Thematische Bibliographien / Tumourigenesis / Zeitschriftenartikel

Zeitschriftenartikel zum Thema „Tumourigenesis“

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Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 6. September 2023

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1

Peiser, J., A. Smith, B. Bapat und H. Stern. „Colorectal tumourigenesis“. Surgical Oncology 3, Nr. 4 (August 1994): 195–201. http://dx.doi.org/10.1016/0960-7404(94)90034-5.

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2

Warfel, Noel A., und Wafik S. El-Deiry. „p21WAF1 and tumourigenesis“. Current Opinion in Oncology 25, Nr. 1 (Januar 2013): 52–58. http://dx.doi.org/10.1097/cco.0b013e32835b639e.

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3

Chang, Xiaotian, und Kehua Fang. „PADI4 and tumourigenesis“. Cancer Cell International 10, Nr. 1 (2010): 7. http://dx.doi.org/10.1186/1475-2867-10-7.

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4

Reincke, M., F. Beuschlein, M. Slawik und K. Borm. „Molecular adrenocortical tumourigenesis“. European Journal of Clinical Investigation 30 (Dezember 2000): 63–68. http://dx.doi.org/10.1046/j.1365-2362.2000.0300s3063.x.

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5

Hickman, J. „Apoptosis and tumourigenesis“. Current Opinion in Genetics & Development 12, Nr. 1 (01.02.2002): 67–72. http://dx.doi.org/10.1016/s0959-437x(01)00266-0.

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6

BUCKLEY, I. „Tumourigenesis: A malignant scenario“. Cell Biology International Reports 15, Nr. 7 (Juli 1991): 545–49. http://dx.doi.org/10.1016/0309-1651(91)90001-y.

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7

Heijmans, J., N. V. J. A. Büller, E. Hoff, A. A. Dihal, T. van der Poll, M. A. D. van Zoelen, A. Bierhaus et al. „Rage signalling promotes intestinal tumourigenesis“. Oncogene 32, Nr. 9 (02.04.2012): 1202–6. http://dx.doi.org/10.1038/onc.2012.119.

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8

Fu, K., F. Lloyd, C. Forrest, B. Klopcic und I. Lawrance. „P036 SPARC affects colorectal tumourigenesis“. Journal of Crohn's and Colitis 7 (Februar 2013): S24—S25. http://dx.doi.org/10.1016/s1873-9946(13)60059-8.

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9

Froldi, Francesca, Milán Szuperák und Louise Y. Cheng. „Neural stem cell derived tumourigenesis“. AIMS Genetics 2, Nr. 1 (2015): 13–24. http://dx.doi.org/10.3934/genet.2015.1.13.

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10

Kishida, S., und K. Kadomatsu. „Involvement of midkine in neuroblastoma tumourigenesis“. British Journal of Pharmacology 171, Nr. 4 (24.01.2014): 896–904. http://dx.doi.org/10.1111/bph.12442.

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11

Ernst, Matthias, und Tracy L. Putoczki. „Stat3: Linking inflammation to (gastrointestinal) tumourigenesis“. Clinical and Experimental Pharmacology and Physiology 39, Nr. 8 (25.07.2012): 711–18. http://dx.doi.org/10.1111/j.1440-1681.2011.05659.x.

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12

Hickman, John A. „Suppression of tumourigenesis by cell death“. Toxicology 226, Nr. 1 (September 2006): 12–13. http://dx.doi.org/10.1016/j.tox.2006.05.019.

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13

Tominaga, Y. „Mechanism of parathyroid tumourigenesis in uraemia“. Nephrology Dialysis Transplantation 14, Nr. 90001 (01.01.1999): 63–65. http://dx.doi.org/10.1093/ndt/14.suppl_1.63.

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14

Thornalley, Paul J., und Naila Rabbani. „Glyoxalase in tumourigenesis and multidrug resistance“. Seminars in Cell & Developmental Biology 22, Nr. 3 (Mai 2011): 318–25. http://dx.doi.org/10.1016/j.semcdb.2011.02.006.

