Дисертації з теми "Cancer transcription"
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Rheinheimer, Brenna Ann. "Alternative Transcription Of The SLIT2/Mir-218-1 Transcriptional Axis Mediates Pancreatic Cancer Invasion." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/605118.
Повний текст джерелаVance, Keith. "Cell type specific regulation of papillomavirus transcription." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340281.
Повний текст джерелаPomeranz, Karen M. "Regulation of FoxO transcription factors in breast cancer." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4253.
Повний текст джерелаSmith, Richard LeRoy. "Cis-regulatory Sequence and Co-regulatory Transcription Factor Functions in ERα-Mediated Transcriptional Repression". BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2261.
Повний текст джерелаTse, Yuen-yu Belinda, and 謝宛余. "Expression of FOXP1 in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193527.
Повний текст джерелаpublished_or_final_version
Pathology
Master
Master of Medical Sciences
Essack, Magbubah. "Transcription Regulation and Candidate Diagnostic Markers of Esophageal Cancer." Thesis, University of the Western Cape, 2009. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5306_1267148426.
Повний текст джерелаThis thesis reports on the development of a novel comprehensive database (Dragon Database of Genes Implicated in Esophageal Cancer, DDEC) as an integrated knowledge database aimed at representing a gateway to esophageal cancer related data. More importantly, it illustrates how the biocurated genes in the database may represent a reliable starting point for divulging transcriptional regulation, diagnostic markers and the biology related to esophageal cancer.
Williams, Christopher M. J. "Transcription factor AP-2 regulatory signatures in breast cancer." Thesis, Queen Mary, University of London, 2007. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1644.
Повний текст джерелаWiseman, Elizabeth Fiona. "Novel FOXM1 transcription factor target genes in oesophageal cancer." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/novel-foxm1-transcription-factor-target-genes-in-oesophageal-cancer(24278706-fa41-41b9-bf59-1902b1c4ba3d).html.
Повний текст джерелаGherardi, Samuele <1981>. "Myc-mediated control of gene transcription in cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2809/1/Gherardi_Samuele_Tesi.pdf.
Повний текст джерелаGherardi, Samuele <1981>. "Myc-mediated control of gene transcription in cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2809/.
Повний текст джерелаMorachis, José Manuel. "Cancer, cell fate, and transcription regulation of the p53 transcriptional response by structurally diverse core promoters /." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3390092.
Повний текст джерелаTitle from first page of PDF file (viewed Feb. 24, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Alghamdi, Youssef Saeed H. "Transcriptional and translational control of the expression of the EMT transcription factor ZEB2 in cancer cells." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37698.
Повний текст джерелаChen, Chien-Cheng. "Mechanisms of transcriptional activation of estrogen responsive genes in breast cancer cells." Thesis, [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1869.
Повний текст джерелаWu, Lai-han. "Expression of FOXO3a in breast cancer /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38284376.
Повний текст джерелаNicolle, Rémy. "Regulatory networks driving bladder cancer." Thesis, Evry-Val d'Essonne, 2015. http://www.theses.fr/2015EVRY0009/document.
