Relevant bibliographies by topics / Fos oncogenes

Academic literature on the topic 'Fos oncogenes'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Fos oncogenes"

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Claycomb, W. C., and N. A. Lanson. "Proto-oncogene expression in proliferating and differentiating cardiac and skeletal muscle." Biochemical Journal 247, no. 3 (November 1, 1987): 701–6. http://dx.doi.org/10.1042/bj2470701.

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We have examined the expression of 13 proto-oncogenes in proliferating and terminally differentiated cardiac and skeletal muscle. Total RNA was prepared from intact ventricular cardiac-muscle tissue and from purified ventricular cardiac-muscle cells of neonatal and adult rats and from cultured proliferating and terminally differentiated L6A1 rat skeletal-muscle cells. cDNA probes for histone H4, thymidine kinase, myosin heavy chain and M-creatine kinase were used to assess cellular proliferation and differentiation. Oncogenes c-myc, c-raf, c-erb-A, c-ras-H, c-ski, and c-sis were expressed in both proliferating and differentiated cardiac muscle tissue and cells, whereas c-myb expression was not observed in either. c-src was expressed only in neonatal cardiac muscle tissue and cells. c-fms, c-abl, and c-ras-K were expressed in tissue from both neonatal and adult animals but only in purified cells from neonatal animals. c-fes/fps was expressed only in neonatal cardiac muscles cells. c-fos expression was not observed in cardiac-muscle tissue from either neonatal or adult rats, but surprisingly was abundantly expressed in freshly isolated cardiac-muscle cells from animals of both ages. These results emphasize that biochemical analysis using intact cardiac-muscle tissue may not necessarily reflect muscle-specific cell processes. They also show that the expression of c-fos can be activated by the cell isolation procedure. c-myc, c-ski, c-ras-H, c-ras-K, c-abl, c-raf and c-erb-A were expressed in both proliferating and terminally differentiated skeletal-muscle cells, whereas c-myb, c-fos, c-src and c-fms transcripts were observed only in proliferating cells. c-fes/fps and c-sis were not expressed in dividing or fused skeletal-muscle cells. These results demonstrate unique tissue and cell-specific patterns of proto-oncogene expression and suggest that these genes may be involved with the regulation of cellular proliferation and terminal differentiation in striated muscle.
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Introna, M., T. A. Hamilton, R. E. Kaufman, D. O. Adams, and R. C. Bast. "Treatment of murine peritoneal macrophages with bacterial lipopolysaccharide alters expression of c-fos and c-myc oncogenes." Journal of Immunology 137, no. 8 (October 15, 1986): 2711–15. http://dx.doi.org/10.4049/jimmunol.137.8.2711.

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Abstract Expression of the c-fos, c-myc, and c-fms proto-oncogenes has been studied in thioglycollate-elicited murine peritoneal macrophages after exposure to lipopolysaccharide (LPS). After incubation with LPS (20 ng/ml), a transient and rapid induction of the expression of c-fos and c-myc oncogenes could be observed, whereas the RNA levels for c-fms were not affected. Treatment with lipid A, the active moiety of the LPS molecule, increased the c-fos and c-myc expression to a comparable degree. Similar induction of c-fos and c-myc was observed after treatment with phorbol myristate acetate, suggesting that this effect of LPS on murine macrophages might be mediated through stimulation of protein kinase C. Under similar experimental conditions, LPS treatment of macrophages did not trigger DNA synthesis. Treatment with LPS blocked DNA synthesis in macrophages treated with L cell-conditioned medium containing colony-stimulating factor. Thus changes in c-fos and c-myc expression may be elements in the complex series of biochemical events that contribute to macrophage activation and are not necessarily related to induction or priming for cellular proliferation.
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Chrysovergis, Aristeidis, Vasileios Papanikolaou, Nicholas Mastronikolis, Despoina Spyropoulou, Maria Adamopoulou, Evangelos Tsiambas, Vasileios Ragos, et al. "C-Fos Digital Expression Analysis in Human PapillomavirusRelated Oral Squamous Cell Carcinoma." Asian Pacific Journal of Cancer Biology 6, no. 2 (May 14, 2021): 117–21. http://dx.doi.org/10.31557/apjcb.2021.6.2.117-121.

