Disease relevance of Genes, Neoplasm

• Cancer gene therapy using a survivin mutant adenovirus [1].
• Since linkage of the familial breast-ovarian cancer gene (BRCA1) to chromosome 17, the critical region has been narrowed to 1.0-1.5 Mb by recombination studies, a detailed physical map has been constructed and much of the region has been cloned in yeast artificial chromosome, bacteriophage P1 and cosmid vectors [2].
• Among 13 myeloid leukemias induced by transplanting into mice bone marrow cells infected in vitro with a replication-defective retrovirus carrying the Sox4 oncogene, 9 contained insertional mutations at known or suspected cancer genes [3].
• The disease locus [previously termed the "tylosis oesophageal cancer gene' (TOC) locus] has been mapped to 17q23-qter by linkage analysis [4].
• Recent evidence suggests that the gene responsible for neurofibromatosis, type 1 (NF-1), belongs to this class of heritable cancer genes [5].

High impact information on Genes, Neoplasm

• These results suggest that combined delivery of two cooperating genes like p16 and p53 could be the basis for the development of a new strategy for cancer gene therapy [6].
• These data suggest that viral vector transduction of the dCK gene followed by treatment with ara-C represents a new chemosensitization strategy for cancer gene therapy [7].
• Probability of carrying a mutation of breast-ovarian cancer gene BRCA1 based on family history [8].
• BRCA2 as a low-penetrance cancer gene [9].
• This evidence now supports the placement of telomerase among the cancer gene elite [10].

Chemical compound and disease context of Genes, Neoplasm

• Bystander effect in herpes simplex virus-thymidine kinase/ganciclovir cancer gene therapy: role of gap-junctional intercellular communication [11].
• CONCLUSIONS: This combination strategy may be very useful in the treatment of 5-FU-resistant colorectal cancers and may also be more generally helpful in minimizing the dose of therapeutic vectors used in cancer gene therapy [12].
• Bifidobacterium longum as a delivery system for cancer gene therapy: selective localization and growth in hypoxic tumors [13].
• Tetracycline-mediated suppression of target cell recognition by engineered T cells may be a useful strategy to limit the toxicity of the approach to cancer gene therapy [14].
• Crystal structure to 1.7 a of the Escherichia coli pyrimidine nucleoside hydrolase YeiK, a novel candidate for cancer gene therapy [15].

Biological context of Genes, Neoplasm

• This may suggest that there is a second tumor suppressor or recessive cancer gene on chromosome 13 in bladder cancer and/or that the mechanism of RB inactivation in bladder cancer frequently involves independent mutations of each RB allele [16].
• These observations strongly support that p16INK4 is a tumor suppressor gene and is a candidate for cancer gene replacement therapy [17].
• The finding of frequent epigenetic inactivation of RASSF1A in papillary RCCs despite previous studies reporting infrequent 3p21 allele loss in this tumor type illustrates how the systematic identification of all major human cancer genes will require detailed analysis of the cancer genome and epigenome [18].
• When expressed alone, E4orf4 induces a novel form of p53-independent apoptosis in cancer cells but not in normal human cells, thus making it of potential use in cancer gene therapy [19].
• We constructed an adenoviral vector containing human p16 cDNA in order to evaluate the cytotoxic effects of exogenous p16 expression on cancer cell proliferation and to explore the potential use of p16 in cancer gene therapy [20].

Anatomical context of Genes, Neoplasm

• To develop a novel cancer gene therapy strategy based on suppression of tumor angiogenesis, we examined the feasibility of targeting and preferential killing of proliferating endothelial cells by use of the von Willebrand factor (vWf) promoter and herpes simplex virus thymidine kinase gene (HSV-TK) [21].
• This mouse model not only demonstrates the depletion of CD4(+) T cells as a useful strategy for cancer gene therapy with interleukin-12 but also provides a model for human melanoma-associated vitiligo.J Invest Dermatol 115:1059-1064 2000[22]
• A candidate for cancer gene therapy: MIP-1 alpha gene transfer to an adenocarcinoma cell line reduced tumorigenicity and induced protective immunity in immunocompetent mice [23].
• Additionally, the characterization of the recovered mutants and a comparison of the mutation spectrum in the rat lymphocyte system to the spectrum in cancer genes, such as H-ras and p53, and the spectrum in transgenic systems, such as lacI, are included [24].

Associations of Genes, Neoplasm with chemical compounds

• Potentiation of cytochrome P450/cyclophosphamide-based cancer gene therapy by coexpression of the P450 reductase gene [25].
• The enzyme/prodrug strategy using bacterial cytosine deaminase (bCD) and 5-fluorocytosine (5-FC) is currently under investigation for cancer gene therapy [26].
• The efficacy of cancer gene therapy using bacterial cytosine deaminase (bCD)/5-fluorocytosine (5-FC) enzyme/prodrug strategy is limited by the inefficiency of cytosine deaminase (CD)-catalyzed conversion of 5-FC into 5-fluorouracil (5-FU) [27].
• Enhanced mutant NTRs such as F124K should improve the efficacy of the NTR/CB1954 combination in cancer gene therapy [28].
• Methioninase cancer gene therapy with selenomethionine as suicide prodrug substrate [29].

Gene context of Genes, Neoplasm

• The vascular endothelial growth factor receptor (VEGFR) is an important angiogenic target for cancer gene therapy [30].
• These observations were strikingly similar to those described for the MDS1-EVI1 cancer gene, which also normally gives rise to a PR domain-lacking product, EVI1, because of an internal promoter [31].
• MEN1 is thus the expression of a cancer gene but without available prevention or cure for malignancy [32].
• Chromosome 13 contains at least two cancer genes, the well-characterized RB1 gene located at 13q14 and the breast cancer-susceptibility gene, BRCA2, recently localized to 13q12 [33].
• We have thus demonstrated the cancer-specific down-regulation of DEFB1 in a large sample of prostatic and renal carcinomas and validated one of the key findings of previous cancer gene profiling studies of prostatic and renal neoplasia [34].

Analytical, diagnostic and therapeutic context of Genes, Neoplasm

• Altogether, these data indicate that AdNIS is very efficient in triggering significant iodide uptake by a tumor, outlining the potential of this novel cancer gene therapy approach for a targeted radiotherapy [35].
• Granulocyte-macrophage colony-stimulating factor and interleukin-2 fusion cDNA for cancer gene immunotherapy [36].
• Further, by profiling gene expression using the same microarray platform, we identified within CNAs the relevant subset of candidate cancer genes displaying comparably altered expression, including Mcl1 (myeloid cell leukemia sequence 1), a highly expressed antiapoptotic gene residing within the chr 3 amplicon peak [37].
• We demonstrate that a deficiency of the primary cellular receptor on the tumour cells restricts the efficacy of adenoviral vectors in two distinct cancer gene therapy approaches, TP53 gene replacement therapy and herpes simplex virus thymidine kinase/ganciclovir suicide gene therapy [38].
• These data indicate that although cationic lipid DNA complexes may differ in their inflammatory properties, the natural killer activation and interferon-gamma secretion that follow lipoplex administration should provide a functional adjuvant for cancer gene therapies that benefit from immunostimulation [39].

References