, but were particularly common (27% incidence) in M4 and M5 myeloid leukemia with monocytic differentiation and in Philadelphia chromosome (Ph1)-positive leukemia of lymphoid phenotype (11% to 29% incidence). Changes in Rb were observed early in the transition to acute leukemia in cases of myelodysplastic syndrome and in the accelerated phase of chronic myelocytic leukemia in transition to blast crisis. In one case, molecular changes in Rb could be correlated with leukemia remission and relapse. We conclude that the Rb antioncogene is commonly involved in the evolution of human acute leukemias, particularly in those of a monocytic phenotype and in lymphoid leukemia in which there is an antecedent alteration of the Ph1 chromosome.

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Liu, L., Y. Wang, R. Bai, K. Yang, and Z. Tian. "MiR-186 inhibited aerobic glycolysis in gastric cancer via HIF-1α regulation." Oncogenesis 5, no. 5 (May 2016): e224-e224. http://dx.doi.org/10.1038/oncsis.2016.35.

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Abstract Deregulation of microRNAs in human malignancies has been well documented, among which microRNA-186 (miR-186) has an antiproliferative role in some carcinomas. Here we demonstrate that low expression of miR-186 facilitates aerobic glycolysis in gastric cancer. MiR-186 suppresses cell proliferation induced by hypoxia inducible factor 1 alpha (HIF-1α) in gastric cancer cell lines MKN45 and SGC7901. Cellular glycolysis, including cellular glucose uptake, lactate, ATP/ADP and NAD+/NADH ratios, are also inhibited by miR-186. The negative regulation of miR-186 on HIF-1α effects its downstream targets, including programmed death ligand 1 and two glycolytic key enzymes, hexokinase 2 and platelet-type phosphofructokinase. The antioncogenic effects of miR-186 are proved by in vivo xenograft tumor experiment. The results demonstrate that the miR-186/HIF-1α axis has an antioncogenic role in gastric cancer.

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AKIYAMA, TETSU, TOHRU OHUCHI, SHUJI SUMIDA, SHI-QIONG XU, and KUMAO TOYOSHIMA. "Phosphorylation of the Antioncogene Products and Control of the Cell Cycle." Tohoku Journal of Experimental Medicine 168, no. 2 (1992): 153–57. http://dx.doi.org/10.1620/tjem.168.153.

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Thomas, G., O. Delattre, J. Zucman, P. Merel, P. Dejong, G. Rouleau, and A. Aurias. "Oncogene and antioncogene from the 22q12 region involved in neuroectodermal tumours." Cancer Genetics and Cytogenetics 77, no. 2 (October 1994): 156. http://dx.doi.org/10.1016/0165-4608(94)90263-1.

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Frisch, S. M. "Antioncogenic effect of adenovirus E1A in human tumor cells." Proceedings of the National Academy of Sciences 88, no. 20 (October 15, 1991): 9077–81. http://dx.doi.org/10.1073/pnas.88.20.9077.

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Xu, Jin, Zengliang Wang, Zhichao Liao, Dong Dai, and Xinlong Ma. "MicroRNA-150 functions as an antioncogenic regulator in osteosarcoma." Oncology Letters 14, no. 2 (June 16, 2017): 2483–90. http://dx.doi.org/10.3892/ol.2017.6393.

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Cacemiro, Maira da Costa, Maria Gabriela Berzoti-Coelho, Juçara Gastaldi Cominal, Sandra Mara Burin, and Fabíola Attié de Castro. "Hippo pathway deregulation: implications in the pathogenesis of haematological malignancies." Journal of Clinical Pathology 70, no. 1 (October 26, 2016): 9–14. http://dx.doi.org/10.1136/jclinpath-2016-204055.

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The Hippo pathway participates in the regulation of cell proliferation, differentiation and apoptosis. It is composed by a large array of proteins whose deregulation has been associated with pro-oncogenic and antioncogenic processes. The present review focuses on the Hippo pathway signalling network and discusses its dual role in oncogenesis, particularly in haematological malignancies.

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Zhang, Q., CM Hu, Y. S. Yuan, C. H. He, Q. Zhao, and N. Z. Liu. "Expression of Mina53 and its Significance in Gastric Carcinoma." International Journal of Biological Markers 23, no. 2 (April 2008): 83–88. http://dx.doi.org/10.1177/172460080802300204.

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Aim To study the expression of Mina53 and its relationships with clinicopathological characteristics, antioncogene inactivation and tumor proliferation in human gastric carcinoma, and to explore the role of Mina53 in carcinogenesis and tumor progression. Methods Expression of Mina53 and proliferating cell nuclear antigen (PCNA) was determined in gastric carcinoma (n=79), gastric dysplasia (n=21) and normal gastric tissues (n=20), while p53 was measured in gastric carcinoma tissues by immunohistochemistry. Results Mina53 was negatively expressed in all normal mucosa tissues. Dysplasia specimens showed weakly positive staining for Mina53 in 3 of 21 cases. Elevated expression of Mina53 was observed in 72 (91.1%) of the gastric carcinomas. No significant associations were found between Mina53 and clinicopathological characteristics such as sex, age, histological differentiation, distant metastasis and lymph node metastasis (p>0.05). There was a significant association with depth of invasion (χ2=5.385, p<0.05) and TMN stage (χ2=6.255, p<0.05). In gastric carcinoma, positive staining for p53 was detected in 53 of 79 cases (67.1%), showing a significant association with Mina53 (χ2=5.161, p<0.05). The mean (± SD) PCNA labeling index for gastric carcinoma was 39.47±16.92%. Mina53 expression was positively associated with PCNA level (r=0.756, p<0.01). Conclusion Mina53 was overexpressed in gastric carcinoma and associated with tumor proliferation and antioncogene inactivation. Mina53 could therefore play an important role in the carcinogenesis and progression of gastric carcinoma.