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Background: Fos Proto-Oncogene (c-Fos) represents a well analyzed gene involved in solid malignancies’ development and progression. The corresponding protein forms heterodimer with c-jun, a strong transcription factor. C-Fos/c-Jun complex influences critically the intracellular signal transduction to the nucleus. Our aim was to detect and evaluate c-Fos protein expression patterns in oral squamous cell carcinomas (OSCC) tissues. Materials and Methods: Fifty (n=50) formalin-fixed, paraffin-embedded primary OSCCs tissue sections were used. Immunohistochemistry and digital image analysis were implemented for identifying and evaluating c-Fos protein expression levels, respectively. Results: C-Fos protein over expression (moderate to high imunostaining intensity values) was observed in 28/50 (56%) tissue cores, whereas low expression rates were detected in the rest of the examined cases (22/50- 44%). C-Fos overall expression was strongly associated with the stage and grade of the examined tumors (p=0.014, p=0.003, respectively) and also with Human papillomavirus (HPV) persistent infection (p=0.004). c-Fos up regulation is frequently observed in OSCCs. Conclusion: C-Fos high expression levels are correlated with an aggressive phenotype (advanced stage/lymph node metastasis) in patients with OSCC, especially in HPV positive cases, especially High Risk subtypes. Due to its elevated oncogenic activity, c-Fos should be a target for novel therapeutic strategies in OSCC combined or not with other oncogenes involving in signaling transduction pathways.
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Sariban, E., T. Mitchell, J. Griffin, and D. W. Kufe. "Effects of interferon-gamma on proto-oncogene expression during induction of human monocytic differentiation." Journal of Immunology 138, no. 6 (March 15, 1987): 1954–58. http://dx.doi.org/10.4049/jimmunol.138.6.1954.

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Abstract Activation of the proto-oncogenes c-fos, c-fms, and c-sis has been associated with monocytic differentiation. In the present study, we monitored the relationship of c-myc, c-fos, c-fms, and c-sis expression to interferon-gamma (IFN-gamma)-induced monocytic differentiation of human HL-60 promyelocytic leukemia cells. Treatment of HL-60 cells with 500 U/ml IFN-gamma arrested cell proliferation after 3 days. Appearance of the monocytic phenotype was manifested within 24 hr of IFN-gamma exposure by: increased nitroblue tetrazolium reduction; increased cell surface expression of the HLA-DR, Mo1, and MY4 antigens; and induction of transcripts for the second component of complement (C2) and tumor necrosis factor. In contrast, c-myc expression decreased as a later event after 72 hr of IFN-gamma exposure, and c-fos transcripts remained undetectable until 5 days of treatment. Furthermore, c-fms RNA and transcripts for the macrophage marker apolipoprotein E were induced only after 7 days. Finally, expression of the c-sis proto-oncogene at the RNA and protein levels remained undetectable after induction with IFN-gamma. These findings would thus suggest that declines in c-myc RNA, as well as induction of c-fos, c-fms, and c-sis expression, are not requisite events in the commitment of HL-60 cells to IFN-gamma-induced monocytic differentiation. Expression of c-fos and c-fms, however, is associated with acquisition of markers associated with maturation to macrophages.
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Kousvelari, E., C. K. Yeh, P. M. Mertz, and M. Chinchetru. "Regulation of Proto-Oncogenes and Salivary Gland Cell Proliferation." Advances in Dental Research 4, no. 1 (June 1990): 61–68. http://dx.doi.org/10.1177/08959374900040010901.

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The proto-oncogenes c-fos and c-jun express proteins targeted into the nucleus. The fos and jun proteins form a heterodimeric complex that binds to regulatory elements in the promoter region of specific genes to influence their transcription. Through such a mechanism, the fos and jun proteins have been suggested to link extracellular stimuli to short- and long-term functional changes in cells. Recently we have shown that β-adrenergic receptor stimulation of rat parotid acinar cells in vitro or addition of 8-BrcAMP in a rat submandibular cell line (RSMT-A5) increases the expression of the c-fos gene in a time-dependent manner. Maximal responses were found at 60 min. The expression of the c-fos gene did not correlate with DNA synthesis in either cell type, and c-fos transcripts were undetectable in the glands of animals treated for eight days with isoproterenol. The new data presented here extended our observations to c-jun gene expression in both salivary cell types where a similar pattern of expression for this proto-oncogene was seen. Conversely, treatment of rats with isoproterenol for nine days resulted in the appearance of two c-abl mRNAs of unique size, in addition to the known 5.3-kb c-abl transcripts. The data suggest that β-adrenergic receptor stimulation or exposure to 8-BrcAMP induces the early expression of the "nuclear proto-oncogenes" c-fos and c-jun before changes are noted in salivary epithelial cell proliferation. Differences in c-abl mRNA size, occurring later, may be associated with the morphological and biochemical changes known to occur in rat parotid glands after chronic β-adrenoreceptor stimulation.
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Kaufmann, Y., T. Silverman, B. Z. Levi, and K. Ozato. "Induction of c-ets and c-fos gene expression upon antigenic stimulation of a T cell hybridoma with inducible cytolytic capacity." Journal of Experimental Medicine 166, no. 3 (September 1, 1987): 810–15. http://dx.doi.org/10.1084/jem.166.3.810.

