File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Mouse models of human chromosomal translocations and approaches to cancer therapy

TitleMouse models of human chromosomal translocations and approaches to cancer therapy
Authors
Issue Date2001
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybcmd
Citation
Blood Cells, Molecules, And Diseases, 2001, v. 27 n. 1, p. 249-259 How to Cite?
AbstractCancer arises because of genetic changes in somatic cells, eventually giving rise to overt malignancy. Principle among genetic changes found in tumor cells are chromosomal translocations which give rise to fusion genes or enforced oncogene expression. These mutations are tumor-specific and result in production of tumor-specific mRNAs and proteins and are attractive targets for therapy. Also, in acute leukemias, many of these molecules are transcription regulators which involve cell-type-specific complexes, offering an alternative therapy via interfering with protein-protein interaction. We are studying these various features of tumor cells to evaluate new therapeutic methods. We describe a mouse model of de novo chromosomal translocations using the Cre-loxP system in which interchromosomal recombination occurs between the Mll and Af9 genes. We are also developing other in vivo methods designed, like the Cre-loxP system, to emulate the effects of these chromosomal abnormalities in human tumors. In addition, we describe new technologies to facilitate the intracellular targeting of fusion mRNAs and proteins resulting from such chromosomal translocations. These include a masked antisense RNA method with the ability to discriminate between closely related RNA targets and the selection and use of intracellular antibodies to bind to target proteins in vivo and cause cell death. These approaches should also be adaptable to targeting point mutations or to differentially expressed tumor-associated proteins. We hope to develop therapeutic approaches for use in cancer therapy after testing their efficacy in our mouse models of human cancer. © 2001 Academic Press.
Persistent Identifierhttp://hdl.handle.net/10722/162499
ISSN
2015 Impact Factor: 2.731
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRabbitts, THen_US
dc.contributor.authorAppert, Aen_US
dc.contributor.authorChung, Gen_US
dc.contributor.authorCollins, ECen_US
dc.contributor.authorDrynan, Len_US
dc.contributor.authorForster, Aen_US
dc.contributor.authorLobato, MNen_US
dc.contributor.authorMccormack, MPen_US
dc.contributor.authorPannell, Ren_US
dc.contributor.authorSpandidos, Aen_US
dc.contributor.authorStocks, MRen_US
dc.contributor.authorTanaka, Ten_US
dc.contributor.authorTse, Een_US
dc.date.accessioned2012-09-05T05:20:33Z-
dc.date.available2012-09-05T05:20:33Z-
dc.date.issued2001en_US
dc.identifier.citationBlood Cells, Molecules, And Diseases, 2001, v. 27 n. 1, p. 249-259en_US
dc.identifier.issn1079-9796en_US
dc.identifier.urihttp://hdl.handle.net/10722/162499-
dc.description.abstractCancer arises because of genetic changes in somatic cells, eventually giving rise to overt malignancy. Principle among genetic changes found in tumor cells are chromosomal translocations which give rise to fusion genes or enforced oncogene expression. These mutations are tumor-specific and result in production of tumor-specific mRNAs and proteins and are attractive targets for therapy. Also, in acute leukemias, many of these molecules are transcription regulators which involve cell-type-specific complexes, offering an alternative therapy via interfering with protein-protein interaction. We are studying these various features of tumor cells to evaluate new therapeutic methods. We describe a mouse model of de novo chromosomal translocations using the Cre-loxP system in which interchromosomal recombination occurs between the Mll and Af9 genes. We are also developing other in vivo methods designed, like the Cre-loxP system, to emulate the effects of these chromosomal abnormalities in human tumors. In addition, we describe new technologies to facilitate the intracellular targeting of fusion mRNAs and proteins resulting from such chromosomal translocations. These include a masked antisense RNA method with the ability to discriminate between closely related RNA targets and the selection and use of intracellular antibodies to bind to target proteins in vivo and cause cell death. These approaches should also be adaptable to targeting point mutations or to differentially expressed tumor-associated proteins. We hope to develop therapeutic approaches for use in cancer therapy after testing their efficacy in our mouse models of human cancer. © 2001 Academic Press.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybcmden_US
dc.relation.ispartofBlood Cells, Molecules, and Diseasesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDrug Delivery Systems - Methodsen_US
dc.subject.meshHumansen_US
dc.subject.meshMice - Geneticsen_US
dc.subject.meshNeoplasms - Therapyen_US
dc.subject.meshTranslocation, Genetic - Geneticsen_US
dc.titleMouse models of human chromosomal translocations and approaches to cancer therapyen_US
dc.typeArticleen_US
dc.identifier.emailTse, E:ewctse@hku.hken_US
dc.identifier.authorityTse, E=rp00471en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1006/bcmd.2000.0371en_US
dc.identifier.pmid11358385-
dc.identifier.scopuseid_2-s2.0-0035054171en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035054171&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume27en_US
dc.identifier.issue1en_US
dc.identifier.spage249en_US
dc.identifier.epage259en_US
dc.identifier.isiWOS:000167738300029-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRabbitts, TH=7103136845en_US
dc.identifier.scopusauthoridAppert, A=6602281646en_US
dc.identifier.scopusauthoridChung, G=9246670000en_US
dc.identifier.scopusauthoridCollins, EC=7201612726en_US
dc.identifier.scopusauthoridDrynan, L=6505956605en_US
dc.identifier.scopusauthoridForster, A=7201638425en_US
dc.identifier.scopusauthoridLobato, MN=35870245400en_US
dc.identifier.scopusauthoridMcCormack, MP=7006728062en_US
dc.identifier.scopusauthoridPannell, R=7004261694en_US
dc.identifier.scopusauthoridSpandidos, A=6506753927en_US
dc.identifier.scopusauthoridStocks, MR=36756716600en_US
dc.identifier.scopusauthoridTanaka, T=7406725547en_US
dc.identifier.scopusauthoridTse, E=7005019454en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats