Buy RAB39 elisa kit, Mouse RAB39, member RAS oncogene family ELISA Kit-NP_780771.1 (MBS9340534) product datasheet at MyBioSource, ELISA Kits
Alterations involving the ROS (v-ros UR2 sarcoma virus oncogene homolog 1) gene such as mutations, overexpression and gene rearrangements has been implicated in carcinogenesis and has been demonstrated to be a relevant target for ALK inhibitors. While emerging reports have demonstrated the role of ROS rearrangement in non-small cell lung cancer and cholangiocarcinoma, the functional significance of ROS dysregulation in solid tumors remain largely unstudied. The investigators aims are: (1) To characterize the frequency of ROS gene fusion, ROS protein overexpression and ROS gene mutations in cell lines and tumors from patients with hepatocellular carcinoma, colorectal, gastric, breast, ovarian, cholangiocarcinoma and non-small cell lung cancer, (2) To identify novel ROS gene variants in human solid tumors harboring ROS aberrations using next generation sequencing (NGS), (3) To determine the functional relevance of novel ROS gene variants identified with NGS, (4) To characterize the sensitivity of ...
Understanding the genetic mechanisms which underlie tumor development will provide a foundation for developing new generations of better and more effective cancer therapies. To address this fundamental issue, new technologies are needed that are superior to those currently available. Current state of the art mouse models enable testing the stochastic activation of oncogenes in a cell type specific fashion and provide a mechanism for testing targeted therapies. Despite these desirable features, their limited accessibility and feasibility precludes their implementation in most laboratories. Moreover, as the list of oncogenes continues to grow, reliable and efficient technologies are needed that can assess several oncogenes simultaneously in order to facilitate rapid analysis of tumorigenicity and their responses to therapy. This application provides a solution to all these issues by developing an innovative transgenic mouse platform (Crainbow) to rapidly, efficiently, and cost effectively create ...
Cancer is caused by an accumulation of genetic alterations that confer a survival advantage to the neoplastic cell. J. L. Jameson(p73) Oncogenes are "[g]enes that normally play a role in growth but, when overexpressed or mutated, can foster the growth of cancer." Oncogenes were discovered and characterized in viruses and animal experimental systems. These genes exist widely outside the systems in which they were discovered, and their normal cellular homologues are important in cell division and differentiation. Human oncogenes should be expressed according to style for human gene symbols (see , Human Gene Nomenclature). Mouse oncogenes (and other nonhuman oncogenes) should Less ...
Cancer is caused by an accumulation of genetic alterations that confer a survival advantage to the neoplastic cell. J. L. Jameson(p73) Oncogenes are "[g]enes that normally play a role in growth but, when overexpressed or mutated, can foster the growth of cancer." Oncogenes were discovered and characterized in viruses and animal experimental systems. These genes exist widely outside the systems in which they were discovered, and their normal cellular homologues are important in cell division and differentiation. Human oncogenes should be expressed according to style for human gene symbols (see , Human Gene Nomenclature). Mouse oncogenes (and other nonhuman oncogenes) should Less ...
Hypomethylation of ras oncogenes in primary human cancers.: We have examined the methylation status of two cellular oncogenes, c-Ha-ras and c-Ki-ras, in primary
In cancer cells associated with human papillomavirus (HPV) infections, the viral genome is very often found integrated into the cellular genome. The viral oncogenes E6 and E7 are transcribed from the viral promoter, and integration events that alter transcriptional regulation of this promoter contribute to carcinogenic progression. In this study, we detected highly enriched binding of the super-enhancer markers Brd4, MED1, and H3K27ac, visible as a prominent nuclear focus by immunofluorescence, at the tandemly integrated copies of HPV16 in cells of the cervical neoplasia cell line W12 subclone 20861. Tumor cells are often addicted to super-enhancer-driven oncogenes and are particularly sensitive to disruption of transcription factor binding to the enhancers. Treatment of 20861 cells with bromodomain inhibitors displaced Brd4 from the HPV integration site, greatly decreased E6/E7 transcription, and inhibited cellular proliferation. Thus, Brd4 activates viral transcription at this integration ...
