H‐<i>ras</i> Ribozyme‐Mediated, Alteration of the Human Melanoma Phenotypea

Ohta, Y.; Tone, Takeshi; Shitara, Tetsuya; Funato, Tadao; Jiao, Lu; Kashfian, Brandon I.; Yoshida, E.; Horng, Mark S.; Tsai, Patricia; Lauterbach, Karen; Kashani‐Sabet, Mohammed; Florenes, Viva Ann; Fodstad, Øystein; Scanlon, Kevin J.

doi:10.1111/j.1749-6632.1994.tb21716.x

Cited by 29 publications

(9 citation statements)

References 38 publications

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“…15,18,19 Previous studies indicated that anti-oncogene Rzs effectively suppress the expression of targeted genes and cause reversal of the malignant phenotype in cancer cells. [23][24][25][32][33][34][35][36]47 However, it has not yet been clarified whether apoptosis is associated with this Rz-mediated growth suppression of the cancer cells.…”

Section: Discussionmentioning

confidence: 99%

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Adenovirus-mediated anti-K-ras ribozyme induces apoptosis and growth suppression of human pancreatic carcinoma

et al. 2000

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Human pancreatic cancer is a lethal malignancy, and the lesions show a very high incidence of point mutations of the K-ras oncogene. These alterations can be used as potential targets for specific ribozyme (Rz)-mediated growth suppression of the cancer cells. We designed an anti-K-ras Rz against mutant K-ras gene transcripts (codon 12, GGT to GTT) and generated a recombinant adenovirus (rAd) to express the Rz (rAd/anti-K-ras Rz). More than 95% of Capan-1 human pancreatic cells were infected with rAd/anti-K-ras Rz when treated with the virus at 200 plaque-forming units/cell. The virus, rAd/anti-K-ras Rz, significantly suppressed mutant K-ras gene expression and inhibited the growth of Capan-1 cells. At 3 days postinfection, we observed maximum growth suppression of the cells, characteristic morphological changes of apoptosis such as nuclear condensation and oligonucleosomal DNA fragmentation, and suppression of bcl-2 oncoprotein. These changes were not found in control virus-infected cells. Our results indicated that the virus rAd/anti-K-ras Rz specifically down-regulated the K-ras/bcl-2 pathway and induced apoptotic changes in Capan-1 pancreatic carcinoma cells. High-efficiency adenovirus-mediated delivery of anti-K-ras Rz could become a significant gene therapy strategy against human pancreatic cancer. Cancer Gene Therapy (2000) 7, 373-383

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Section: Discussionmentioning

confidence: 99%

“…[32][33][34][35][36] However, it has not yet been clarified whether apoptotic changes are associated with this Rz-mediated growth suppression of cancer cells.…”

Section: 31mentioning

confidence: 99%

Adenovirus-mediated anti-K-ras ribozyme induces apoptosis and growth suppression of human pancreatic carcinoma

et al. 2000

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“…In addition, specific approaches have been developed to accomplish targeted abrogation of overexpressed dominant oncoproteins. These approaches have been based largely upon the employment of antisense methods to achieve selected knockout of a target oncoprotein at the transcriptional (5,6) or posttranscriptional level (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Targeted tumor killing via an intracellular antibody against erbB-2.

Deshane¹,

Siegal²,

Alvarez³

et al. 1995

J. Clin. Invest.

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Specific killing of erbB-2-overexpressing tumor cells can be achieved using expression of an intracellular antibody directed against the erbB-2 oncoprotein. We have developed a strategy using a recombinant adenovirus encoding an anti-erbB-2 single chain antibody to achieve targeted tumor cell killing in vivo and can show significantly prolonged survival of animals carrying a human ovarian carcinoma tumor burden within their peritoneal cavities. This strategy of gene therapy for ovarian carcinoma offers the potential to achieve highly specific, targeted killing of human tumor cells and thus establishes the rationale to undertake human clinical trials on this basis. (J. Clin. Invest. 1995. 96:2980-2989

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“…Antisense-H-ras [118] AS-K-ras [56, 108,188] AS-BCR-abl [98] Suicide genes HSV-tk b [107] VZV-tk [6] Cytosine deaminase b [111] Drug-resistance genes Multidrug-resistance (MDR-1) gene b [157], DHRF gene [31]…”

Section: Gene Therapy Strategiesmentioning

confidence: 99%

“…However, techniques using antisense oligonucleotides [26] and ribozymes to inhibit oncogene expression are by far the most used [82]. The ribozyme recognizes its target through complementary antisense nucleotide sequences, then binds and cleaves the mRNA molecule [118]. Antisense mRNA specifically switches off the production of the abnormal protein product.…”

Section: Protecting Normal Tissue From the Toxic Effects Of Chemotherapymentioning

confidence: 99%

Cancer and gene therapy

Schmidt-Wolf

Schmidt‐Wolf

1996

Ann Hematol

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The authors review the current literature pertaining to gene therapy as related to human cancer, covering gene therapy strategies, techniques of gene transfer, and targeted gene delivery. Gene therapy has various applications. Many technical obstacles in gene delivery need to be overcome. The safe delivery and expression of a gene to its destination are essential for clinical use. A greater understanding of the genetic basis of cancer and tumor immunology is necessary before the goal of cancer gene therapy can be fully realized.

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H‐ras Ribozyme‐Mediated, Alteration of the Human Melanoma Phenotypea

Cited by 29 publications

References 38 publications

Adenovirus-mediated anti-K-ras ribozyme induces apoptosis and growth suppression of human pancreatic carcinoma

Adenovirus-mediated anti-K-ras ribozyme induces apoptosis and growth suppression of human pancreatic carcinoma

Targeted tumor killing via an intracellular antibody against erbB-2.

Cancer and gene therapy

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