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Osipovich, O. A., A. B. Sudarikov, T. S. Kolesnikova, N. I. Misuno, and N. N. Voitenok. "Differences in “antioncogene” p53 expression in human monocytes and lymphocytes in vitro." Bulletin of Experimental Biology and Medicine 113, no. 6 (June 1992): 856–59. http://dx.doi.org/10.1007/bf00790114.

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Wu, Hucong, Jiaqi Liu, Yi Yin, Dong Zhang, Pengpeng Xia, and Guoqiang Zhu. "Therapeutic Opportunities in Colorectal Cancer: Focus on Melatonin Antioncogenic Action." BioMed Research International 2019 (September 17, 2019): 1–6. http://dx.doi.org/10.1155/2019/9740568.

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Colorectal cancer (CRC) influences individual health worldwide with high morbidity and mortality. Melatonin, which shows multiple physiological functions (e.g., circadian rhythm, immune modulation, and antioncogenic action), can be present in almost all organisms and found in various tissues including gastrointestinal tract. Notably, melatonin disruption is closely associated with the elevation of CRC incidence, indicating that melatonin is effective in suppressing CRC development and progression. Mechanistically, melatonin favors in activating apoptosis and colon cancer immunity, while reducing proliferation, autophagy, metastasis, and angiogenesis, thereby exerting its anticarcinogenic effects. This review highlights that melatonin can be an adjuvant therapy and be beneficial in treating patients suffering from CRC.

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Son, Young-Ok, Poyil Pratheeshkumar, Ram Vinod Roy, John Andrew Hitron, Lei Wang, Sasidharan Padmaja Divya, Mei Xu, et al. "Antioncogenic and Oncogenic Properties of Nrf2 in Arsenic-induced Carcinogenesis." Journal of Biological Chemistry 290, no. 45 (September 18, 2015): 27090–100. http://dx.doi.org/10.1074/jbc.m115.675371.

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Ferrari, P., G. Ferrari, G. Castagnetti, A. Dotti, B. Baisi, and G. Galizia. "I markers biologici. Introduzione:Biological markers. Introduction." Urologia Journal 62, no. 2 (April 1995): 209–15. http://dx.doi.org/10.1177/039156039506200207.

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Molecular biology has made giant strides over the last ten years and provides an immense field of research. The Authors first review the concepts of neoplastic proliferation and transformation of the phenotype, analysing cell constitution and its relations with the intercellular space. The most important moment in molecular research was the identification of the growth factors and consequently the process of transduction of signals from the outside into the cell and the retroinhibiting mechanisms of the same signals. The terms oncogene and antioncogene are defined as well as their most significant expressions.

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Fujimoto, H., N. Onishi, N. Kato, M. Takekawa, X. Z. Xu, A. Kosugi, T. Kondo, et al. "Regulation of the antioncogenic Chk2 kinase by the oncogenic Wip1 phosphatase." Cell Death & Differentiation 13, no. 7 (November 25, 2005): 1170–80. http://dx.doi.org/10.1038/sj.cdd.4401801.

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Carneiro, C., D. Sanguinetti, G. Martinez, M. C. Pastoriza, J. Martin-Caballero, J. M. Cameselle-Teijeiro, J. Forteza, F. Dominguez, J. Seoane, and A. Vidal. "407 Nur77 is a Tumor Suppressor That Mediates P53 Antioncogenic Activities." European Journal of Cancer 48 (July 2012): S98. http://dx.doi.org/10.1016/s0959-8049(12)71089-4.

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Son, Young-Ok, Poyil Pratheeshkumar, Ram Vinod Roy, John Andrew Hitron, Lei Wang, Sasidharan Padmaja Divya, Mei Xu, et al. "Withdrawal: Antioncogenic and oncogenic properties of Nrf2 in arsenic-induced carcinogenesis." Journal of Biological Chemistry 293, no. 40 (October 5, 2018): 15456. http://dx.doi.org/10.1074/jbc.w118.005758.

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Giannios, J. N., P. Ginopoulos, and J. A. Karagiannis. "Induction of apoptosis after combined antioncogene and cytotoxic treatment in chemoresistant hepatocellular carcinoma cells." Gastroenterology 114 (April 1998): A1246—A1247. http://dx.doi.org/10.1016/s0016-5085(98)85056-7.

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Zang, K. D., and N. Blin. "Search for a new kind of antioncogene on human chromosome 22q. — Facts and fancies." Cancer Genetics and Cytogenetics 41, no. 2 (September 1989): 228–29. http://dx.doi.org/10.1016/0165-4608(89)90270-7.

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Demyashkin, G. A., and P. V. Nikitin. "IDH1- and IDH2-mutations in brain glial tumors - the new antioncogenic mechanism." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 118, no. 4 (2018): 134. http://dx.doi.org/10.17116/jnevro201811841134-139.

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