Cancer statistics, 1998

Landis, Sarah H.; Murray, Taylor; Bolden, Sherry; Wingo, Phyllis A.

doi:10.3322/canjclin.48.1.6

Cited by 2,435 publications

(1,236 citation statements)

References 3 publications

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“…Since 1987, more women have died of lung cancer than breast cancer (Landis et al, 1998). Unfortunately, the severe morbidity of lung cancer and the poor 5-year relative survival rate (only 14%) have not been improved by current treatments.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of apoptosis induced by the synthetic retinoid CD437 in human non-small cell lung carcinoma cells

Sun

Yue²,

et al. 1999

Oncogene

116

103

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The novel synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) has been shown to induce apoptosis in various tumor cell lines including human non-small cell lung carcinoma (NSCLC) cells, which are resistant to the natural alltrans retinoic acid and to many synthetic receptorselective retinoids. Although the mechanism of this e ect was not elucidated, it was found to be independent of nuclear retinoid receptors. In the present study, we analysed the mechanisms by which CD437 induces apoptosis in two human NSCLC cell lines: H460 with wild-type p53 and H1792 with mutant p53. Both cell lines underwent apoptosis after exposure to CD437, although the cell line with wild-type p53 (H460) was more sensitive to the induction of apoptosis. CD437 increased the activity of caspase in both cell lines, however, the e ect was much more pronounced in the H460 cells. The caspase inhibitors (Z-DEVD-FMK and Z-VAD-FMK) suppressed CD437-induced CPP32-like caspase activation and apoptosis in both cell lines. CD437 induced the expression of the p53 gene and its target genes, p21, Bax, and Killer/DR5, only in the H460 cells. These results suggest that CD437-induced apoptosis is more extensive in NSCLC cells that express wild-type p53, possibly due to the involvement of the p53 regulated genes Killer/DR5, and Bax although CD437 can also induce apoptosis by means of a p53-independent mechanism. Both pathways of CD437-induced apoptosis appear to involve activation of CPP32-like caspase.

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Section: Introductionmentioning

confidence: 99%

Mechanisms of apoptosis induced by the synthetic retinoid CD437 in human non-small cell lung carcinoma cells

Sun

Yue²,

et al. 1999

Oncogene

116

103

View full text Add to dashboard Cite

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“…Lung cancer is the third most common non-cutaneous cancer and is the leading cause of death from cancer in the United States, with 171 500 new cases and 165 600 deaths projected for 1998 (Landis et al, 1998). Lung cancer cases are sporadic, and tobacco product usage is the strongest risk factor identi®ed to date: 80 ± 90% of all patients are past or current smokers and 10% of all smokers will develop lung cancer after a latency period of years to decades (Shopland et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Modeling human lung cancer in mice: similarities and shortcomings

1999

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Lung cancer kills more Americans yearly than any other neoplastic process. Mortality rates have changed little over the past several decades, despite improvements in surgical techniques, radiation therapy and chemotherapy. The identi®cation of mutations in oncogenes and tumor suppressor genes in human lung tumor specimens, including K-ras, p53, p16 INK4a and Rb, o ers molecular explanations for tumor development and resistance to therapy. Mouse models of human lung cancer may advance our understanding of this disease. The examination of mice which develop lung cancer either spontaneously or due to carcinogen exposure, and the creation of mouse strains harboring the speci®c genetic mutations found in human lung cancer are among strategies being pursued.

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“…1 Despite aggressive efforts toward earlier detection and treatment, the mortality resulting from distant metastasis of prostate cancer remains high. The most common site of prostate cancer metastasis is bone, with skeletal metastases identified at the time of autopsy up to 90% in patients dying from prostate cancer.…”

mentioning

confidence: 99%

Cotargeting tumor and tumor endothelium effectively inhibits the growth of human prostate cancer in adenovirus-mediated antiangiogenesis and oncolysis combination therapy

et al. 2004

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Tumor-endothelial interaction contributes to local prostate tumor growth and distant metastasis. In this communication, we designed a novel approach to target both cancer cells and their ''crosstalk'' with surrounding microvascular endothelium in an experimental hormone refractory human prostate cancer model. We evaluated the in vitro and in vivo synergistic and/or additive effects of a combination of conditional oncolytic adenovirus plus an adenoviral-mediated antiangiogenic therapy. In the in vitro study, we demonstrated that human umbilical vein endothelial cells (HUVEC) and human C4-2 androgen-independent (AI) prostate cancer cells, when infected with an antiangiogenic adenoviral (Ad)-Flk1-Fc vector secreting a soluble form of Flk1, showed dramatically inhibited proliferation, migration and tubular formation of HUVEC endothelial cells. C4-2 cells showed maximal growth inhibition when coinfected with Ad-Flk1-Fc and Ad-hOC-E1, a conditional replication-competent Ad vector with viral replication driven by a human osteocalcin (hOC) promoter targeting both prostate cancer epithelial and stromal cells. Using a threedimensional (3D) coculture model, we found that targeting C4-2 cells with Ad-hOC-E1 markedly decreased tubular formation in HUVEC, as visualized by confocal microscopy. In a subcutaneous C4-2 tumor xenograft model, tumor volume was decreased by 40-60% in animals treated with Ad-Flk1-Fc or Ad-hOC-E1 plus vitamin D 3 alone and by 90% in a combined treatment group, compared to untreated animals in an 8-week treatment period. Moreover, three of 10 (30%) pre-established tumors completely regressed when animals received combination therapy. Cotargeting tumor and tumor endothelium could be a promising gene therapy strategy for the treatment of both localized and metastatic human prostate cancer.

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Cancer statistics, 1998

Cited by 2,435 publications

References 3 publications

Mechanisms of apoptosis induced by the synthetic retinoid CD437 in human non-small cell lung carcinoma cells

Mechanisms of apoptosis induced by the synthetic retinoid CD437 in human non-small cell lung carcinoma cells

Modeling human lung cancer in mice: similarities and shortcomings

Cotargeting tumor and tumor endothelium effectively inhibits the growth of human prostate cancer in adenovirus-mediated antiangiogenesis and oncolysis combination therapy

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