A new filamentous phage cloning vector: fd-tet

Zacher, Allan N.; Stock, Carolyn; Golden, James W.; Smith, George P.

doi:10.1016/0378-1119(80)90171-7

Cited by 111 publications

(58 citation statements)

References 11 publications

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“…␣v integrin-binding (10,14,15), IL11R-binding (21), and APA-binding (22) phage were described; the insertless fd-tet phage (13) or phage displaying unrelated peptide sequences served as controls. Design and genetic construction of targeted AAVP-based vectors is detailed in ref.…”

Section: Methodsmentioning

confidence: 99%

“…We have introduced a hybrid vector that enables convergence of ligand-directed targeting and molecular imaging (10)(11)(12); such vector incorporates genomic cis-elements of adeno-associated virus (AAV) and of an M13-derived (13) phage [AAV phage (AAVP)]. Our prototype displays CDCRGDCFC (RGD-4C) to target ␣v integrins (14,15) and systemically deliver transgenes to tumors (10)(11)(12).…”

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confidence: 99%

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A preclinical model for predicting drug response in soft-tissue sarcoma with targeted AAVP molecular imaging

Hajitou

Lev

Hannay

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Human sarcomas are rare but diverse malignant tumors derived from mesenchymal tissue. Clinical response to therapy is currently determined by the modified World Health Organization (WHO) criteria or the Response Evaluation Criteria in Solid Tumors (RECIST), but these standards correlate poorly with sarcoma patient outcome. We introduced ligand-directed particles with elements of AAV and phage (AAVP) to enable integration of tumor targeting to molecular imaging. We report drug-response monitoring and prediction in a nude rat model of human sarcoma by AAVP imaging. As a proof-of-concept, we imaged Herpes simplex thymidine kinase in a clinic-ready setting with PET to show that one can a priori predict tumor response to a systemic cytotoxic. Given the target expression in patient-derived sarcomas, this platform may be translated in clinical applications. Sarcoma-specific ligands and promoters may ultimately lead to an imaging transcriptome.H uman sarcomas are rare yet heterogeneous malignant tumors from mesenchymal tissues (1). Monitoring drug responses in soft-tissue sarcoma has long been clinically problematic. Currently, responses are determined by the modified World Health Organization (WHO) criteria (2-4) or the Response Evaluation Criteria in Solid Tumors (RECIST) (5-7), which require marked tumor size decrease for patients to be considered responding to therapy. A major assumption of these criteria is that a solid tumor volume is directly proportional to the cancer cell number. However, in soft-tissue sarcomas, there are reasons to challenge such an assumption (8). First, in addition to tumor cells, sarcomas contain nonmalignant stromal cells and extracellular matrix (ECM) that do not disappear, even if the malignant component is treated. Moreover, when cytotoxics are used against sarcomas, there is often associated necrosis resulting in reduced total cell number but not necessarily overall tumor size changes. Finally, even if a soft-tissue sarcoma is predominantly or entirely composed of cancer cells, its remnant composition may not be fully eliminated when tumor cells are destroyed by therapy, because myxoid-type degeneration is not always promptly removed. Ultimately, the modified WHO criteria and RECIST correlate poorly with drug response and outcome in patients with soft-tissue sarcomas; validation in this setting is sporadic and restricted. In another level of complexity, drug responses in patients with soft-tissue sarcoma are determined through standard methods, such as CT, MRI, or PET scans. However, because systematic quantitative measurements have not been established because of the rarity and diversity of soft-tissue sarcomas, decreases in tumor size and/or density are not accepted as unequivocal evidence of response. Consequently, many conventional soft-tissue sarcoma responses in individual patients are evaluated qualitatively. Thus, new or alternative quantitative imaging criteria to improve management and follow-up of responses were proposed in ref. 9.We have introduced a hybrid vector that ena...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

A preclinical model for predicting drug response in soft-tissue sarcoma with targeted AAVP molecular imaging

Hajitou

Lev

Hannay

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…Plasmid pJH16 is a pACYC184 derivative that contains a cat gene and the fl origin and packaging signal; it was constructed and kindly provided by J. Heitman. Bacteriophages fd tet (27), an infectious filamentous phage that contains the tetracycline resistance gene from TnJO, and fKN16, a derivative of fd tet containing a 507-base deletion in gene III (17), were obtained from G. Smith.…”

