Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently it has been suggested that proto-oncogene plays a role not only in cellular proliferation, development and differentiation, but also in neoplastic transformation. We now show the expression and its localization of c-myc, c-fms and c-sis proto-oncogenes in human developing chorionic tissue and fresh surgical specimens of mole and choriocarcinoma with the method of Northern blotting and In-situ hybridization. The 2.4kb c-myc transcript has been localized to the cytotrophoblast in early placenta and also localized to the C and S typed trophoblastic cells in mole and choriocarcinoma. The 4.0kb c-fms transcript has been localized to the syncytiotrophoblast, especially the highly differentiated syncytiotrophoblast in the second and third trimesters and S typed trophoblastic cells in mole and choriocarcinoma. Moreover, the 4.0kb c-sis transcript has been localized to the cytotrophoblast in early placenta, but not detected in mole or choriocarcinoma. First, these results suggest that the stage and site specific expression of c-myc, c-fms and c-sis proto-oncogenes are clearly related to the proliferation, development and differentiation of normal trophoblastic cells. Second, the expression of c-myc, c-fms proto-oncogenes may be of particular importance in the tumorigenesis and progression of trophoblastic disease.
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PMID:[The expression of c-myc, c-fms, c-sis oncogenes in the trophoblast of normal pregnancy and trophoblastic disease]. 285 Mar 28

The expression of c-fos, c-myc, Ha-ras, N-ras, EGF-receptor, and cardiac actin genes was examined in 7 normal epidermis, 3 cellular nevi, and 8 skin tumors including 6 malignant and 2 benign tumors of human origin. These genes were transcribed in most normal and tumor tissues, though no tumor-specific expression of proto-oncogenes (c-fos, c-myc, Ha-ras, and N-ras) could be detected. However, there was a characteristic parallelism between the expression of c-fos and c-myc in normal epidermis, while the parallelism was not always definite in skin tumors. The ratio of c-fos/c-myc transcripts in normal epidermis was constant compared with the expression of other genes examined. These data suggest that c-fos and c-myc are expressed in all normal skin tissues, and that maintenance of a constant ratio of c-fos/c-myc is closely related to ordered cell growth of the tissues.
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PMID:Expression of proto-oncogenes in normal and tumor tissues of human skin. 289 96

Regulatory or structural alterations of c-onc genes including amplification, rearrangement and point mutation was implicated in the causation of various malignant tumors. However, such changes of molecular levels have not been reported so far in choriocarcinoma cells. In the present study, thus, 5 choriocarcinoma cell lines were analyzed by hybridization using 16 oncogene probes. By Southern blot hybridization of DNA extracted from these cells, 8 fold amplification of c-myc gene and rearrangement of c-fms gene were shown in ENAMI cells, although the role of these alterations remained unknown. Northern blot hybridization performed simultaneously demonstrated multiple expression of c-onc genes. 4 choriocarcinoma cell lines (HCCM, CHl, CCl, ENAMI) expressed at least 11 c-onc genes (H-ras, K-ras, N-ras, c-myc, N-myc, fos, fms, src, yes, erb B and raf); though the degree of expression of H-ras, C-myc, erb B and fms in these cells was either similar or enhanced as compared with normal fibroblast, the expression of two c-onc genes (N-myc and fos) was extremely enhanced. However, expression of K-ras and myb was either low or not detected. The multiple expression of c-onc genes seems to reflect partly on growth advantages of trophoblast. Transfection assay using NIH3T3 cells failed to form any transformed foci. Since choriocarcinoma cells which derived from the transformation of trophoblast of complete mole possess the genetic characteristics identical to the one of cells of complete mole, chromosomal instability was assumed to play a major role for multiple oncogene expression in choriocarcinoma cells.
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PMID:[Analysis of c-onc genes in choriocarcinoma cells]. 369 32