How is growth controlled in normal cells? How are the growth control mechanisms perturbed in cancer cells? This book provides an up-to-date description of research aimed at resolving these questions. It is organized into four sections, each containing a series of short reviews written by experts in the field. The general headings are: growth factors, receptors, and related oncogenes: transduction of mitogenic signals and ras oncogenes; nuclear oncogenes and regulation of gene expression; and multiple steps involved in malignant transformation. The articles emphasize concepts rather than detailed facts and are intended not only for specialists in the field but also for interested readers, such as physicians and advanced students, who wish to stay abreast of developments in one of the most exciting fields in current biomedical research.
This gene is a member of the Rab family of small G proteins and plays a role in regulating membrane trafficking between trans-Golgi network (TGN) and recycling endosomes (RE). The encoded protein is involved in the assembly of tight junctions, which are components of the apical junctional complex (AJC) of epithelial cells. The AJC plays a role in forming a barrier between luminal contents and the underlying tissue. Additional functions associated with the protein include endocytic recycling of occludin, regulation of epithelial cell scattering, neuronal regeneration and regulation of neurite outgrowth. Alternately spliced transcript variants have been observed for this gene. A pseudogene associated with this gene is located on chromosome 12. [provided by RefSeq, Jan 2013 ...
The KOMP Repository is located at the University of California Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...
Cancer is a genetic disease that evolves over years with accumulating genetic and epigenetic abnormalities that confer an enhanced capacity to proliferate and evade apoptosis, eventually compromising the host (1, 2). Although cancer exhibits complex genetic aberrations and functional deregulations, it has been shown that abrogation of certain apical oncogenes can effectively inhibit cancer cell growth and prolong patient survival-a phenomenon termed "oncogene addiction" (3). In accordance with this concept, molecularly targeted drugs have been developed and successfully used in treating cancer patients, exemplified by the use of imatinib for chronic myelogenous leukemia, erlotinib for lung cancer, and sunitinib for kidney cancer (4). Despite these recent strides against cancer, most end-stage cancer patients still succumb to their diseases, highlighting the urgent need for novel anticancer therapeutic strategies. Recently, the "non-oncogene addiction" hypothesis was proposed based on the heavy ...
References. Calabretta B, Kaczmarek LL, Selleri L, Torelli G, Ming PML, Ming SC and Mercer WE (1986) Growth-dependent expression of human Mr 53,000 tumor antigen messenger RNA in normal and neoplastic cells. Cancer. Res. 46: 5738-5742.. Deppert W, Buschhausendenker G, Patschinsky T and Steinmeyer K (1990) Cell cycle control of p53 in normal (3T3) and chemically transformed (Meth-A) mouse cells . II. requirement for cell cycle progression. Oncogene 5: 1701-1706.. Eliyahu D, Raz A, Gruss P, Givol D and Oren M (1984) Participation of p53 cellular tumour antigen in transformation of normal embryonic cells. Nature 312: 646-649.. Jenkins JR, Rudge K, Chumakov P and Currie GA (1985) The cellular oncogene p53 can be activated by mutagenesis. Nature 317: 816-818.. Jenkins JR, Rudge K and Currie GA (1984) Cellular immortalization by a cDNA clone encoding the transformation-associated phosphoprotein p53. Nature 312: 651-654.. Mercer WE, Avignolo C and Baserga R (1984) Role of the p53 protein in cell ...
miRNAs modulate gene expression programs to control cellular processes. Analyses of bulk tissue from epithelial cancers have indicated that the levels of miR-143 and miR-145, two miRNAs shown to repress the expression of several oncogenes, are decreased compared to adjacent normal tissue, suggesting a tumor-suppressive role. In contrast, in normal tissues, the miR-143/145 cluster is expressed in the stroma and promotes epithelial growth during injury responses. To clarify the role of miR-143/145 in tumorigenesis and to elucidate the cell-type specificity of miR-143/145 expression in cancer, Dimitrova, Gocheva, and colleagues evaluated an autochthonous mouse model of Kras-mutant/Trp53-null (KP)-driven lung adenocarcinomas. Tumor-specific deletion or induced overexpression of miR-143/145 in KP mice did not affect tumor development or overall survival; however, organism-wide loss of miR-143/145 in vivo resulted in decreased lung tumor burden, suggesting that stromal miR-143/145 supports lung tumor ...