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15

Junien, Claudine. „Beckwith-wiedemann syndrome, tumourigenesis and imprinting“. Current Opinion in Genetics & Development 2, Nr. 3 (Januar 1992): 431–38. http://dx.doi.org/10.1016/s0959-437x(05)80154-6.

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16

Junien, Claudine. „Beckwith-Wiedemann syndrome, tumourigenesis and imprinting“. Current Biology 2, Nr. 6 (Juni 1992): 321. http://dx.doi.org/10.1016/0960-9822(92)90888-h.

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17

Frappier, Lori. „Role of EBNA1 in NPC tumourigenesis“. Seminars in Cancer Biology 22, Nr. 2 (April 2012): 154–61. http://dx.doi.org/10.1016/j.semcancer.2011.12.002.

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18

Poulard, Coralie, Juliette Rambaud, Emilie Lavergne, Julien Jacquemetton, Jack-Michel Renoir, Olivier Trédan, Sylvie Chabaud, Isabelle Treilleux, Laura Corbo und Muriel Le Romancer. „Role of JMJD6 in Breast Tumourigenesis“. PLOS ONE 10, Nr. 5 (07.05.2015): e0126181. http://dx.doi.org/10.1371/journal.pone.0126181.

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19

Wilkinson, Simon, und Kevin M. Ryan. „Autophagy: an adaptable modifier of tumourigenesis“. Current Opinion in Genetics & Development 20, Nr. 1 (Februar 2010): 57–64. http://dx.doi.org/10.1016/j.gde.2009.12.004.

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20

Quail, Daniela F., Gabrielle M. Siegers, Michael Jewer und Lynne-Marie Postovit. „Nodal signalling in embryogenesis and tumourigenesis“. International Journal of Biochemistry & Cell Biology 45, Nr. 4 (April 2013): 885–98. http://dx.doi.org/10.1016/j.biocel.2012.12.021.

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21

Atkinson, Stuart P., und W. Nicol Keith. „Epigenetic control of cellular senescence in disease: opportunities for therapeutic intervention“. Expert Reviews in Molecular Medicine 9, Nr. 7 (März 2007): 1–26. http://dx.doi.org/10.1017/s1462399407000269.

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AbstractUnderstanding how senescence is established and maintained is an important area of study both for normal cell physiology and in tumourigenesis. Modifications to N-terminal tails of histone proteins, which can lead to chromatin remodelling, appear to be key to the regulation of the senescence phenotype. Epigenetic mechanisms such as modification of histone proteins have been shown to be sufficient to regulate gene expression levels and specific gene promoters can become epigenetically altered at senescence. This suggests that epigenetic mechanisms are important in senescence and further suggests epigenetic deregulation could play an important role in the bypass of senescence and the acquisition of a tumourigenic phenotype. Tumour suppressor proteins and cellular senescence are intimately linked and such proteins are now known to regulate gene expression through chromatin remodelling, again suggesting a link between chromatin modification and cellular senescence. Telomere dynamics and the expression of the telomerase genes are also both implicitly linked to senescence and tumourigenesis, and epigenetic deregulation of the telomerase gene promoters has been identified as a possible mechanism for the activation of telomere maintenance mechanisms in cancer. Recent studies have also suggested that epigenetic deregulation in stem cells could play an important role in carcinogenesis, and new models have been suggested for the attainment of tumourigenesis and bypass of senescence. Overall, proper regulation of the chromatin environment is suggested to have an important role in the senescence pathway, such that its deregulation could lead to tumourigenesis.
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22

Bai, Xiao-Hui, Hae-Ra Cho, Serisha Moodley und Mingyao Liu. „XB130—A Novel Adaptor Protein: Gene, Function, and Roles in Tumorigenesis“. Scientifica 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/903014.