Повний текст джерелаCarcinogenesis is a consequence of the unceasing activation of cell proliferation. In normal cells, mito-genic stimuli are processed by a complex network of protein interactions and enzymatic reactions, often referred to as pathways, which can eventually trigger the activation of new genes to engage the cell into mitosis. During developmental or wound healing processes, this complex regulation of cellular phenotypes results in a tight control of the number and behavior of cells and therefore contributes to the maintenance of a functional and healthy tissue architecture. Based on genomic, transcriptomic and proteomic profiles of bladder tumors and transcriptomes of nor-mal urothelial cells at various states of proliferation and differentiation, I devised novel methodologies to characterize the pathways driving bladder cancer. I first developed a set of tools to identify and visualize sample and subtype-specific transcriptional pro-grams through the inference of a co-regulatory network and the prediction of transcription factor activity. These methods were embedded in a Bioconductor package entitled CoRegNet (bioconductor.org). The measure of transcriptional activity is based on the influence of a transcription factor on the expression of its target genes and was used to characterize the most active regulators of each bladder cancer subtypes. The integration of genomic profiles highlighted two altered transcription factors with driver roles in lumi-nal-like and basal-like bladder cancer, one of which was experimentally validated. The use of CoRegNet to model the contribution of regulatory programs of normal proliferation and diffe-rentiation in bladder cancers underlined a strong preservation of normal networks during tumorigenesis. Furthermore, a regulator of normal proliferation was found to be constitutively activated by genetic al-terations and its influence on bladder cancer cell proliferation was experimentally validated. In addition, a master regulator of urothelial differentiation was found to have a loss of activity in nearly all tumors. This was then associated to the discovery of frequent inactivating mutations and further analysis unco-vered a major role in differentiated tumors. In order to characterize signaling pathways from proteomic pull-down assays, I then designed a novel algorithm to grow a densely connected network from a set of proteins and a repository of protein interac-tions. The proposed algorithm was made available as a Cytoscape application named Pepper for Protein Complex Expansion using Protein- Protein interaction networks (apps.cytoscape.org). Finally, using both a proteomic pull-down assay of the bladder cancer oncogene FGFR3 and a transcrip-tomic profiling of its downstream regulated genes, I applied Pepper to characterize the full FGFR3 signa-ling pathway from its protein partners to the downstream transcriptional regulators. In particular, this uncovered a regulatory link between FGFR3 and the tumor suppressor TP53
Cutress, Ramsey Ian. "BAG 1 expression and function in breast cancer." Thesis, University of Southampton, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289513.
Повний текст джерелаTam, Christine. "Defining microenvironment-induced transcription profiles in breast cancer liver metastases." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=123094.
Повний текст джерелаLe cancer du sein est le cancer le plus fréquent chez la femme au Canada. Les métastases demeurent la principale cause de décès associée au cancer du sein. Chez ces patients, le foie est le troisième site le plus fréquent pour la formation de métastases. À ce jour, très peu est connu concernant les interactions éventuelles entre le microenvironnement hépatique et les cellules cancéreuses qui y croissent. Pour ce faire, nous avons utilisé un processus de sélection in vivo pour générer, à partir des cellules 4T1, des sous-populations de cellules murines de cancer du sein. Ainsi, les cellules obtenues ont pour caractéristique principale de former des tumeurs mammaires mais surtout de préférentiellement former des métastases hépatiques dans les souris Balb/c. Dans le but de déterminer les changements d'expression des gènes qui se produisent pendant le processus de développement des métastases au foie, nous avons initialement collecté des tumeurs primaires et des métastases hépatiques après trois différentes périodes de temps. Par la suite, nous avons utilisé la microdissection par capture laser pour isoler différentes régions dans les tumeurs ou les métastases, soit le centre des lésions, la périphérie des lésions ou des régions de foie non cancéreuses adjacentes ou distales aux lésions. L'analyse de l'expression des gènes a révélé de nombreuses différences dans l'expression des gènes entre les tumeurs mammaires et les métastases hépatiques. Ainsi, en comparant les métastases hépatique aux tumeurs primaires, nous avons identifié la surexpression d'un ensemble de gènes normalement exprimés par les cellules myéloïdes ou granulocytaires. Parmi ces gènes, Lcn2 et S100a8/S100a9 sont exprimé exclusivement par les cellules immunitaires présentes au niveau des métastases, surtout au niveau des plus petites lésions. Considérant que des études conduites dans notre laboratoire ont également démontré un recrutement similaire de cellules immunitaire Gr1+/NE+ (neutrophiles) au niveau des métastases au foie, il appert que Lcn2 et S100a8/a9 représentent des candidats intéressants pour l'étude des interactions entre système immunitaire et cellules cancéreuses pour le développement de métastases hépatiques dérivées du cancer du sein.