Section: Methodsmentioning

confidence: 99%

Low-frequency infection of F- bacteria by transducing particles of filamentous bacteriophages

et al. 1988

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Filamentous particles containing single-stranded plasmid and bacteriophage DNA are able to infect FEscherichia coli at frequencies of approximately 10-6. This infection is dependent on an intact particle and requires the products of the tolQ, tolR, and toUl genes of the bacteria. The addition of CaCl2 can increase the frequency about 100-fold, presumably by increasing the concentration of particles at the bacterial surface.The filamentous bacteriophages fl, fd, and M13 form plaques only on Escherichia coli that have F pili, while the related filamentous phage Ike forms plaques only on E. coli that have N pili. These pili are extracellular structures that confer donor activity in bacterial conjugation (4, 10, 18). Pilin, the major structural protein of pili, and additional proteins required for its assembly are encoded by genes carried on the F or N conjugative plasmids. The filamentous phages require pili for entry of the genome into the bacterium but not for replication and assembly, as E. coli lacking the F factor produce phage efficiently when fl DNA is introduced into them by transformation (13).A number of studies have strongly suggested that infection by filamentous phage is a multistep process. Initially, the particle binds to the tip of the pilus via an interaction with the phage-encoded gene III protein located at one end of the phage particle (for reviews, see references 15 and 19). It is postulated that the pilus subsequently depolymerizes into the membrane, thereby bringing the tip of the phage particle to the surface of the bacterium. There the particle must interact with additional proteins in order for the viral DNA to translocate into the cytoplasm (24,25). This step in the entry pathway is defined by mutations in the tolQ, tolR, and tolA genes of E. coli which render F+ bacteria uninfectable by filamentous phages. These mutant bacteria are still fully competent to undergo conjugation and are able to bind filamentous phages to the tips of their pili (24). In addition, tol mutants are not killed by (they are tolerant to) the colicins El, E2, and E3 (16, 25), although they retain the ability to bind the colicins to a specific receptor defined by the bacterial btuB locus (5, 11).These observations suggest that pili serve as the primary receptors for the filamentous phages, providing both an attachment site and perhaps a mechanism for bringing the particle close to the bacterial membrane where the ToIQ, ToiR, and TolA proteins are located (24). This paper supports this idea by demonstrating that transducing particles of filamentous phages can bypass the pilus and infect F-E. coli at low efficiencies.MATERIALS AND METHODS Strains and plasmids. The F-strains of E. coli used in this study are shown in Table 1 and are all derivatives of the K-12 strain C600. The mutations in orf-J, tolQ, toIR, and tolA were introduced into K17 by P1 transduction. The * Corresponding author. rfaC2::TnJO allele from CS1700 (provided by C. Schnaitman) was introduced into A593 by P1 transduction. The plasmids pD8, pKUN1, pKA...

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“…Recently, a hybrid vector using elements of adenoassociated virus (AAV) and fd-tet phage, 10 an M13-based bacteriophage, was developed. 9 Bacteriophage vectors have no native tropism for mammalian cells; however, they can be engineered to target specific eukaryotic cells by altering the expression of surface peptides.…”

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confidence: 99%

Tumor vasculature‐targeted delivery of tumor necrosis factor‐α*

Tandle

Hanna

Lorang

et al. 2008

Cancer

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BACKGROUND: Recently, considerable efforts have been directed toward antivascular therapy as a new modality to treat human cancers. However, targeting a therapeutic gene of interest to the tumor vasculature with minimal toxicity to other tissues remains the objective of antivascular gene therapy. Tumor necrosis factor‐α (TNF‐α) is a potent antivascular agent but has limited clinical utility because of significant systemic toxicity. At the maximum tolerated doses of systemic TNF‐α, there is no meaningful antitumor activity. Hence, the objective of this study was to deliver TNF‐α targeted to tumor vasculature by systemic delivery to examine its antitumor activity. METHODS: A hybrid adeno‐associated virus phage vector (AAVP) was used that targets tumor endothelium to express TNF‐α (AAVP‐TNF‐α). The activity of AAVP‐TNF‐α was analyzed in various in vitro and in vivo settings using a human melanoma tumor model. RESULTS: In vitro, AAVP‐TNF‐α infection of human melanoma cells resulted in high levels of TNF‐α expression. Systemic administration of targeted AAVP‐TNF‐α to melanoma xenografts in mice produced the specific delivery of virus to tumor vasculature. In contrast, the nontargeted vector did not target to tumor vasculature. Targeted AAVP delivery resulted in expression of TNF‐α, induction of apoptosis in tumor vessels, and significant inhibition of tumor growth. No systemic toxicity to normal organs was observed. CONCLUSIONS: Targeted AAVP vectors can be used to deliver TNF‐α specifically to tumor vasculature, potentially reducing its systemic toxicity. Because TNF‐α is a promising antivascular agent that currently is limited by its toxicity, the current results suggest the potential for clinical translation of this strategy. Cancer 2009. Published 2008 by the American Cancer Society.

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A new filamentous phage cloning vector: fd-tet

Cited by 111 publications

References 11 publications

A preclinical model for predicting drug response in soft-tissue sarcoma with targeted AAVP molecular imaging

A preclinical model for predicting drug response in soft-tissue sarcoma with targeted AAVP molecular imaging

Low-frequency infection of F- bacteria by transducing particles of filamentous bacteriophages

Tumor vasculature‐targeted delivery of tumor necrosis factor‐α*

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