Gene in a virus that is able to produce a malignant change in an infected cell; several have been identified in human tissue as potential causes of cancer. Researchers are attempting to isolate anti-oncogenes that suppress tumours and may be used in the treatment of cancer. Certain oncogenes may play a role in normal growth and development; if they are damaged or mutated, cancer may result ...
In virtually all epithelial tumors, growth factor receptor activity is deregulated by activated mutations, genomic amplification, and autocrine loops. The dependence of tumor cell survival upon the driving oncogene has been called "oncogene addiction" and demonstrates the acute sensitivity of cancer cells to inhibition of the pathways driving their proliferation, growth and survival. Major questions regarding the sensitivity of solid tumors to targeted kinase inhibitors is why some tumors respond and others do not and why ones which respond still are able to develop resistance through the activation of other pathways. Robust, but not durable, response to receptor tyrosine kinase inhibitors (RTKIs) highlights the need to inhibit pathway activity at multiple levels.. In this study, we identify extensive signaling networks downstream of receptor tyroine kinases (RTKs) across multiple spaces, including phosphorylation, acetylation, and methylation. We used the established method of TMT labeling ...
Some tumors addiction to the over-expression of a single oncogene provides a weakness for a molecularly targeted therapy to exploit. A number of targeted
pep:known chromosome:VEGA66:5:115631908:115647736:1 gene:OTTMUSG00000014704 transcript:OTTMUST00000034877 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Rab35 description:RAB35 member RAS oncogene family ...
RAB17 antibody [4E7] (RAB17, member RAS oncogene family) for ICC/IF, IHC-P, WB. Anti-RAB17 mAb (GTX83739) is tested in Human samples. 100% Ab-Assurance.
RAB4A antibody [4E11] (RAB4A, member RAS oncogene family) for ELISA, FACS, IHC-P, WB. Anti-RAB4A mAb (GTX60601) is tested in Human, Mouse, Monkey samples. 100% Ab-Assurance.
Looking for online definition of cellular oncogene c-fos in the Medical Dictionary? cellular oncogene c-fos explanation free. What is cellular oncogene c-fos? Meaning of cellular oncogene c-fos medical term. What does cellular oncogene c-fos mean?
Looking for online definition of RAB41, member RAS oncogene family in the Medical Dictionary? RAB41, member RAS oncogene family explanation free. What is RAB41, member RAS oncogene family? Meaning of RAB41, member RAS oncogene family medical term. What does RAB41, member RAS oncogene family mean?
Acquisition of genes via horizontal transfer rather than by inheritance is frequently observed in bacteria. Now, Swedish researchers demonstrate that a similar phenomenon can occur between eucaryotic cells. Oncogenes from a dying cell can be transferred to a nearby cell via phagocytosis, a process through which one cell engulfs another. If the recipient cell is already genetically unstable, the newly acquired oncogenes can lead to tumor formation.. The researchers propose that this horizontal transfer of genes could be one route by which cells accumulate genetic abnormalities. The study also indicates that even after a cell dies, its genetic material entire chromosomes in some cases can be rescued by other cells.. The scientists mixed dying rat cells carrying cancer-causing oncogenes with mouse cells lacking p53, a tumor-suppressing gene. The p53-deficient cells developed tumor-like characteristics. The same experiment was done with mouse cells carrying p53. In contrast, however, the rat cells ...
