Tumour markers in oncology: past, present and future

Magdelénat, H.

doi:10.1016/0022-1759(92)90072-2

Cited by 34 publications

(18 citation statements)

References 39 publications

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“…To investigate this possibility, we stained tumor sections form treated or untreated animals for expression of the nuclear antigen, Ki67/MIB1, a marker selectively expressed in actively proliferating cells [30][31][32][33]. Our results clearly show that liposomal sclareol inhibits expression of Ki67 indicating a direct effect on cell proliferation.…”

Section: Discussionmentioning

confidence: 75%

“…Further, we investigated whether sclareol treatment affects proliferation of cancer cells in the section by detecting the presence of the nuclear Ki67/MIB1 protein, a marker indicative of active cell proliferation (reviewed in refs. [30][31][32][33]). More than 80% of the cells stained positive for Ki67 in the untreated tumor ( Fig.…”

Section: Characteristics Of Sclareol-treated Tumorsmentioning

confidence: 97%

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Sclareol induces apoptosis in human HCT116 colon cancer cells in vitro and suppression of HCT116 tumor growth in immunodeficient mice

et al. 2007

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Labd-14-ene-8, 13-diol (sclareol) is a labdane-type diterpene, which has demonstrated significant cytotoxic activity against human leukemic cell lines, but its effect on solid tumor-derived cells is uknown. Here, we demonstrate that addition of sclareol to cultures of human colon cancer HCT116 cells results in inhibition of DNA synthesis, arrest of cells at the G(1) phase of the cell cycle, activation of caspases-8, -9, PARP degradation, and DNA fragmentation, events characteristic of induction of apoptosis. Intraperitoneal (ip) administration of sclareol alone, at the maximum tolerated dose, was unable to induce suppression of growth of HCT116 tumors established as xenografts in immunodeficient SCID mice. In contrast, ip administration of liposome-encapsulated sclareol, following a specific schedule, induced suppression of tumor growth by arresting tumor cell proliferation as assessed by detecting the presence of the cell proliferation-associated nuclear protein, Ki67, in thin tumor sections. These findings suggest that sclareol incorporated into liposomes may possess chemotherapeutic potential for the treatment of colorectal and other types of human cancer.

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Section: Discussionmentioning

confidence: 75%

Section: Characteristics Of Sclareol-treated Tumorsmentioning

confidence: 97%

Sclareol induces apoptosis in human HCT116 colon cancer cells in vitro and suppression of HCT116 tumor growth in immunodeficient mice

et al. 2007

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“…One approach to cancer therapy is elimination of tumor cells based on their inappropriate expression of genes normally expressed either in other cell types or during the early to middle stages of embryogenesis (40). Using RDA PCR, we identified 12 E2a-Pbx1-induced RNAs that reveal some basic principles about the transforming mechanisms of E2a-Pbx1.…”

Section: Discussionmentioning

confidence: 99%

E2a-Pbx1 Induces Aberrant Expression of Tissue-Specific and Developmentally Regulated Genes When Expressed in NIH 3T3 Fibroblasts

Kamps

1997

Molecular and Cellular Biology

100

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The E2a-Pbx1 oncoprotein contains the transactivation domain of E2a joined to the DNA-binding homeodomain (HD) of Pbx1. In mice, E2a-Pbx1 transforms T lymphoblasts and fibroblasts and blocks myeloblast differentiation. Pbx1 and E2a-Pbx1 bind DNA as heterodimers with other HD proteins whose expression is tissue specific. While the transactivation domain of E2a is required for all forms of transformation, DNA binding by the Pbx1 HD is essential for blocking myeloblast differentiation but dispensable for fibroblast or T-lymphoblast transformation. These properties suggest (i) that E2a-Pbx1 causes cellular transformation by activating gene transcription, (ii) that transcription of E2a-Pbx1 target genes is normally regulated by ubiquitous Pbx proteins and tissue-specific partners, and (iii) that DNA-binding mutants of E2a-Pbx1 activate a subset of all gene targets. To test these predictions, genes induced in NIH 3T3 fibroblasts by E2a-Pbx1 were identified and examined for tissue-and stage-specific expression and their differential abilities to be upregulated by E2a-Pbx1 in NIH 3T3 fibroblasts and myeloblasts and by a DNA-binding mutant of E2a-Pbx1 in NIH 3T3 cells. Of 12 RNAs induced by E2a-Pbx1, 4 encoded known proteins (a J-C region of the immunoglobulin kappa light chain, natriuretic peptide receptor C, mitochondrial fumarase, and the 3,5-cyclic nucleotide phosphodiesterase, PDE1A) and 5 encoded new proteins related to angiogenin, ion channels, villin, epidermal growth factor repeat proteins, and the human 2.19 gene product. Expression of many of these genes was tissue specific or developmentally regulated, and most were not expressed in fibroblasts, indicating that E2a-Pbx1 can induce ectopic expression of genes associated with lineage-specific differentiation.

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“…In the management of cancer patients, tumor-associated antigens in serum have been used in noninvasive tests for relapse detection [1]. Carcinoembryonic antigen (CEA), an important tumor-associated antigen, is an acidic glycoprotein with a molecular weight of about 200 kDa and has been expressed in many malignancies [2,3].…”

Section: Introductionmentioning

confidence: 99%

Noncompetitive enzyme immunoassay for carcinoembryonic antigen by flow injection chemiluminescence

Jun

Yan

2004

Clinica Chimica Acta

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Tumour markers in oncology: past, present and future

Cited by 34 publications

References 39 publications

Sclareol induces apoptosis in human HCT116 colon cancer cells in vitro and suppression of HCT116 tumor growth in immunodeficient mice

Sclareol induces apoptosis in human HCT116 colon cancer cells in vitro and suppression of HCT116 tumor growth in immunodeficient mice

E2a-Pbx1 Induces Aberrant Expression of Tissue-Specific and Developmentally Regulated Genes When Expressed in NIH 3T3 Fibroblasts

Noncompetitive enzyme immunoassay for carcinoembryonic antigen by flow injection chemiluminescence

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