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Several adaptor proteins have previously been shown to play an important role in the promotion of tumourigenesis. XB130 (AFAP1L2) is an adaptor protein involved in many cellular functions, such as cell survival, cell proliferation, migration, and gene and miRNA expression. XB130’s functional domains and motifs enable its interaction with a multitude of proteins involved in several different signaling pathways. As a tyrosine kinase substrate, tyrosine phosphorylated XB130 associates with the p85αregulatory subunit of phosphoinositol-3-kinase (PI3K) and subsequently affects Akt activity and its downstream signalling. Tumourigenesis studies show that downregulation of XB130 expression by RNAi inhibits tumor growth in mouse xenograft models. Furthermore, XB130 affects tumor oncogenicity by regulating the expression of specific tumour suppressing miRNAs. The expression level and pattern of XB130 has been studied in various human tumors, such as thyroid, esophageal, and gastric cancers, as well as, soft tissue tumors. Studies show the significant effects of XB130 in tumourigenesis and suggest its potential as a diagnostic biomarker and therapeutic target for cancer treatments.
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23

Wu, X., X. Liu, N. Lan, X. Zheng, Y. Chen, Z. Cai, P. Lan und X. Wu. „P069 CD73 promotes colitis-associated tumourigenesis in mice“. Journal of Crohn's and Colitis 14, Supplement_1 (Januar 2020): S170. http://dx.doi.org/10.1093/ecco-jcc/jjz203.198.

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Abstract Background Patients with inflammatory bowel disease (IBD) are at a higher risk of developing colitis-associated colorectal cancer. The aim of the present study was to investigate the role of CD73 in IBD-associated tumourigenesis. Methods A mouse model of colitis-associated tumourigenesis (CAT) induced by azoxymethane and dextran sulphate sodium (AOM/DSS) was successfully constructed. Model mice were injected with CD73 inhibitor or adenosine receptor agonist. Colon length, body weight loss and tumour formation were assessed macroscopically. Measurement of inflammatory cytokines and RNA sequencing on colon tissues were performed. Results Inhibition of CD73 by adenosine 5′-(α,β-methylene) diphosphate (APCP) suppressed the severity of CAT with attenuated weight loss, longer colons, lower tumour number and smaller tumour size when compared with the model group. On the other hand, activation of adenosine receptors using 1-(6-amino-9H-purin-9-yl)-1-deoxy-N-ethyl-β-d-ribofuranuronamide (NECA) exacerbated CAT. Histological assessment indicated that inhibition of CD73 reduced while activation of adenosine receptors exacerbated the histological damage of the colon compared with the model group. Increased expression of pro-inflammatory cytokines (tumour necrosis factor-α and interleukin-6) in colonic tissue was detected in the NECA group. According to the results of RNA sequencing, potential oncogenes such as ALOX15, Bcl2l15 and Nat8l were found to be downregulated in the APCP group and upregulated in the NECA group compared with the model group. Conclusion Therefore, inhibition of CD73 attenuated IBD-associated tumourigenesis, while activation of adenosine receptors exacerbated tumourigenesis in a C57BL/6J mouse model. This effect may be associated with the expression of pro-inflammatory cytokines and the regulation of ALOX15, Bcl2l15 and Nat8l.
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24

Aranha, M. M., P. M. Borralho, P. Ravasco, I. B. Moreira da Silva, L. Correia, A. Fernandes, M. E. Camilo und C. M. P. Rodrigues. „NF-?B and apoptosis in colorectal tumourigenesis“. European Journal of Clinical Investigation 37, Nr. 5 (Mai 2007): 416–24. http://dx.doi.org/10.1111/j.1365-2362.2007.01801.x.

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25

Levy, Andy. „Molecular and Trophic Mechanisms of Pituitary Tumourigenesis“. Hormone Research in Paediatrics 76, s1 (2011): 2–6. http://dx.doi.org/10.1159/000329114.

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26

Ioannou, Savvas, und Michael Voulgarelis. „Toll-Like Receptors, Tissue Injury, and Tumourigenesis“. Mediators of Inflammation 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/581837.