Ki-ras and c-myc oncogene mRNA in carcinoma tissue was quantitatively detected by the coamplification polymerase chain reaction. After the reverse transcription of the mRNA mixture with random hexanucleotide primer the coamplification polymerase chain reaction of the oncogene and the internal standard beta-actin cDNA was done. The amount of oncogene mRNA was calculated from the coamplified product ratio. Ki-ras expression in a human gastric cancer strain H-111 was estimated to 5 percent of beta-actin. The expression of c-myc mRNA in colorectal carcinoma tissue was observed to be ten to one hundred times higher than normal mucosa. Gene expression was compared numerically in mole/liter without using hybridization and radioactive probes.
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PMID:Ki-ras and c-myc oncogene expression measured by coamplification polymerase chain reaction. 800 89

The expression of c-myc protein was studied in formalin-fixed, paraffin-embedded sections of 16 compound Spitz nevi (SNs), 20 ordinary compound melanocytic nevi (MNs) and 30 malignant melanomas (MMs), using monoclonal antibody 9E10 and an immunoperoxidase technique. Nine (56%) SNs, 16 (80%) MNs and 23 (77%) MMs showed positive reactions in some of the tumor cells (P = non-significant). The staining reactions were mostly cytoplasmic, and moderate to strong in intensity. The frequencies of positively stained cells were higher in the MN and SN groups. Most of the lesions with a significant dermal component did not show stratification of staining with progressive descent into the dermis. Therefore, the mode of expression of c-myc in routinely processed specimens does not differentiate between SNs, MNs and MMs. One possible reason is that the increased expression of the c-myc protein is not sufficient alone to promote proliferation and malignant transformation in these types of tumors.
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PMID:Mode of c-myc protein expression in Spitz nevi, common melanocytic nevi and malignant melanomas. 913 12

Amplification and overexpression of the c-myc gene have been associated with neoplastic transformation in a plethora of malignant tumours. We applied interphase fluorescence in situ hybridization (FISH) with a locus-specific probe for the c-myc gene (8q24) in combination with a corresponding chromosome 8 alpha-satellite probe to evaluate genetic alterations in 8 primary melanomas and 33 advanced melanomas and compared it to 12 melanocytic nevi, 7 safety margins and 2 cases of normal skin. Additionally, in metaphase spreads of 7 melanoma cell lines a whole chromosome 8 paint probe was used. We investigated the functionality of the c-myc gene by detecting c-myc RNA expression with RT-PCR and c-myc protein by immunohistochemistry. 4/8 primary melanomas and 11/33 melanoma metastases showed additional c-myc signals relative to the centromere of chromosome 8 copy number. None of the nevi, safety margins or normal skin samples demonstrated this gain. In 2/7 melanoma cell lines (C32 and WM 266-4) isochromosome 8q formation with a relative gain of c-myc copies and a loss of 8p was observed. The highest c-myc gene expression compared to GAPDH was found in melanoma metastases (17.5%). Nevi (6.6%) and primary melanomas (5.0%) expressed the c-myc gene on a lower level. 72.7% of the patients with c-myc extra copies had visceral melanoma metastases (UICC IV), patients without c-myc gain in 35.0% only. The collective with additional c-myc copies also expressed the gene on a significantly higher level. These results indicate that a c-myc gain in relation to the centromere 8 copy number might be associated with advanced cutaneous melanoma.
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PMID:Extra c-myc oncogene copies in high risk cutaneous malignant melanoma and melanoma metastases. 1113 16