Maritz, Michelle Frances. "Inhibition of the transcription factor AP-1 in cervical cancer." Master's thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/3138.
Повний текст джерелаAP-I is a dimeric transcription factor comprised primarily of Jun and Fos family proteins, that regulates numerous genes involved in cell proliferation, differentiation and oncogenesis. The expression of AP-I is shown to play an important role in many human cancers and plays a key role in the regulation of the E6 and E7 oncoproteins of high-risk Human Papillomaviruses (HPV) that are etiologically associated with cervical cancer. The c-Jun and Jun B components of AP-I were shown to be expressed at higher levels in cervical cancer patients compared to nonnal patient tissue while Jun D levels were largely unchanged. To define the role of AP-I in cervical cancer, the effect of inhibiting AP-I actvity was determined using a dominantnegative deletion mutant T AM67. CaSki cervical cancer cells with a doxycycline inducible T AM67 demonstrated that inhibition of AP-I activity and expression resulted in an altered cell morphology, a significant decrease in cell proliferation and inhibition of colony formation. This was accompanied by a slower progression of T AM67 expressing cells through the cell cycle, with an accompanying increase in G21M phase. An increase in the expression of the cell cycle regulatory protein, p21 CIPI, was observed that appeared independent of p53 expression. siRNA directed at inhibiting individual AP-I components showed that Jun B was an important regulator of CaSki cell proliferation. These results suggest that AP-I is involved in the cell proliferation and tumourigenic phenotype of cervical cancer cells, such as CaSki cells, possibly via a direct repression of cell cycle regulator p21 CIP1
Johnson, Kevin. "PTP1B regulation of the transcription factor Stat5 in breast cancer." Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/454241197/viewonline.
Повний текст джерелаDAS, VIVEK. "LEVERAGING TRANSCRIPTOMIC ANALYSIS TO IDENTIFY TRANSCRIPTION FACTORS ORCHESTRATING CANCER PROGRESSION." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/559711.
Повний текст джерелаCrighton, Diane. "Regulation of RNA polymerase III transcription by the tumour suppessor p53." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252510.
Повний текст джерелаBrulliard, Marie. "Infidélité de transcription et carcinogénèse. Analyse bioinformatique et preuves de concept biologiques." Thesis, Vandoeuvre-les-Nancy, INPL, 2009. http://www.theses.fr/2009INPL037N/document.
Повний текст джерелаOne of the aim of the fight against cancer is to understand the heterogeneity of cancer cells. The goal of our work has been to explore cancer cell mRNA heterogeneity. ESTs (Expressed Sequence Tags) extracted from normal and cancer tissues have been aligned to mRNA reference sequences. This allowed identification of non-random sequence variations that occurred at statistically significant increased rates in cancer compared to normal libraries. This analysis first focused on 17 abundant transcripts and was next extended to whole human genome, as well as to that of Mus musculus. The results show an increase of transcription infidelity events in cancer tissues. Three types of events occur, i.e. base substitutions, deletions and insertions. Bioinformatics results have been validated through different biological methods. First, the cloning and sequencing of mRNA from lung cancer human with a deletion occurring at bioinformatically predicted position in absence of somatic mutation has been achieved. Then, mass spectrometry analysis confirmed the existence of protein variants resulting from translation of mRNA bypassing stop codon. Finally, we showed that transcription infidelity peptides contain specific epitopes of immunoglobulins ; detection of changes in immunoglobulins in patients with cancers opens a novel path toward early stage cancer diagnosis. This increased transcription infidelity in cancer contributes to the heterogeneity of cancer cells. This finding opens novel perspectives and strategies toward understanding carcinogenesis and diagnostic of the disease
Zhao, Fung, and 趙楓. "Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/211053.
Повний текст джерелаpublished_or_final_version
Pathology
Doctoral
Doctor of Philosophy
Brulliard, Marie Bihain Bernard Méjean Luc. "Infidélité de transcription et carcinogénèse. Analyse bioinformatique et preuves de concept biologiques." S. l. : S. n, 2009. http://www.scd.inpl-nancy.fr/theses/2009_BRULLIARD_M.pdf.