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Toll-like receptors (TLRs) belong to a class of molecules known as pattern recognition receptors, and they are part of the innate immune system, although they modulate mechanisms that impact the development of adaptive immune responses. Several studies have shown that TLRs, and their intracellular signalling components, constitute an important cellular pathway mediating the inflammatory process. Moreover, their critical role in the regulation of tissue injury and wound healing process as well as in the regulation of apoptosis is well established. However, interest in the role of these receptors in cancer development and progression has been increasing over the last years. TLRs are likely candidates to mediate effects of the innate immune system within the tumour microenvironment. A rapidly expanding area of research regarding the expression and function of TLRs in cancer cells and its association with chemoresistance and tumourigenesis, and TLR-based therapy as potential immunotherapy in cancer treatment is taking place over the last years.
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27

Nemenoff, Raphael A., und Robert A. Winn. „Role of nuclear receptors in lung tumourigenesis“. European Journal of Cancer 41, Nr. 16 (November 2005): 2561–68. http://dx.doi.org/10.1016/j.ejca.2005.08.015.

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28

Chatterjee, Aniruddha, Euan J. Rodger und Michael R. Eccles. „Epigenetic drivers of tumourigenesis and cancer metastasis“. Seminars in Cancer Biology 51 (August 2018): 149–59. http://dx.doi.org/10.1016/j.semcancer.2017.08.004.

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29

Sidhu, Stan, Christine Gicquel, Christopher P. Bambach, Peter Campbell, Christopher Magarey, Bruce G. Robinson und Leigh W. Delbridge. „Clinical and molecular aspects of adrenocortical tumourigenesis“. ANZ Journal of Surgery 73, Nr. 9 (September 2003): 727–38. http://dx.doi.org/10.1046/j.1445-2197.2003.02746.x.

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30

Biswas, S., D. Holyoake und T. S. Maughan. „Molecular Taxonomy and Tumourigenesis of Colorectal Cancer“. Clinical Oncology 28, Nr. 2 (Februar 2016): 73–82. http://dx.doi.org/10.1016/j.clon.2015.11.001.

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31

Lebelo, Maphuti T., Anna M. Joubert und Michelle H. Visagie. „Warburg effect and its role in tumourigenesis“. Archives of Pharmacal Research 42, Nr. 10 (31.08.2019): 833–47. http://dx.doi.org/10.1007/s12272-019-01185-2.

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32

Koutsi, Aikaterini, Angeliki Papapanagiotou und Athanasios G. Papavassiliou. „Thrombomodulin: From haemostasis to inflammation and tumourigenesis“. International Journal of Biochemistry & Cell Biology 40, Nr. 9 (Januar 2008): 1669–73. http://dx.doi.org/10.1016/j.biocel.2007.06.024.

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33

Jäger, Richard, und Howard O. Fearnhead. „“Dead Cells Talking”: The Silent Form of Cell Death Is Not so Quiet“. Biochemistry Research International 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/453838.

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After more than twenty years of research, the molecular events of apoptotic cell death can be succinctly stated; different pathways, activated by diverse signals, increase the activity of proteases called caspases that rapidly and irreversibly dismantle condemned cell by cleaving specific substrates. In this time the ideas that apoptosis protects us from tumourigenesis and that cancer chemotherapy works by inducing apoptosis also emerged. Currently, apoptosis research is shifting away from the intracellular events within the dying cell to focus on the effect of apoptotic cells on surrounding tissues. This is producing counterintuitive data showing that our understanding of the role of apoptosis in tumourigenesis and cancer therapy is too simple, with some interesting and provocative implications. Here, we will consider evidence supporting the idea that dying cells signal their presence to the surrounding tissue and, in doing so, elicit repair and regeneration that compensates for any loss of function caused by cell death. We will discuss evidence suggesting that cancer cell proliferation may be driven by inappropriate or corrupted tissue-repair programmes that are initiated by signals from apoptotic cells and show how this may dramatically modify how we view the role of apoptosis in both tumourigenesis and cancer therapy.
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Heiliger, Katrin-Janine, Julia Hess, Donata Vitagliano, Paolo Salerno, Herbert Braselmann, Giuliana Salvatore, Clara Ugolini et al. „Novel candidate genes of thyroid tumourigenesis identified in Trk-T1 transgenic mice“. Endocrine-Related Cancer 19, Nr. 3 (26.03.2012): 409–21. http://dx.doi.org/10.1530/erc-11-0387.