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Expression of cellular oncogenes was studied in a T cell hybridoma that undergoes cytolytic activation when stimulated by specific antigen or by anti-Thy-1 antibody. The activation occurs without induction of hybridoma proliferation, providing a model to examine oncogene expression during functional differentiation of lymphocytes. We found that c-fos and c-ets-1 mRNAs were transiently induced at high levels in the hybridoma 30 min and 4 h after stimulation, respectively. c-myc and c-ets-2 oncogenes were constitutively expressed in the hybridoma and their mRNA levels were unaffected during 4 h of stimulation, although c-myc expression was reduced in the later stage of stimulation. Inhibitors of T cell activation, cyclosporin A and anti-LFA-1 antibody, blocked the induction of c-fos and c-ets-1 mRNAs without reducing the levels of c-myc and c-ets-2. The results indicate that the functional activation of the CTL hybridoma is associated with induction of c-fos and c-ets-1 genes.
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Ransone, Lynn J., and Inder M. Verma. "Nuclear Proto-Oncogenes Fos and Jun." Annual Review of Cell Biology 6, no. 1 (November 1990): 539–57. http://dx.doi.org/10.1146/annurev.cb.06.110190.002543.

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Zabulionis, R. B., B. G. Atkinson, J. D. Procunier, and D. B. Walden. "Maize (Zea mays L.) DNA sequences homologous to the oncogenes myb, ras, and src." Genome 30, no. 5 (October 1, 1988): 820–24. http://dx.doi.org/10.1139/g88-132.

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The presence of genes that may govern cell division and differentiation is being investigated in the agronomically important higher plant Zea mays. Heterologous animal oncogene probes (v-myb, v-fos, v-src, and v-Ki-ras) were hybridized to Southern-blotted endonuclease-restricted fragments of maize DNA under conditions that allowed up to 28% mismatch between the probe and genomic sequence. Human, yeast, and Escherichia coli endonuclease restricted DNA served as controls for the hybridization conditions used. The Southern blotted DNAs were hybridized with probes to ribosomal DNA and pBR322 to ensure that the observed hybridization signals were not due to spurious binding or contamination of the oncogene probes. Maize DNA sequences homologous to v-myb, v-src, and v-Ki-ras were detected. No maize sequences homologous to the v-fos probe were detected. The oncogene probes did not detect any homologous sequences in E. coli DNA and all the reported homologous bands in human and yeast DNA were observed. These results illustrate the evolutionary conservation of animal proto-oncogenes within the plant kingdom, and suggest that these sequences may play a role in the replication and differentiation of plant cells.Key words: oncogenes, v-myb, v-fos, v-src, v-Ki-ras, Zea mays.
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Gutman, A., C. Wasylyk, and B. Wasylyk. "Cell-specific regulation of oncogene-responsive sequences of the c-fos promoter." Molecular and Cellular Biology 11, no. 10 (October 1991): 5381–87. http://dx.doi.org/10.1128/mcb.11.10.5381-5387.1991.

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We have identified oncogene-responsive sequences in the human c-fos promoter that mediate induction of transcription by several nonnuclear oncoproteins and the tumor promoter TPA. These sequences are regulated in a cell-specific manner. (i) In NIH 3T3 cells, the CArG box of the c-fos promoter is sufficient to mediate activation by oncogenes. (ii) In contrast, in HeLa cells, additional flanking sequences are also required, including the outer arm of the serum response element and the FAP site. We also show that the serum response factor, which binds to the CArG box, activates transcription in vivo in NIH 3T3 cells but not in HeLa cells. Finally, we present evidence that the intracellular level of the c-Fos protein could be a major determinant of cell-specific regulation of these oncogene-responsive elements of the c-fos promoter.
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Gutman, A., C. Wasylyk, and B. Wasylyk. "Cell-specific regulation of oncogene-responsive sequences of the c-fos promoter." Molecular and Cellular Biology 11, no. 10 (October 1991): 5381–87. http://dx.doi.org/10.1128/mcb.11.10.5381.

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We have identified oncogene-responsive sequences in the human c-fos promoter that mediate induction of transcription by several nonnuclear oncoproteins and the tumor promoter TPA. These sequences are regulated in a cell-specific manner. (i) In NIH 3T3 cells, the CArG box of the c-fos promoter is sufficient to mediate activation by oncogenes. (ii) In contrast, in HeLa cells, additional flanking sequences are also required, including the outer arm of the serum response element and the FAP site. We also show that the serum response factor, which binds to the CArG box, activates transcription in vivo in NIH 3T3 cells but not in HeLa cells. Finally, we present evidence that the intracellular level of the c-Fos protein could be a major determinant of cell-specific regulation of these oncogene-responsive elements of the c-fos promoter.
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Dissertations / Theses on the topic "Fos oncogenes"

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TEYSSIER, MAGALI. "Expression des oncogenes c-fos et c-myc et immunomodulation de la lignee monocytaire." Paris 11, 1992. http://www.theses.fr/1992PA112239.