Повний текст джерелаNixon, Paula. "Patterns of gene expression controlled by AP 2 in breast cancer." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271013.
Повний текст джерелаLin, Yiwei. "THE LINKAGE BETWEEN TRANSCRIPTION CONTROL AND EPIGENETIC REGULATION: THE SNAIL STORY AND BEYOND." UKnowledge, 2012. http://uknowledge.uky.edu/pharmacol_etds/2.
Повний текст джерелаRoberts, Melyssa Susann. "TARGETING BREAST CANCER TRANSCRIPTION-DRIVEN SIGNALING PATHWAYS TO IMPROVE THERAPEUTIC RESPONSE IN TRIPLE NEGATIVE BREAST CANCER." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1586195580085135.
Повний текст джерелаSharili, Amir Shaya. "The role of Snail2 transcription factor in osteosarcoma." Thesis, Royal Veterinary College (University of London), 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572481.
Повний текст джерелаLow, Carolyn M. "Genomic interactions of the transcription factor VEZF1." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/5078/.
Повний текст джерелаTang, Yuk-fong, and 鄧玉芳. "The expression of transcription factors Pea3 and Snail in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4467076X.
Повний текст джерелаHasleton, Mark Daniel. "Regulation of transcription factor AP-2 expression in breast cancer cells." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248230.
Повний текст джерелаMore, Piyush [Verfasser]. "Relevance of transcription to topoisomerase II-mediated cancer treatments / Piyush More." Mainz : Universitätsbibliothek Mainz, 2019. http://d-nb.info/1185541527/34.
Повний текст джерелаWu, Pei Hsin, and 吳佩欣. "The expression of transcription factors TWIST and Snail in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47468907.
Повний текст джерелаpublished_or_final_version
Pathology
Master
Master of Medical Sciences
Ferrari, Nicola. "Investigating RUNX transcription factors in mammary gland development and breast cancer." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4790/.
Повний текст джерелаKaradedou, Christina Theano. "Forkhead transcription factors in the regulation of VEGF in breast cancer." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7113.
Повний текст джерелаSchmidt, Xénia. "TOX3 – A candidate breast cancer predisposition gene." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21831/document.
Повний текст джерелаTwo thirds of breast cancers express the estrogen receptor alpha (ERα) and are estrogen-dependent for growth. In contrast, expression of ERα induces differentiation and senescence in normal human mammary epithelial cells. Both embryonic development and lineage commitment in the adult mammary gland are governed by transcriptional regulators, many of which have also been implicated in tumourigenesis. Genome-wide association studies have identified the previously uncharacterised putative transcription factor TOX high mobility group box family member 3 (TOX3) as a new candidate breast cancer susceptibility gene.In the present study, I aimed to characterise TOX3 function in the normal human mammary epithelium and in breast cancer.I have examined TOX3 expression in primary breast tumours and in the normal mammary gland using micorarray data. The influence of TOX3 expression on lineage commitment was investigated using the colony forming cell (CFC) assay and FACS analysis. I further carried out microarray analysis of luminal breast cancer cells ectopically expressing TOX3 to identify TOX3 target genes as well as tandem affinity purification of TOX3 to identify TOX3 interacting proteins. Finally, the oncogenic potential of TOX3 was investigated in a human-in-mouse xenograft model
Wu, Lai-han, and 胡麗嫻. "Expression of FOXO3a in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011515.
Повний текст джерелаTreilleux, Isabelle. "Cancer du sein et oestrogènes : régulation de l'expression du récepteur aux oestrogènes humain." Lyon 1, 1997. http://www.theses.fr/1997LYO1T161.
Повний текст джерела陳鴻霖 and Hong-lin Chen. "Transcription of the epstein-barr virus genome in nasopharyngeal carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1992. http://hub.hku.hk/bib/B31232486.