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For an identification of novel candidate genes in thyroid tumourigenesis, we have investigated gene copy number changes in aTrk-T1transgenic mouse model of thyroid neoplasia. For this aim, 30 thyroid tumours fromTrk-T1transgenics were investigated by comparative genomic hybridisation. Recurrent gene copy number alterations were identified and genes located in the altered chromosomal regions were analysed by Gene Ontology term enrichment analysis in order to reveal gene functions potentially associated with thyroid tumourigenesis. In thyroid neoplasms fromTrk-T1mice, a recurrent gain on chromosomal bands 1C4–E2.3 (10.0% of cases), and losses on 3H1–H3 (13.3%), 4D2.3–E2 (43.3%) and 14E4–E5 (6.7%) were identified. The genesTwist2,Ptma,Pde6d,Bmpr1b,Pdlim5,Unc5c,Srm,Trp73,Ythdf2,Taf12andSlitrk5are located in these chromosomal bands. Copy number changes of these genes were studied by fluorescencein situhybridisation on 30 human papillary thyroid carcinoma (PTC) samples and altered gene expression was studied by qRT-PCR analyses in 67 human PTC. Copy number gains were detected in 83% of cases forTWIST2and in 100% of cases forPTMAandPDE6D. DNA losses ofSLITRK1andSLITRK5were observed in 21% of cases and ofSLITRK6in 16% of cases. Gene expression was significantly up-regulated forUNC5CandTP73and significantly down-regulated forSLITRK5in tumours compared with normal tissue. In conclusion, a global genomic copy number analysis of thyroid tumours fromTrk-T1transgenic mice revealed a number of novel gene alterations in thyroid tumourigenesis that are also prevalent in human PTCs.
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35

Michel, E., C. Rohrer Bley, M. P. Kowalewski, S. K. Feldmann und I. M. Reichler. „Prolactin - to be reconsidered in canine mammary tumourigenesis?“ Veterinary and Comparative Oncology 12, Nr. 2 (28.06.2012): 93–105. http://dx.doi.org/10.1111/j.1476-5829.2012.00337.x.

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36

Chang, F., S. Syrjänen, A. Tervahauta und K. Syrjänen. „Tumourigenesis associated with the p53 tumour suppressor gene“. British Journal of Cancer 68, Nr. 4 (Oktober 1993): 653–61. http://dx.doi.org/10.1038/bjc.1993.404.

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37

Loveridge, Carolyn J., Sarah Slater, Kirsteen J. Campbell, Noor A. Nam, John Knight, Imran Ahmad, Ann Hedley et al. „BRF1 accelerates prostate tumourigenesis and perturbs immune infiltration“. Oncogene 39, Nr. 8 (18.11.2019): 1797–806. http://dx.doi.org/10.1038/s41388-019-1106-x.

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AbstractBRF1 is a rate-limiting factor for RNA Polymerase III-mediated transcription and is elevated in numerous cancers. Here, we report that elevated levels of BRF1 associate with poor prognosis in human prostate cancer. In vitro studies in human prostate cancer cell lines demonstrated that transient overexpression of BRF1 increased cell proliferation whereas the transient downregulation of BRF1 reduced proliferation and mediated cell cycle arrest. Consistent with our clinical observations, BRF1 overexpression in a Pten-deficient mouse (PtenΔ/ΔBRF1Tg) prostate cancer model accelerated prostate carcinogenesis and shortened survival. In PtenΔ/ΔBRF1Tg tumours, immune and inflammatory processes were altered, with reduced tumoral infiltration of neutrophils and CD4 positive T cells, which can be explained by decreased levels of complement factor D (CFD) and C7 components of the complement cascade, an innate immune pathway that influences the adaptive immune response. We tested if the secretome was involved in BRF1-driven tumorigenesis. Unbiased proteomic analysis on BRF1-overexpresing PC3 cells confirmed reduced levels of CFD in the secretome, implicating the complement system in prostate carcinogenesis. We further identify that expression of C7 significantly correlates with expression of CD4 and has the potential to alter clinical outcome in human prostate cancer, where low levels of C7 associate with poorer prognosis.
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38

Gonzalez-Meljem, Jose Mario, John Richard Apps, Helen Christina Fraser und Juan Pedro Martinez-Barbera. „Paracrine roles of cellular senescence in promoting tumourigenesis“. British Journal of Cancer 118, Nr. 10 (19.04.2018): 1283–88. http://dx.doi.org/10.1038/s41416-018-0066-1.

