S100-Beta, Melanoma-Inhibiting Activity, and Lactate Dehydrogenase Discriminate Progressive From Nonprogressive American Joint Committee on Cancer Stage IV Melanoma

Deichmann, Martin; Benner, Axel; Bock, Michael; Jäckel, Andreas; Uhl, K.; Waldmann, V.; Näher, Helmut

doi:10.1200/jco.1999.17.6.1891

Cited by 221 publications

(161 citation statements)

References 20 publications

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“…Inositol 1, 4, 5-triphospate receptor type 3 (IP(3)R3) is frequently expressed in secretion cells and known to be related to the IP3 signalling pathway, Ca 2+ influx, enzyme secretion and cell motility (Broad et al, 2001;Lee and Laychock, 2001), but its role in peritoneal dissemination is still unclear. Aldoketoreductase and aldehyde dehydrogenase (ALDH) belong to a family of several isoenzymes important in cell defence against both exogenous and endogenous aldehydes (Deichmann et al, 1999;Canuto et al, 2001). Compared with expression of ALDH in normal hepatocytes, several changes were observed in rat hepatoma cells (Canuto et al, 2001).…”

Section: Genetics and Genomicsmentioning

confidence: 99%

Differential gene expression profiles of gastric cancer cells established from primary tumour and malignant ascites

et al. 2002

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Advanced gastric cancer is often accompanied by metastasis to the peritoneum, resulting in a high mortality rate. Mechanisms involved in gastric cancer metastasis have not been fully clarified because metastasis involves multiple steps and requires a combination of altered expressions of many different genes. Thus, independent analysis of any single gene would be insufficient to understand all of the aspects of gastric cancer peritoneal dissemination. In this study, we performed a global analysis of the differential gene expression of a gastric cancer cell line established from a primary main tumour (SNU-1) and of other cell lines established from the metastasis to the peritoneal cavity (SNU-5, SNU-16, SNU-620, KATO-III and GT3TKB). The application of a high-density cDNA microarray method made it possible to analyse the expression of approximately 21 168 genes. Our examinations of SNU-5, SNU-16, SNU-620, KATO-III and GT3TKB showed that 24 genes were upregulated and 17 genes down-regulated besides expression sequence tags. The analysis revealed the following altered expression such as: (a) up-regulation of CD44 (cell adhesion), keratins 7, 8, and 14 (epitherial marker), aldehyde dehydrogenase (drug metabolism), CD9 and IP3 receptor type3 (signal transduction); (b) down-regulation of IL2 receptor g, IL4-Stat (immune response), p27 (cell cycle) and integrin b4 (adhesion) in gastric cancer cells from malignant ascites. We then analysed eight gastric cancer cell lines with Northern blot and observed preferential up-regulation and down-regulation of these selected genes in cells prone to peritoneal dissemination. Reverse transcriptase -polymerase chain reaction confirmed that several genes selected by DNA microarray were also overexpressed in clinical samples of malignant ascites. It is therefore considered that these genes may be related to the peritoneal dissemination of gastric cancers. The results of this global gene expression analysis of gastric cancer cells with peritoneal dissemination, promise to provide a new insight into the study of human gastric cancer peritoneal dissemination.

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Section: Genetics and Genomicsmentioning

confidence: 99%

Differential gene expression profiles of gastric cancer cells established from primary tumour and malignant ascites

et al. 2002

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“…In addition, MIA is synthesized by preosteoblasts during tooth healing (Shyng et al, 1999). Virtually all primary and metastatic melanoma cells, but not normal melanocytes, express and secrete MIA to a high extent, such that MIA serum levels serve as a marker for malignant melanoma (Bosserhoff et al, 1997b, a;Deichmann et al, 1999). Neoplastic expression of MIA has also been observed in mammacarcinoma (Bosserhoff et al, 1999b), ovarian cancer (Bosserhoff et al, 1999a), and various gastrointestinal carcinomas (Wagner et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Identification and Characterization of an Inner Ear-Expressed Human Melanoma Inhibitory Activity (MIA)-like Gene (MIAL) with a Frequent Polymorphism That Abolishes Translation