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The p388d1 murine macrophage cell line has been chosen to study events resulting from the transduction of immunomodulatory signals. Owing to the frequent implication of the c-myc gene in the tumorigenicity of hematopoietic cells, the normal c-myc status in this cell line is demonstrated by southern analysis. The early modulation of the c-fos and c-myc proto-oncogene expression has been studied by northern analysis and the dna synthesis by #3h-thymidine incorporation after treatment of p388d1 cells by tpa, calcium ionophore a23187, mdp and csf-1. No correlation could be evidenced in this cell line between the mitogenic effect and the c-fos and c-myc modulation induced by these immunomodifiers. The impact of lps, tpa and dibutyryl-cyclic amp on mhc class ii antigen (ia) has been revealed by radio-immuno-assay. These compounds inhibited constitutive or induced by interferon-gamma ia expression. This inhibition seemed to be in relation with c-fos expression. The ia expression was therefore analysed either after c-fos translation blockage by a dna antisense either after overexpression of c-fos by transfection of p388d1 cells with a plasmid containing the c-fos gene. The first results seemed to confirm an inverse correlation between the c-fos induction and the inhibition of ia expression
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Tiniakos, Konstantina G. "Production, characterisation and clinical application of monoclonal antibodies to the human c-jun and c-fos oncoproteins." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246089.

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Jang, Woochan. "The presence of fos-like immunoreactivity in neurons in the vomeronasal epithelium of mice /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9842591.

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Bauters, Christophe. "Expression des oncogenes nucleaires c-myc et c-fos dans les surcharges hemodynamiques du coeur de rat adulte." Lille 2, 1990. http://www.theses.fr/1990LIL2M006.

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Spray, Kristina Jean. "Neural circuitry underlying expression of fos-like immunoreactivity in intermediate nucleus of the solitary tract following expression of taste aversion learning /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/8998.

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Whitelaw, Philippa F. "The expression of cellular oncogenes c-myc and c-fos in rat skeletal muscle : changes during development and hypertrophy." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295585.

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A study has been made on the expression of cellular oncogenes c-myc and c-fos in rate skeletal muscle both in vitro in cell lines and primary culture and in vivo during development and after the induction of two models of hypertrophy. Using the technique of Northern hybridisation, results showed that the pattern of expression of c-myc and c-fos mRNA in primary myoblast cells and in established myoblast and fibroblast cells in culture were similar; stimulation of quiescent cells to proliferate induced expression from the c-fos gene within 30 minutes and the c-myc gene by 2 hours. The findings demonstrate that c-myc and c-fos mRNA levels are increased in terminally differentiated rat skeletal muscle both in vitro and in vivo. They confirm work which showed that c-myc is not exclusively connected with cell proliferation (Endo and Nadal-Ginard 1986) and extend previous work into the increased expression of c-myc and c-fos mRNA in cardiac muscle induced to hypertrophy (Mulvagh et al., 1987; Izumo et al., 1988; Komuro et al., 1988). The possible location of the elevated expression within the muscle after hypertrophy and the relative contributions from an inflammatory response, satellite cells and myofibres are discussed. Elevation of c-myc and c-fos mRNA in hypertrophy induced both surgically by tenotomy and pharmocologically with clenbuterol argue against a significant contribution from infiltrating fibroblasts, while from the literature, the activation of satellite cells appears to occur later. It is concluded that the elevated expression of c-myc in skeletal muscle is probably located within the myofibres and may be linked to mechanisms of cell enlargement. However further confirmation with in situ hybridisation and immunohistochemistry is required.
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Allbutt, Haydn. "The rat spinal cord following traumatic injury: An anatomical and behavioural study examining NADPH-d and fos." University of Sydney, 2004. http://hdl.handle.net/2123/1335.

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Doctor of Philosophy
The general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.
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Hamon, Martial. "Expression des oncogenes nucleaires dans l'aorte de lapin apres angioplastie : influence de l'heparine sur l'expression de c-myc, c-fos et c-jun." Lille 2, 1991. http://www.theses.fr/1991LIL2M347.

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Van, Belle Eric. "Effets de l'inhibition de l'enzyme de conversion de l'angiotensine sur l'expression des oncogenes nucleaires c-myc, c-fos et c-jun et sur l'hyperplasie intimale induites par l'angioplastie experimentale." Lille 2, 1993. http://www.theses.fr/1993LIL2M261.