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39

Reed, Karen R., Simon J. Tunster, Madeleine Young, Adam Carrico, Rosalind M. John und Alan R. Clarke. „Entopic overexpression ofAscl2does not accelerate tumourigenesis in ApcMinmice“. Gut 61, Nr. 10 (03.12.2011): 1435–38. http://dx.doi.org/10.1136/gutjnl-2011-300842.

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40

SATO, Fumiaki, Shunsaku SASAKI, Fumitoshi CHINO und Daiji ENDOH. „Tumourigenesis by partial body X-irradiation in mice.“ Japanese Journal of Veterinary Science 50, Nr. 6 (1988): 1161–68. http://dx.doi.org/10.1292/jvms1939.50.1161.

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41

Muşat, Mădălina, Damian G. Morris, Márta Korbonits und Ashley B. Grossman. „Cyclins and their related proteins in pituitary tumourigenesis“. Molecular and Cellular Endocrinology 326, Nr. 1-2 (15.09.2010): 25–29. http://dx.doi.org/10.1016/j.mce.2010.03.017.

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42

Miyazawa, K. „Phosphoinositide 5-phosphatases: how do they affect tumourigenesis?“ Journal of Biochemistry 153, Nr. 1 (26.09.2012): 1–3. http://dx.doi.org/10.1093/jb/mvs107.

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43

Shirakawa, R., und H. Horiuchi. „Ral GTPases: crucial mediators of exocytosis and tumourigenesis“. Journal of Biochemistry 157, Nr. 5 (20.03.2015): 285–99. http://dx.doi.org/10.1093/jb/mvv029.

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44

Gardiner, Jennifer R., Yuichi Shima, Ken-ichirou Morohashi und Amanda Swain. „SF-1 expression during adrenal development and tumourigenesis“. Molecular and Cellular Endocrinology 351, Nr. 1 (März 2012): 12–18. http://dx.doi.org/10.1016/j.mce.2011.10.007.

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45

Angel, Peter. „AP-1-dependent gene expression during skin tumourigenesis“. European Journal of Cancer Supplements 4, Nr. 6 (Juni 2006): 4. http://dx.doi.org/10.1016/j.ejcsup.2006.04.004.

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46

Ma, Yanlei, Peng Zhang, Feng Wang, Jianjun Yang, Zhe Yang und Huanlong Qin. „The relationship between early embryo development and tumourigenesis“. Journal of Cellular and Molecular Medicine 14, Nr. 12 (Dezember 2010): 2697–701. http://dx.doi.org/10.1111/j.1582-4934.2010.01191.x.

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47

Diener, Kerrilyn R., Eleanor F. Need, Grant Buchanan und John D. Hayball. „TGF-β signalling and immunity in prostate tumourigenesis“. Expert Opinion on Therapeutic Targets 14, Nr. 2 (08.01.2010): 179–92. http://dx.doi.org/10.1517/14728220903544507.

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48

Myant, Kevin. „COLGENES - Defining novel mechanisms critical for colorectal tumourigenesis“. Impact 2017, Nr. 10 (25.11.2017): 12–14. http://dx.doi.org/10.21820/23987073.2017.10.12.

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Myant, Kevin. „COLGENES - Defining novel mechanisms critical for colorectal tumourigenesis“. Impact 2018, Nr. 7 (15.10.2018): 74–76. http://dx.doi.org/10.21820/23987073.2018.7.74.

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Radford, I. R. „Chromosomal rearrangement as the basis for human tumourigenesis“. International Journal of Radiation Biology 80, Nr. 8 (August 2004): 543–57. http://dx.doi.org/10.1080/09553000412331283489.

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