Apoptosis is an important co-factor in the pathogenesis of a plethora of malignancies. Enhanced c-myc activation can result either in proliferation or apoptosis. Coexpression with antiapoptotic bcl-2, which abrogates the apoptotic function of c-myc might lead to an enormous growth advantage of cells. In order to elucidate the role of c-myc and bcl-2 as well as the coexpression of both genes in human melanoma, their expression was studied in four samples of normal skin (SK), 15 surgical margins (SM), 20 benign melanocytic nevi (MN), 20 primary melanomas (MM), and 30 melanoma metastases (MMET) by RT-PCR. These results were compared with immunohistochemistry (IH) in 7 SK, 7 SM, 26 MN, 50 MM, and 34 MMET. Similar results were found with both methods. However, MMET expressed c-myc (PCR 28/30, IH 23/34) as well as bcl-2 (PCR 27/30, IH 24/34) more frequently. Primary melanomas showed a similar expression pattern as SM and nevi. Moreover, in contrast to SK, SM, MN, and MM coexpression of bcl-2 and c-myc was found more frequently in MMET (PCR 25/30, p < 0.01, IH 19/34, p < 0.01). These results indicate that coexpression of c-myc and bcl-2 appears to be associated with advanced melanoma and contributes to the malignant phenotype.
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PMID:Expression of c-myc and bcl-2 in primary and advanced cutaneous melanoma. 1244 22

More than 85% of c-myc transcription is controlled by the nuclease hypersensitive element III(1) upstream of the P1 promoter of this oncogene. The purine-rich sequence in the anti-sense strand forms a G-quadruplex, which has been recently implicated in colorectal cancer, and is proposed as a silencer element [Proc. Natl. Acad. Sci. USA 101 (2004) 6140]. This prompted us to characterize the thermodynamics and proton/counterion effect of the complementary pyrimidine-rich sequence, which forms a C-tetraplex. We report the thermodynamic parameters for folding of the pyrimidine-rich DNA fragment from this region into a C-tetraplex. At 20 degrees C, we observed a DeltaG of -10.36+/-0.13kcalmol(-1) with favorable enthalpy (DeltaH=75.99+/-0.99kcalmol(-1)) and unfavorable entropy (TDeltaS=65.63+/-0.88 kcalmol(-1)) at pH 5.3 in 20mM NaCl for tetraplex folding. Similar characteristic stabilizing enthalpy and destabilizing entropy were observed at other pH and ionic strengths. Folding was induced by uptake of about two to three protons per mole of tetraplex while a marginal (0.5-1mol/mol) counterion uptake was observed. In the context of current understanding of c-myc transcription we envisage a role of the i-motif in remodeling the G-quadruplex silencer.
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PMID:Thermodynamics of i-tetraplex formation in the nuclease hypersensitive element of human c-myc promoter. 1524 20

The muroid rodents are the largest superfamily of mammals, containing nearly one third of all mammal species. We report on a phylogenetic study comprising 53 genera sequenced for four nuclear genes, GHR, BRCA1, RAG1, and c-myc, totaling up to 6400 nucleotides. Most relationships among the subfamilies are resolved. All four genes yield nearly identical phylogenies, differing only in five key regions, four of which may represent particularly rapid radiations. Support is very strong for a fundamental division of the mole rats of the subfamilies Spalacinae and Rhizomyinae from all other muroids. Among the other "core" muroids, a rapid radiation led to at least four distinct lineages: Asian Calomyscus, an African clade of at least four endemic subfamilies, including the diverse Nesomyinae of Madagascar, a hamster clade with maximum diversity in the New World, and an Old World clade including gerbils and the diverse Old World mice and rats (Murinae). The Deomyinae, recently removed from the Murinae, is well supported as the sister group to the gerbils (Gerbillinae). Four key regions appear to represent rapid radiations and, despite a large amount of sequence data, remain poorly resolved: the base of the "core" muroids, among the five cricetid (hamster) subfamilies, within a large clade of Sigmodontinae endemic to South America, and among major geographic lineages of Old World Murinae. Because of the detailed taxon sampling within the Murinae, we are able to refine the fossil calibration of a rate-smoothed molecular clock and apply this clock to date key events in muroid evolution. We calculate rate differences among the gene regions and relate those differences to relative contribution of each gene to the support for various nodes. The among-gene variance in support is greatest for the shortest branches. We present a revised classification for this largest but most unsettled mammalian superfamily.
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PMID:Phylogeny and divergence-date estimates of rapid radiations in muroid rodents based on multiple nuclear genes. 1537 Dec 45