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MATSUYAMA, MUTSUSHI, R. KAZUHIKO UTSUMI, AKIRA MASUDA, MASAHIDE TAKAHASHI, WORAWIDH WAJJWALKUI, and YOSHIHISA SAKAI. "Expression of Proto-Oncogenes and Tumor Suppressor Genes in in vitro Cell Lines Derived from a Thymus, Thymoma, and Malignant Thymoma of Rats." Nagoya University School of Medicine, 1993. http://hdl.handle.net/2237/17542.

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Books on the topic "Fos oncogenes"

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E, Angel Peter, and Herrlich Peter 1940-, eds. The fos and jun families of transcription factors. Boca Raton: CRC Press, 1994.

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Angier, Natalie. Natural obsessions: The search for the oncogene. Boston: Houghton Mifflin, 1988.

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The biology of cancer. New York: Garland Science, 2007.

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Angel, Peter E., and Peter Herrlich. FOS and JUN Families of Transcription Factors. Taylor & Francis Group, 2017.

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FOS and JUN Families of Transcription Factors. Taylor & Francis Group, 2017.

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Angel, Peter E., and Peter Herrlich. FOS and JUN Families of Transcription Factors. Taylor & Francis Group, 2017.

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Angel, Peter E., and Peter Herrlich. FOS and JUN Families of Transcription Factors. Taylor & Francis Group, 2017.

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Merl, Dan, Joseph Lucas, Joseph Nevins, Haige Shen, and Mike West. Trans-study projection of genomic biomarkers in analysis of oncogene deregulation and breast cancer. Edited by Anthony O'Hagan and Mike West. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780198703174.013.6.

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This article focuses on the use of Bayesian concepts and methods in the trans-study projection of genomic biomarkers for the analysis of oncogene deregulation in breast cancer. The objective of the study is to determine the extent to which patterns of gene expression associated with experimentally induced oncogene pathway deregulation can be used to investigate oncogene pathway activity in real human cancers. This is often referred to as the in vitro to in vivo translation problem, which is addressed using Bayesian sparse factor regression analysis for model-based translation and refinement of in vitro generated signatures of oncogene pathway activity into the domain of human breast tumour tissue samples. The article first provides an overview of the role of oncogene pathway deregulation in human cancers before discussing the details of modelling and data analysis. It then considers the findings based on biological evaluation and Bayesian pathway annotation analysis.
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Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.
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Angier, Natalie. Natural Obsessions: The Search for the Oncogene. HarperCollins Publishers, 1999.

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Book chapters on the topic "Fos oncogenes"

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Müller, R., and R. Bravo. "c-fos and Growth Control." In Cell Cycle and Oncogenes, 69–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71686-7_8.

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Jenuwein, Thomas, and Rolf Müller. "The fos Oncogene and Transformation." In Oncogenes and Growth Control, 278–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-73325-3_38.

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Bannister, Andrew J., and Tony Kouzarides. "Structure/Function and Oncogenic Conversion of Fos and Jun." In Oncogenes as Transcriptional Regulators, 223–47. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-8889-9_6.

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Newbould, Susan A., and I. Gibson. "Expression of ras, myc and fos Oncogenes During the DMSO-Induced Detransformation of a Colon Carcinoma Line (HT29)." In ras Oncogenes, 175–89. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_24.

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Verma, Inder M., Lynn J. Ransone, Jane Visvader, Paolo Sassone-Corsi, and William W. Lamph. "Fos-Jun Conspiracy: Implications for the Cell." In Ciba Foundation Symposium 150 - Proto-Oncogenes in Cell Development, 128–46. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513927.ch9.

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Verma, I. M., T. Curran, A. D. Miller, and C. Van Beveren. "Viral and Cellular Fos Gene." In RNA Tumor Viruses, Oncogenes, Human Cancer and AIDS: On the Frontiers of Understanding, 14–24. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2583-3_2.

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Bravo, Rodrigo, and Rolf Müller. "Involvement of Proto-Oncogenes in Growth Control: The Induction of c-fos and c-myc by Growth Factors." In Oncogenes and Growth Control, 253–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-73325-3_34.

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Holt, Jeffrey. "Fos and Jun: Inducible transcription factors regulating growth of normal and transformed cells." In Oncogenes and Tumor Suppressor Genes in Human Malignancies, 301–11. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3088-6_15.

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Adamson, Eileen D., and Steven A. Edwards. "Oncogenes in Development: C-FOS and EGR-1 Studies in Embryonal Carcinoma Cells." In Uterine and Embryonic Factors in Early Pregnancy, 205–18. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3380-1_17.