Cancer cells escape normal growth control mechanisms as a consequence of activating (i.e., gain-of-function) mutations and/or increased expression of one or more cellular protooncogenes and/or inactivating (i.e., loss-of function) mutations and/or decreased expression of one or more tumor suppressor genes. Most oncogene and tumor suppressor gene products are components of signal transduction pathways that control cell cycle entry or exit, promote differentiation, sense DNA damage and initiate repair mechanisms, and/or regulate cell death programs. Several oncogenes and tumor suppressor genes belong to the same signaling pathway. Perhaps the best-characterized pathway includes D-type cyclin/cdk complexes, which can be oncogenes, and two tumor suppressor genes, the p16 cyclin/cdk inhibitor and the retinoblastoma gene product (reviewed in ref. 1). Nearly all tumors have mutations in multiple oncogenes and tumor suppressor genes, indicating that cells employ multiple parallel mechanisms to regulate ...
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How might this happen? Several potential regulatory schemes could contribute to the differential decay of prosurvival and proapoptotic signals on oncogene inactivation. For example, it is well documented in numerous cell culture studies that acute inactivation of various oncoproteins leads to the rapid dephosphorylation (and inactivation) of AKT, which is both a key cell survival mediator in tumor cells and a downstream target of many of the common oncoproteins (e.g., tyrosine kinases such as EGFR and Src). Although the molecular pathways that link these active kinases to an apoptotic response are poorly understood, these pathways are likely to involve a cascade of signaling events, some of which culminate in gene expression changes. Inactivation of an upstream kinase may not be sensed by downstream proapoptotic mediators for a longer period of time than that required for AKT inactivation, thereby creating a signaling imbalance that leads to an irreversible apoptotic response. Certainly, ...
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Researchers at the University of Texas M. D. Anderson Cancer Center report they have discovered a potential oncogene in ovarian cancer, which is the leading cause of gynaecological cancer death in U.S. women.
Maestro, R., Dei Tos, A. P., Hamamori, Y., Krasnokutsky, S., Sartorelli, V., Kedes, L., Doglioni, C., Beach, D. H., Hannon, G. J. (1999) Twist is a potential oncogene that inhibits apoptosis. Genes and Development, 13 (17). pp. 2207-17. ISSN 0890-9369 Martienssen, R. (1996) Epigenetic phenomena: Paramutation and gene silencing in plants. Current Biology, 6 (7). pp. 810-813. ISSN 0960-9822 Martienssen, R., Lippman, Z., May, B., Ronemus, M., Vaughn, M. (2004) Transposons, tandem repeats, and the silencing of imprinted genes. Cold Spring Harbor symposia on quantitative biology, 69. pp. 371-9. ISSN 0091-7451 (Print)0091-7451 (Linking) Matapurkar, A., Lazebnik, Y. (2006) Requirement of cytochrome c for apoptosis in human cells. Cell Death Differ, 13 (12). pp. 2062-7. ISSN 1350-9047 (Print) McCaffrey, A. P., Meuse, L., Pham, T. T. T., Conklin, D. S., Hannon, G. J., Kay, M. A. (2002) Gene expression - RNA interference in adult mice. Nature, 418 (6893). pp. 38-39. ISSN 0028-0836 Mittal, V. (2004) ...
Oncogene-encoded proteins c-Myc, n-Myc, and l-Myc function in cell proliferation, differentation and neoplastic disease. A mutated version of Myc is found in many cancers, which causes Myc to be constitutively expressed. This leads to the unregulated expression of many genes, some of which are involved in cell proliferation, and result in the formation of cancer. c-Myc is a transcription factor and is a proto-oncogene that is the focal point in cell cycle regulation, metabolism, apoptosis, differentiation, cell adhesion, and tumorigenesis. A common human translocation involving Myc is t(8;14), which is criticial to the development of most cases of Burkitts Lymphoma. Malfunctions in Myc have also been found in carcinoma of the cervix, colon, breast, lung, and stomach ...
View Notes - Lecture 29 Oncogenes and Tumor Suppressors from PHARM HB at UCSD. Recognize that most cancers originate in tissues and cell types that undergo continuous regeneration Explain the
Cancer is a leading cause of mortality in the world today. Mutation in the K-ras oncogene is common in most human cancers. K-ras oncogene expression was specifically downregulated by 58.7% by K-ras silencing siRNA, and ...
