Anticancer Gene Transfer for Cancer Gene Therapy

Pazarentzos, Evangelos; Mazarakis, Nicholas D.

doi:10.1007/978-1-4471-6458-6_13

Cited by 7 publications

(5 citation statements)

References 120 publications

(123 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In clinical practice, we often need combined application of a number of different drugs to affect the tumor growth [ 154 ]. On the other hand, gene therapy technology can inhibit the expression of drug resistance gene mRNA, with a broad clinical application prospects [ 155 , 156 ]. As the researchers on the tumor resistance mechanism continuously deepening and related treatment technology continuously develop, human can improve the effect of clinical chemotherapy, reverse the resistance of cancer.…”

Section: Discussionmentioning

confidence: 99%

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

et al. 2018

View full text Add to dashboard Cite

Protein tyrosine kinase (PTK) is one of the major signaling enzymes in the process of cell signal transduction, which catalyzes the transfer of ATP-γ-phosphate to the tyrosine residues of the substrate protein, making it phosphorylation, regulating cell growth, differentiation, death and a series of physiological and biochemical processes. Abnormal expression of PTK usually leads to cell proliferation disorders, and is closely related to tumor invasion, metastasis and tumor angiogenesis. At present, a variety of PTKs have been used as targets in the screening of anti-tumor drugs. Tyrosine kinase inhibitors (TKIs) compete with ATP for the ATP binding site of PTK and reduce tyrosine kinase phosphorylation, thereby inhibiting cancer cell proliferation. TKI has made great progress in the treatment of cancer, but the attendant acquired acquired resistance is still inevitable, restricting the treatment of cancer. In this paper, we summarize the role of PTK in cancer, TKI treatment of tumor pathways and TKI acquired resistance mechanisms, which provide some reference for further research on TKI treatment of tumors.

show abstract

Section: Discussionmentioning

confidence: 99%

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

et al. 2018

View full text Add to dashboard Cite

show abstract

“…A number of different vectors are currently being used for gene therapy of malignant tumors. Whereas early vectors were non-specific, novel vectors, especially viruses, have been developed that target cancer cells but leave normal cells unharmed ( 27 ). We have reported that attenuated Salmonella typhimurium has potential utility for transgene delivery, since it shows >1,000-fold preferential accumulation in tumors compared with normal tissues ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-related apoptosis inducing ligand overexpression and Taxol treatment suppresses the growth of cervical cancer cells inï¿½vitro and inï¿½vivo

et al. 2018

View full text Add to dashboard Cite

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a member of tumor necrosis factor (TNF) superfamily and functions to promote apoptosis by binding to cell surface death receptor (DR)4 and DR5. Cancer cells are more sensitive than normal cells to TRAIL-induced apoptosis, and TRAIL-based therapeutic strategies have shown promise for the treatment of cancer. The present study investigated whether enforced overexpression of TRAIL in cervical cancer cells promoted cell death in the presence or absence of Taxol, an important first-line cancer chemotherapeutic drug. Hela human cervical cancer cells were transfected with a TRAIL expression plasmid, and the effects of the combination treatment with Taxol on apoptosis was investigated in vitro and in tumor xenografts in vivo. The results indicated that Taxol treatment and TRAIL overexpression enhanced apoptosis compared with either treatment alone. The present data indicate that Taxol may enhance the pro-apoptotic effects of TRAIL overexpression in HeLa cells by increasing cleaved caspase-3 and DR5 expression levels and decreasing Bcl-2 expression levels. Furthermore, the findings suggest a possible novel treatment option for cervical cancer and uncovers a potential mechanism of the enhancing effects of Taxol on TRAIL-induced apoptosis.

show abstract

“…This effect may be anticipated from the outset of vector development, particularly when utilizing known cytotoxic transgenes, for example, in cancer-killing vectors1029 or anti-HIV-1 genes that encode restriction factors that affect retroviral vectors, for example, APOBEC3G (ref. 30) and TRIMcyp (ref.…”

Section: Discussionmentioning

confidence: 99%

“…Contemporary gene therapy vectors based on RNA viruses such as γ-Retroviruses and Lentiviruses12, and DNA viruses such as Adenovirus3 and Adeno-associated virus (AAV)4 have shown promise in a growing number of human disease indications. These include ex vivo modification of patient cells for hematological conditions56, and in vivo treatment of ophthalmic7, cardiovascular8, neurodegenerative diseases9 and tumour therapy10. Immunogen-encoding vectors based on Poxviruses11 and Avian viruses12 are widely used in human and animal vaccinations.…”

mentioning

confidence: 99%

Enhancing titres of therapeutic viral vectors using the transgene repression in vector production (TRiP) system

et al. 2017

View full text Add to dashboard Cite

A key challenge in the field of therapeutic viral vector/vaccine manufacturing is maximizing production. For most vector platforms, the ‘benchmark' vector titres are achieved with inert reporter genes. However, expression of therapeutic transgenes can often adversely affect vector titres due to biological effects on cell metabolism and/or on the vector virion itself. Here, we exemplify the novel ‘Transgene Repression In vector Production' (TRiP) system for the production of both RNA- and DNA-based viral vectors. The TRiP system utilizes a translational block of one or more transgenes by employing the bacterial tryptophan RNA-binding attenuation protein (TRAP), which binds its target RNA sequence close to the transgene initiation codon. We report enhancement of titres of lentiviral vectors expressing Cyclo-oxygenase-2 by 600-fold, and adenoviral vectors expressing the pro-apoptotic gene Bax by >150,000-fold. The TRiP system is transgene-independent and will be a particularly useful platform in the clinical development of viral vectors expressing problematic transgenes.

show abstract

Anticancer Gene Transfer for Cancer Gene Therapy

Cited by 7 publications

References 120 publications

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

Tumor necrosis factor-related apoptosis inducing ligand overexpression and Taxol treatment suppresses the growth of cervical cancer cells inï¿½vitro and inï¿½vivo

Enhancing titres of therapeutic viral vectors using the transgene repression in vector production (TRiP) system

Contact Info

Product

Resources

About