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Ringertz, Nils, Magnus Rahm, Anna Hultgardh-Nilsson, Pei Jin, and Thomas Sejersen. "Expression of C-MYC, C-FOS and C-JUN Proto-Oncogenes During Muscle Differentiation in Vitro." In Molecular Basis of Human Cancer, 115–26. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2563-3_5.

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Conference papers on the topic "Fos oncogenes"

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Matos, Ana Gabrielly de Melo, ELDEVAN DA SILVA BARBOSA, LARISSA RODRIGUES DE SOUSA, WESLIANY EVERTON DUARTE, and JAQUELINE DINIZ PINHO. "AVANÇOS NA PESQUISA MOLECULAR DO CÂNCER DE CABEÇA E PESCOÇO: UMA BREVE DESCRIÇÃO DA LITERATURA." In I Congresso Nacional de Pesquisas e Estudos Genéticos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/geneticon/9041.

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Introdução: Grande parte dos casos de câncer de cabeça e pescoço (CCP), são originários das células escamosas e inclui tumores que surgem no epitélio da cavidade nasal e oral, seios paranasais, faringe e laringe. O tratamento para essa neoplasia é considerado um desafio, devido sua heterogeneidade intratumoral e os vários subsítios anatômicos. O conhecimento de alterações epigenéticas envolvidas na tumorigênese se expandiu nos últimos anos, o qual possibilitou novos insights sobre a biologia e etiologia do CCP, bem como ofereceu novas ferramentas de diagnóstico e marcadores prognósticos. Objetivo: Diante deste contexto, este trabalho tem como objetivo analisar as informações descritas na literatura a respeito dos avanços na pesquisa molecular do CCP. Metodologia: Foram selecionados 83 artigos, que fornecem uma visão abrangente sobre os avanços na pesquisa molecular do CCP, cuja fonte de pesquisa foi o PubMed e Science Direct, foram excluídos artigos duplicados e/ou que não se enquadraram na temática escolhida. Resultados: Recentes avanços em pesquisas acerca das modificações de histonas, metilação do DNA e expressão de RNAs não codificantes de proteínas demonstram que esses processos estão associados com a carcinogênese e progressão tumoral, reconhecidos como reguladores epigenéticos. Genes epigenéticos que são alvos de mutações somáticas, podem atuar como genes supressores de tumor ou oncogenes. Identificamos que alterações no supressor de tumor p53 estão associadas a menor sobrevida de pacientes com CCP, já o oncogene SKA3 em altos níveis, está intimamente associado à progressão maligna e prognóstico ruim. Verificamos ainda que vias de sinalização podem ser alteradas, a exemplo da via PI3K/AKT/mTOR, a qual tem sido observada frequentemente alterada em CCP, e está associada ao processo de proliferação celular, invasão e metástase. Conclusão: Conforme a literatura, a validação de biomarcadores e assinaturas epigenéticas é necessária, tendo em vista que a elucidação dos mecanismos genéticos e epigenéticos associados à carcinogênese possuem relevante papel na progressão e resposta ao tratamento. Portanto, os avanços na pesquisa molecular no CCP são essenciais para medicina de precisão, pois contribuem para terapias personalizadas e direcionadas aos pacientes.
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Yeh, Hsin-Chih, Christopher M. Puleo, Yi-Ping Ho, and Tza-Huei Wang. "Towards Single-Molecule Diagnostics Using Microfluidic Manipulation and Quantum Dot Nanosensors." In ASME 2007 5th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2007. http://dx.doi.org/10.1115/icnmm2007-30213.

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In this report, we review several single-molecule detection (SMD) methods and newly developed nanocrystal-mediated single-fluorophore strategies for ultrasensitive and specific analysis of genomic sequences. These include techniques, such as quantum dot (QD)-mediated fluorescence resonance energy transfer (FRET) technology and dual-color fluorescence coincidence and colocalization analysis, which allow separation-free detection of low-abundance DNA sequences and mutational analysis of oncogenes. Microfluidic approaches developed for use with single-molecule detection to achieve rapid, low-volume, and quantitative analysis of nucleic acids, such as electrokinetic manipulation of single molecules and confinement of sub-nanoliter samples using microfluidic networks integrated with valves, are also discussed.
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Rodrigues, Antonio Rony da S. P., and Edinalda Maria Cavalcante. "ESTUDO GENÉTICO DO CÂNCER DE TIREOIDE – UMA REVISÃO." In I SIMPÓSIO MARANHENSE DE GENÉTICA E GENÔMICA EM SAÚDE. Doity - Plataforma de Eventos, 2022. http://dx.doi.org/10.55664/simaggens2022.005.