et al. 2001

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To discover new cochlea-specific genes as candidate genes for nonsyndromic hearing impairment, we searched in The Institute of Genome Research database for expressed sequence tags isolated from the cochlea only. This led to the cloning and characterization of a human gene named melanoma inhibitory activity-like (MIAL; HGMW-approved symbol OTOR alias MIAL) gene. In situ hybridization revealed MIAL expression in a cell layer beneath the sensory epithelium of cochlea and vestibule of human fetal inner ear. No other human tissue, except fetal brain, showed expression of MIAL when analyzed by in situ hybridization or reverse transcription-polymerase chain reaction. The cDNA of the mouse homologue was also cloned and mapped about 80 cM from the top of mouse chromosome 2. In mouse, Mial was also expressed in the cochlea and the vestibule of the inner ear, as well as in brain, eye, limb, and ovary. Expression in mammalian cell cultures showed that MIAL is translated as an ϳ15-kDa polypeptide that is assembled into a covalently linked homodimer, modified by sulfation, and secreted from the cells via the Golgi apparatus. In the human MIAL gene, a frequent polymorphism was discovered in the translation initiation codon (ACG instead of ATG). Of 505 individuals, 48 (9.5%) were ATG/ ACG heterozygous and 1 (0.2%) was homozygous for ACG. No MIAL protein was synthesized in cells transfected with cDNA of the ACG allele. The inner earrestricted expression pattern and the existence of an inactive allele suggest that MIAL may contribute to inner-ear dysfunction in humans.

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“…46 In contrast, hMIA promoter activity correlates with melanoma progression. 28,47 Therefore, the MIA promoter may confer melanoma-restricted expression of the suicide gene also in advanced stages of the disease. The successful use of enhancer elements to increase transcriptional activity of weak tissue-specific promoters has been demonstrated in previous studies: a hypoxia-inducible enhancer linked to the human alphafetoprotein promoter has been shown to enhance selective suicide gene expression in hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

MIA (melanoma inhibitory activity) promoter mediated tissue-specific suicide gene therapy of malignant melanoma

Schoensiegel

Paschen

Sieger³

et al. 2004

Cancer Gene Ther

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Suicide gene therapy of malignant melanoma essentially requires efficient gene transfer and highly selective therapeutic gene expression. To achieve this, recombinant adeno-associated virus (rAAV) particles were constructed containing the tissue-specific promoter of the human melanoma inhibitory activity (hMIA) gene combined with four copies of the enhancer element of the murine tyrosinase gene. Three melanoma and one cervix carcinoma cell line were infected with rAAV particles carrying a reporter gene under control of the enhancer/hMIA promoter in order to determine transcriptional activity and specificity of this system. Viral particles containing the enhancer/hMIA promoter mediated reporter gene activity only in melanoma cells, whereas infection with a cytomegalovirus (CMV)-based promoter construct induced unspecific gene expression. Correspondingly, transient transduction with viral particles bearing the HSVtk gene under the control of the enhancer/MIA promoter elements followed by treatment with ganciclovir (GCV) resulted in growth inhibition only in melanoma cells, whereas the CMV promoter-based construct induced unspecific cytotoxicity. In vivo experiments in nude mice demonstrated that tumors originating from human melanoma cells disappeared after stable, but not transient transduction with vectors bearing the HSVtk gene under the control of the enhancer/hMIA promoter in response to GCV application. In face of higher transduction efficiency, these rAAV particles might therefore be a useful tool for suicide gene therapy of malignant melanoma.

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S100-Beta, Melanoma-Inhibiting Activity, and Lactate Dehydrogenase Discriminate Progressive From Nonprogressive American Joint Committee on Cancer Stage IV Melanoma

Abstract: Elevated serum levels of S100beta, MIA, and LDH indicate current disease progression in AJCC stage IV melanoma. LDH was the most relevant overall parameter.

Cited by 221 publications

References 20 publications

Differential gene expression profiles of gastric cancer cells established from primary tumour and malignant ascites

Differential gene expression profiles of gastric cancer cells established from primary tumour and malignant ascites

Identification and Characterization of an Inner Ear-Expressed Human Melanoma Inhibitory Activity (MIA)-like Gene (MIAL) with a Frequent Polymorphism That Abolishes Translation

MIA (melanoma inhibitory activity) promoter mediated tissue-specific suicide gene therapy of malignant melanoma

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