Charles Sawyers, who began his research career just as the genetic details of human oncogenes were emerging, codeveloped Gleevec, the quintessential targeted cancer therapy.. 0 Comments. ...
Charles Sawyers, who began his research career just as the genetic details of human oncogenes were emerging, codeveloped Gleevec, the quintessential targeted cancer therapy.. 0 Comments. ...
Protein syn cael ei godio yn y corff dynol gan y genyn RAB6B yw RAB6B a elwir hefyd yn Ras-related protein Rab-6B a RAB6B, member RAS oncogene family (Saesneg). Segment o DNA ywr genyn, syn amgodio ffwythiant arbennig. Maer genyn yma wedi ei leoli ar yr edefyn ôl o gromosom dynol 3, band 3q22.1.[2] ...
Complete information for RAB40B gene (Protein Coding), RAB40B, Member RAS Oncogene Family, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Top performende anti-Human Cell Adhesion Molecule-Related/down-Regulated By Oncogenes Antikörper für Western Blotting (WB) vergleichen & kaufen.
pep:known chromosome:VEGA66:10:93247414:93311135:-1 gene:OTTMUSG00000033471 transcript:OTTMUST00000084101 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Elk3 description:ELK3, member of ETS oncogene family ...
Mutation or inactivation of RB occurs in most human tumors and results in the deregulation of several E2F family transcription factors. Among the E2F family, E2F3 has been implicated as a key regulator of cell proliferation ...
We isolated cDNA clones containing the entire coding region of the putative oncogene AKT2. Sequence analysis and in vitro translation demonstrated that AKT2 encodes a 56-kDa protein with homology to serine/threonine kinases; moreover, this protein contains a Src homology 2-like domain. AKT2 was shown to be amplified and overexpressed in 2 of 8 ovarian carcinoma cell lines and 2 of 15 primary ovarian tumors. AKT2 was mapped to chromosome region 19q13.1-q13.2 by fluorescence in situ hybridization. In the two ovarian carcinoma cell lines exhibiting amplification of AKT2, the amplified sequences were localized within homogeneously staining regions. We conclude that AKT2 belongs to a distinct subfamily of protein-serine/threonine kinases containing Src homology 2-like domains and that alterations of AKT2 may contribute to the pathogenesis of ovarian carcinomas.. ...
Lung cancer, the leading cause of cancer deaths worldwide, is largely classified into small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) based on histological characteristics. Lung adenocarcinoma (LUAD), the most common subtype of NSCLC, is responsible for more than 40% of lung cancer-related deaths (Imielinski et al., 2012). The recent advances in next generation sequencing (NGS) technologies have allowed high-throughput analyses of cancer genome. This study sought to validate the candidate oncogene (U2AF1) and tumor suppressors (CLEC3B and TNNC1) discovered from a large scale sequencing project using 103 Korean lung adenocarcinoma patient samples. U2AF1 (U2 small nuclear RNA auxiliary factor 1) is a RNA splicing factor. Mutations in spliceosome components have been implicated in carcinogenesis of various types of cancer. One of the most frequently found is U2AF1 S34F missense mutation. Functional analyses of this mutation have been largely limited to hematological ...