Повний текст джерелаTse, Yuk-ting Edith. "Estrogen receptor gene polymorphisms and breast cancer risk in the Chinese population." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38709466.
Повний текст джерелаEllison, Jason. "Identification of target genes of PEA3, an ETS family transcription factor /." *McMaster only, 2001.
Знайти повний текст джерелаBenizri, Emmanuel. "HIF-1alpha : le poumon du cancer." Nice, 2007. http://www.theses.fr/2007NICE4044.
Повний текст джерелаAny alive organism can survive without energy, which involves a satisfactory oxygen and nutriments supply. At the initial phase of tumor progression, cells proliferate without their own vascularization ; indeed, oxygen and nutrients are delivered by simple diffusion. Nevertheless, beyond a certain size, these mechanisms are no more effective and oxygen deficiencies appear. The transcription factor HIF (Hypoxia Inducible Factor) is a key regulator required to maintain oxygen homeostasis. HIF is composed of a constitutive HIF-â sub-unit and a HIF- 1á sub-unit, specific of the hypoxic cascade. Three hifá genes have been identified : hif1a, epas 1 and hif3a that code for HIF-1á, HIF-2á and HIF-3á, respectively. Because of its ubiquitous tissue distribution and its central impact on the regulation of the target genes, HIF- 1á is the mosty studied isoform. During my laboratory training, I have contributed to 3 main projects : • First, I have been focused on the regulatory mechanisms that control HIF-1á stability and more precisely, on the study of the HIF prolyl-hydroxylase (PHDs). Using a RNA interference (RNAi) approach, we have highlighted PHD2 as the key isoform that controls HIF-1á stability in normoxia. Related to clinical studies, we have evaluated the impact of HIF-1á immunostaining in a serie of breast cancer. We have shown that HIF-1á is an independent prognostic factor and a bad preditive factor for classical adjuvant treatments. • Finally, in a pre-clinical study, we have analyzed the impact of HIF-1á invalidation by RNAi in a xenograft melanoma model. We have reported a reduction of tumor growth in mice treated with siRNAs targeting HIF-1á
O'Hanlon, Brown Ciara. "The role of MAF, an androgen regulated transcription factor in prostate cancer." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/39123.
Повний текст джерелаCain, Henry James. "A study of transcription factors STAT3, SP1 and NFkB in breast cancer." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1333.
Повний текст джерелаKeld, Richard. "ETS domain transcription factor PEA3 sub family and oesophageal and gastric cancer." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509380.
Повний текст джерелаKavanagh, Claire Louise. "Investigating the role of specific LEF/TCF transcription factors in colorectal cancer." Thesis, University of Aberdeen, 2008. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU492219.
Повний текст джерелаFilippi, Letizia. "Epigenetic Control of YAP/TAZ-Mediated Transcription." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3425760.
Повний текст джерелаLe cellule tumorali per sostenere l’elevato ritmo di crescita richiamano un maggior numero di fattori trascrizionali e modificatori della cromatina, diventando dipendenti dagli stessi, portando così ad un globale aumento della trascrizione. La “transcriptional addiction” è un tema sempre più emergente nella biologia del cancro, ma ad oggi sia il meccanismo che i fattori coinvolti rimangono sconosciuti. Si è ipotizzato che YAP e TAZ, due cofattori trascrizionali, potessero essere ottimi candidati per mediare queste dipendenze in differenti contesti cellulari. YAP/TAZ ricoprono un ruolo fondamentale nel cancro, prendendo parte nell’iniziazione, progressione ed induzione di metastasi. In questo progetto di ricerca abbiamo identificato un legame fisico e funzionale tra YAP/TAZ e un membro della famiglia delle proteine BET, BRD4. Tramite ChIP-seq abbiamo dimostrato che il già noto legame di YAP/TAZ a siti enhancers media il reclutamento di BRD4 sugli stessi siti e sui promotori dei geni regolati da YAP/TAZ, richiamando l’RNA polimerasi II e permettendo la successiva trascrizione dei geni a valle. La relazione YAP/TAZ-BRD4 conferisce un vantaggio trascrizionale a geni principalmente coinvolti nella proliferazione e nel ciclo cellulare; allo stesso tempo però l’accumulo di BRD4 su queste regioni di cromatina conferisce una certa sensibilità ai target di YAP/TAZ all’azione di inibitori farmacologici delle proteine BET. L’azione inibitoria di queste molecole si è rivelata efficace anche in vivo su modelli di tumore dipendenti da YAP/TAZ e inoltre sulla capacità di sovvertire la resistenza al Vemurafenib in linee cellulari di melanoma. Questi risultati aprono una nuova finestra di opportunità terapeutiche dove i BET-inhibitors usati da soli o in combinazione con farmaci preesistenti possono contrastare l’attività pro-tumorigenica di YAP/TAZ in diversi tessuti.