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INTRODUÇÃO: O câncer de tireoide é um dos agravos mais comuns ao sistema endócrino, com o maior aumento anual de incidência em diferentes países, principalmente devido à melhoria das tecnologias de diagnóstico, sendo mais proeminente em regiões com acesso aos cuidados de saúde amplamente disponíveis. Alguns eventos moleculares são descritos tanto na carciogênese da tireoide quanto na evolução do tumor glandular. Dados do Atlas do câncer no Genoma Humano dividiu os carcinomas papilíferos de tireoide nas categorias BRAF e RAS, com base nos resultados do exoma do sequenciamento de DNA, RNA e perfil proteômico, e padrões de metilação. OBJETIVOS: Observar nos estudos da literatura os marcadores genéticos relacionados ao câncer de tireóide. MÉTODOS MÉTODOS: Para alcançar os objetivos propostos neste estudo, o método eleito foi a Revisão Integrativa que inclui a análise de pesquisas relevantes que dão suporte para a tomada de decisão, permitindo a incorporação desses achados na prática clínica. A partir de então, foi feita uma busca, ocorrida entre fevereiro e março de 2022, em 5 bases de dados: LILACS (Literatura Latino-Americana e do Caribe em Ciências da Saúde) e SciELO (Scientific Electronic Library Online), PubMed (Central: PMC- National Library of Medicine National Institutes of Health), ScienceDirect e IBECS (Índice Bibliográfico Espanhol em Ciências da Saúde). A pesquisa por artigos foi feita através dos termos em língua inglesa: “thyroid cancer”, “risk markers” e “thyroid cancer genetics” junto ao operador booleano AND. Os resultados obtidos foram comparados, estabelecendo-se concordância quanto a formulação da amostra final. Os achados foram apresentados a partir do método de “nuvem de palavras”, utilizando o software wordle. Nuvem de palavras é uma forma de facilitar a demonstração de quais são as palavras mais frequentes quando pesquisado por determinado assunto ou tema. RESULTADOS E DISCUSSÃO: Na etapa de seleção subsequente os artigos foram lidos na íntegra onde 213 artigos foram excluídos por não se apresentarem dentro do objeto estudo, e incluídos 14 trabalhos na versão final da revisão. A análise proteica demostrou projeção da estrutura molecular e homologia proteica dos seguintes marcadores moleculares de câncer de tireoide: proto-oncogene receptor tirosina quinase (RET); proto-oncogene do receptor de tirosina quinase neurotrófico 1 (NTRK1); homólogo de fosfatase tensina (PTEN); gene da proteína tumoral p53 (TP53); fosfoinositida 3-quinase/treonina proteína quinase (PI3K/AKT); catenina beta 1 (CTNNB1); gama de receptor ativado por proliferador de peroxissoma de caixa pareada 8 (PAX8-PPARG); oncogene viral de sarcoma de rato (RAS); proto-oncogene B-raf, serina/treonina quinase (BRAF); e receptor do hormônio estimulante da tireóide (TSHR). Experimentos utilizando o tipo de array identificaram três genes diferencialmente expressos, cuja expressão foi analisada por RT-PCR em 10 amostras de cada tipo de tecido. Dois deles foram capazes de diferenciar carcinomas papilíferos de tecido normal e bócio com 89% de precisão para o tumor maligno e 80% para os tecidos não malignos. Conclusão: Após a análise dos resultados desta RI, foi possível observar alguns marcadores de risco para câncer de tireóide. Desse modo, o presente trabalho contribui para o aprofundamento e desenvolvimento de novas reflexões dos estudos sobre marcadores genéticos canceriginos
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Dupain, C., L. Massaad-Massade, AC Harttrampf, and C. Gracia. "PO-508 Detection and role of novel fusion oncogenes in paediatric cancers." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.523.

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Mudassir, M., MA Kassab, S. Ansari, M. Bhagat, and P. Chattopadhyay. "PO-002 Single siRNA mediated post transcriptional and transcriptional gene silencing of HPV18 oncogenes." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.540.

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Pais, A. Casas, A. Díaz Díaz, V. Calamia, O. Martínez Iglesias, D. Roca Lema, M. Valladares Ayerbes, and V. Chantada. "PO-194 Novel potential targets for hakai oncogene during tumour progression." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.230.

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Farias, Stephanie Freire Soares de, Graziela Gama da Conceição Gomes, Biatriz Costa Diniz, CAIO DE BRITO MATOS, and MARCOS VINÍCIUS SOUZA DE ALMEIDA. "GENES RELACIONADOS AO CÂNCER DE MAMA: UM ESTUDO ACERCA DOS ONCOGENES." In I Congresso Nacional de Pesquisas e Estudos Genéticos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/geneticon/9136.