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A novel oncogene related to c-mil is transduced in chicken neuroretina cells induced to proliferate by infection with an avian lymphomatosis virus.: Non-dividin
p130Cas is a tyrosine phosphorylated scaffold molecule originally identified in cells transformed by v-c-Src and v-Crk oncogenes [1-3]. p130Cas structural motifs and its posttranslational modifications enable interactions with many proteins leading to multi-protein complexes that in normal cells modulate cell motility, survival and proliferation [3]. In addition, p130Cas acts as a primary force sensor, transducing force into mechanical extension [4].. Extensive work on cancer cell models show that p130Cas is involved in cancer initiation, progression and metastasis formation [3]. p130Cas is necessary for transformation by several oncogenes, such as c-Src [5] and Her2 [6, 7] as well as the oncogenic fusion protein nucleophosmin (NPM1)-anaplastic lymphoma receptor tyrosine kinase (ALK) [8]. Recently, p130Cas has been shown to be required for K-Ras, b-Raf, PTEN and PIK3CA oncogene-dependent proliferation [9]. Moreover, we have demonstrated that p130Cas is required for driving invasion and ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Oncogenes and tumor suppressor genes (TSGs) both play a role in oncogenesis via opposite mechanisms. Proto-oncogenes promote normal cell growth. Occasionally, a mutation increases their activity or a duplication, translocation, or other genetic event increases their expression. Under such conditions, these genes, now called oncogenes, cause abnormal unchecked cell growth. Examples of proto-oncogenes include growth factors, tyrosine kinases, regulatory GTPases, and transcription factors. TSGs inhibit cell growth in normal cells. However, decreases in TSG activity, often caused by mutation or promoter hypermethylation, prevents their ability to stop abnormal cell growth. Examples of TSGs include genes that regulate apoptosis, cell adhesion, or DNA damage signaling. Genes may have oncogenic properties, tumor suppressor properties, or both. These properties depend not only on the tumor type, but also on the known or observed differences in gene expression or epigenetic marks. Genetic differences in ...
TransAM Elk-1 is a DNA-binding ELISA that quantifies the activated transcription factor using a method that is faster and more sensitive than gelshift, without radioactivity and gels.
Among the 518 kinases identified in the human genome are many exciting targets for cancer drug discovery (22). Molecular alterations in numerous kinases have been documented to drive malignant proliferation either via overexpression or activation, the latter secondary to an acquired mutation. Where dependence on a kinase is essential to the phenotype of a tumor, the term oncogene addiction has been coined. It is interesting that where such oncogene addiction is observed, the kinase inhibitors can have dramatic effects, whereas a lesser effect is observed on cells with mere overexpression of the target. An example of this is the activity of gefitinib or erlotinib in lung cancers with or without mutations in epidermal growth factor receptor (23). Can this be considered cytotoxicity on the one hand but cytostasis on the other? On examination of these agents, it becomes clear that the outcome, cytostasis or cytotoxicity, may depend less on the agent and more on the cellular context, especially the ...
Tang B, Yoo N, Vu M et al. Transforming growth factor-beta can suppress tumorigenesis through effects on the putative cancer stem or early progenitor cell and committed progeny in a breast cancer xenograft model. Cancer Res 2007; 67:8643-52 ...
Blocking the function of the Ras oncogenes is considered by many scientists to be the holy grail of cancer therapeutics because mutations in these genes drive the growth of so many different types of cancers. The three Ras genes found in humans -- H-Ras, K-Ras and N-Ras --were among the first to be linked to cancer development, and a new study led by VCU Massey Cancer Center researcher Paul Dent, Ph.D., has shown the recently approved breast cancer drug neratinib can block the function of Ras as well as several other oncogenes through an unexpected process.
The theory of oncogenes was foreshadowed by the German biologist Theodor Boveri in his 1914 book Zur Frage der Entstehung Maligner Tumoren (The Origin of Malignant Tumours), Gustav Fisher, Jena, 1914. Oncogenes (Teilungsfoerdernde Chromosomen) that become amplified (im permanenten Übergewicht) during tumour development. Later on the term "oncogene" was rediscovered in 1969 by National Cancer Institute scientists George Todaro and Robert Heubner.[7]. The first confirmed oncogene was discovered in 1970 and was termed sarcom. Sarcoma was in fact first discovered as an oncogene in a chicken retrovirus. Experiments performed by Dr. G. Steve Martin of the University of California, Berkeley demonstrated that the sarcoma was indeed the oncogene of the virus.[8] The first nucleotide sequence of v-sarcoma was sequenced in 1980 by A.P. Czernilofsky et al.[9]. In 1976 Drs. Dominique Stehelin, J. Michael Bishop and Harold E. Varmus of the University of California, San Francisco demonstrated that oncogenes ...