Maquaire, Sabrina. "Rôle de la protéine nucléophosmine (NPM1/B23) dans la physiologie des tissus sensibles aux androgènes et la physiopathologie prostatique." Thesis, Clermont-Ferrand 2, 2011. http://www.theses.fr/2011CLF22162.
Повний текст джерелаSutcliffe, Josephine E. "The regulation of RNA polymerase I and RNA polymerase III transcription by the pocket proteins." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327577.
Повний текст джерелаPascali, Chiara. "Identification à l'échelle génomique de gènes transcrits par deux isoformes de l'ARN polymérase III humaine." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21813/document.
Повний текст джерелаIn eukaryotes, transcription is carried out by DNA-dependent RNA polymerases I, II and III (or I-V inplants). These RNA polymerases are specialized in the transcription of specific groups of genes.Human RNA polymerase III (Pol III) transcribes small noncoding RNAs involved in the regulation oftranscription (7SK RNA), RNA processing (U6 RNA, RNAse P, RNAse MRP), translation (tRNAs,5S RNA) or other cellular processes (vault RNAs [multidrug resistance], adenoviral RNAs [VA-I,VA-II], Epstein-Barr virus RNAs [EBER1, EBER2]). It has furthermore been reported that somemicroRNAs of viral or cellular origin may also be transcribed by Pol III.Interestingly, increased Pol III transcription levels accompany or cause cell transformation. Themechanisms underlying this phenomenon are still largely unknown. Recently, two distinct isoforms ofhuman Pol III have been discovered (Haurie et al., 2010). RPC32β-containing Pol IIIβ is ubiquitouslyexpressed and essential for growth and survival of human cells. In contrast, RPC32α-containing PolIIIα is dispensable for cell survival and its expression is restricted to undifferentiated embryonic stem(ES) cells and to tumor cells.The distinct effects of Pol IIIα and Pol III β on cell growth and transformation may be explained bythe transcription of isoform-specific target genes. To identify such isoform-specific target genes, wespecifically targeted RPC32α and of RPC32β subunits in chromatin immunoprecipitation (ChIP)experiments and analyzed the co-precipitated DNA sequences by high throughput sequencing (ChIPseq.).Genome wide localization of RPC32α and RPC32β subunits of Pol III revealed the presence of bothsubunits on many of the known Pol III-transcribed genes, suggesting redundant activities of bothisoforms of Pol III in transcription of these genes. We also found that some of the genes known to betranscribed by Pol III are only occupied by either RPC32α or by RPC32β, suggesting that these genesare exclusively transcribed by Pol IIIα or by Pol IIIβ, respectively.RPC32α and RPC32β ChIP-seq. results furthermore led to the identification of novel Pol III candidategenes in HeLa cells. Moreover, we found high levels of Pol IIIα or Pol III β at some of the annotatedtRNA pseudogenes, implicating that these genes may be transcribed. The functions of RNAstranscribed from novel putative Pol III genes or from tRNA pseudogenes remain to be determined