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Introdução: O câncer de mama é uma patologia relacionada a mutações genéticas, como alterações patológicas em genes como: BRCA 1 e BRCA 2. De acordo com dados do Instituto Nacional do Câncer, no ano de 2022, é estimado 68.280 novos casos, número que representa uma incidência de 43,74 casos por 100 mil individuos do sexo feminino. Objetivo: entender a relação dos genes com o desenvolvimento do câncer de mama. Materiais e Métodos: foi realizado um levantamento bibliográfico nos bancos de dados online NCBI, Scielo e Lilacs, durante o mês de junho de 2022, utilizando as palavras-chaves, isoladas e combinadas na língua portuguesa: câncer de mama, oncogenes e genes. Os artigos selecionados atendem ao período de 2017 a 2022, abordando a relação de genes com o câncer de mama. Resultados e Discussões: Foram identificados 32 artigos, dos quais 5 foram selecionados. Observou-se que a incidência do câncer de mama em portadores da mutação nos genes BRCA 1 e BRCA 2 são maiores que em vítimas do câncer de mama esporádico. Além disso, apesar de raro, a hereditariedade se configura como fator de risco para o desenvolvimento desse tipo de câncer, pois mutações nos genes BRCA 1 e BRCA 2 podem estar presentes nas células germinativas. Tais genes são designados genes supressores tumorais e se encontram associados à atividade celular, por exemplo o reparo de danos ao DNA, o ajuste da expressão gênica e o comando do ciclo celular. Assim, esses genes têm correspondência e ação essencial no câncer de mama genético, já que mutações nesses genes exprimem 85% dos sucedidos de câncer de mama. Ademais, visto que os genes BRCA1 e BRCA2 estão descritos como genes supressores de tumor, são encarregados pela regulação a proliferação celular de forma negativa e atuam na apoptose, ou seja, uma imperfeição ou outra variação em algum desses genes contribui para o acréscimo da predisposição ao câncer de mama. Conclusão: o câncer de mama é acometido em pacientes com mutações nos genes BRCA 1 e BRCA 2, sendo fundamental aprofundar pesquisas para melhor entender a atuação desses genes na fisiopatologia do câncer de mama.
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García Puga, M., CG Estefanía, SA Ander, AL Sara, and M. Ander. "PO-297 Oncogenic activity of SOX1 in gastric cancer." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.328.

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Sheetz, M. P. "Local Force on Cell Cytoskeletons Causes Binding of Focal Contact Proteins Dependent Upon Tyrosine Phosphatase/Kinases." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23074.

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Abstract Cellular responses to mechanical force are critical for the shaping of cells and for many physiological functions that need to be satisfied in functionally engineered tissues. From several recent observations, there is the suggestion that physical force developed by a cell or its environment can signal to the cell through oncogenic tyrosine kinase/phosphatase pathways and alter the program of the cell. These responses occur in seconds and lead to the localization of focal contact proteins at the sites of maximum force on the cytoskeleton. We suggest that forces directly applied to cytoskeleton proteins cause the activation of the cellular responses.
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Pirogova, Elena, Vuk Vojisavljevic, and Irena Cosic. "Prediction of protein active and/or binding site using time-frequency analysis: Application to ras oncogene proteins." In 2012 ISSNIP Biosignals and Biorobotics Conference: Biosignals and Robotics for Better and Safer Living (BRC). IEEE, 2012. http://dx.doi.org/10.1109/brc.2012.6222173.

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Reports on the topic "Fos oncogenes"

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Byers, Stephen W. Targeting of Oncogenic Proteins for Intracellular Degradation. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada421110.

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Byers, Stephen. Targeting of Oncogenic Proteins for Intracellular Degradation. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada391534.

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Byers, Stephen W. Targeting of Oncogenic Proteins for Intracellular Degradation (97breast). Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada390580.

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Gregg, Jeffrey P., and Sheryl R. Krig. The ZNF217 Breast Cancer Oncogene Amplified at 20q13: A Potential Marker for Invasiveness. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada564327.

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Keleti, David. Identification of Novel Molecular Targets for Pleckstrin Homology (PH) Domains Found in Oncogenes Implicated in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada435560.

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Keleti, David. Identification of Novel Molecular Targets for Pleckstrin Homology (PH) Domains Found in Oncogenes Implicated in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada485939.

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Keleti, David. Investigation of Novel Molecular Targets for Pleckstrin Homology (PH) Domains Found in Oncogenes Implicated in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada455267.

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Keleti, David, and Mark A. Lemmon. Investigation of Novel Molecular Targets for Pleckstrin Homology (PH) Domains Found in Oncogenes Implicated in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada469536.

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Simons, Brian. Defining a Role for the Oncogene Beta-Catenin in Prostate Epithelial Growth and Invasion. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada574100.

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Sicinski, Piotr. The Unique Role for Cyclin D1 in Mammary Gland Oncogenesis and Development. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396559.

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