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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The putative transregulatory activity of the RB (retinoblastoma tumor suppressor) gene product on the expression of the c-myc and c-fos proteins during the cell cycle was assessed in HL-60 promyelocytic leukemia cells. Multiparameter flow cytometry was used to simultaneously measure nuclear DNA content, RB protein, and MYC or FOS protein per cell. The amount of RB protein per cell increased with progression through the cell cycle. As the amount of RB protein increased, the ratio of RB to MYC or to FOS protein could be determined per cell as a function of cell cycle phase. Although the amount of RB protein per cell increased with progression through successive cell cycle phases, during S phase the relative rate of increase was not as rapid as that of nuclear DNA. The amount of MYC and FOS per cell also increased throughout the cell cycle, but also more slowly than DNA during S. The ratio of the amount of RB protein to MYC protein remained constant throughout the cell cycle, consistent with putative co-regulation suggested by previous studies of promoter structure. In contrast, the ratio of RB protein to FOS protein increased with progression through the phases of the cell cycle, consistent with a putative negative effect of RB on FOS which was found in previous studies with transgenes and reporters. There was no significant change in these ratios with myelo-monocytic differentiation. Although MYC and FOS have both been implicated as growth-promoting oncogenes putatively transregulated by RB, their behavior during the cell cycle relative to RB is thus distinguishable. Interestingly, in the case of all three of these putative cell cycle regulatory proteins, their cell cycle phase-specific expression levels are consistent with a minimum amount per cell that is necessary but not sufficient for progression to the next cell cycle phase.
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PMID:The ratio of retinoblastoma (RB) to fos and RB to myc expression during the cell cycle. 853 57

The etiology of breast cancer involves a complex interplay of various factors, including genetic alterations. Many studies have been devoted to the identification and characterization of mutations that occur frequently during breast tumorigenesis. The major types of genetic abnormalities that are frequently observed in breast tumors are amplification of protooncogenes (MYC, ERBB2) and DNA from chromosome band 11q13; mutation of TP53; and loss of heterozygosity from chromosomes and chromosome arms 1, 3p, 6q, 7q, 8p, 11, 13q, 16q, 17, 18q, and 22q. The latter may correspond to losses or inactivations of tumor suppressor genes. Recently, linkage analyses of large families with a predisposition to breast cancer have been performed in order to map breast cancer susceptibility genes (TP53, BRCA1, BRCA2). The findings have thrown light on the molecular mechanisms of breast cancer and have enabled various genetic markers to be used in clinical oncology.
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PMID:Genetic alterations in breast cancer. 860 12

The L-MYC restriction fragment-length polymorphism (RFLP) revealed by EcoR1 has been suggested to be of prognostic significance in lung, breast, and kidney cancer. The presence of the smaller allele, in either the homozygotic (S-S) or heterozygotic form (L-S), is felt to convey a worse prognosis than the homozygotic form for the larger allele (L-L). The significance of this relationship in lung cancer has been questioned recently. The objective of the present study was to test the prognostic significance of the L-MYC allelotype in a group of renal cell carcinoma (RCC) patients. Tumor and normal tissue were obtained from 59 patients who underwent radical nephrectomy for RCC between 1986 and 1990. EcoR1 restriction digests were performed on isolated DNA and hybridized with the L-MYC probe. Allelotypes were correlated with pathologic parameters and clinical outcome using the chi 2 test. The L-MYC alleolotype (L-L versus L-S and S-S) did not correlate with any pathologic parameter or likelihood of disease recurrence and does not offer any clinical utility in patients with RCC.
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PMID:L-MYC allelotype in renal cell carcinoma. 863 Sep 82

The classical follicular variant of follicle center lymphoma (FCL-fo) is associated with the chromosomal translocation t(14;18)(q32;q21). However, the sole presence of this translocation is not sufficient for malignant transformation, as demonstrated by experiments in a transgenic mouse model. Most of the secondary changes, which play a central role in tumor development and progression and which are presumed to be of prognostic value, are gains and losses of chromosomal material. We analyzed 28 FCL-fo patients using comparative genomic hybridization (CGH). The most frequent imbalances were gains on chromosomes X, 7, 8, 12, and 18 as well as losses of material on chromosome arm 6q. For chromosomes X, 8, 12, and 18, the CGH data allowed further narrowing of the relevant subregions. In addition, novel high-level DNA amplifications were identified in five instances mapping to chromosome bands 1p36, 6p21, 8q24 (2 patients), and 12q13-14. Previously, such amplifications have been identified very rarely in lymphomas. In the 2 patients with amplifications mapping to chromosomal band 8q24, involvement of the MYC proto-oncogene in the amplification unit was demonstrated by Southern blot analysis. These data provide further entry points for studies to identify genes relevant for tumor progression in FCL-fo.
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PMID:High incidence of chromosomal imbalances and gene amplifications in the classical follicular variant of follicle center lymphoma. 869 64

Human carcinomas are generally considered to develop through the accumulation of various genetic abnormalities. The major types of genetic alterations that are frequently observed in breast cancer are amplification of protooncogenes (MYC, ERBB2); mutation of TP53; and loss of heterozygosity on chromosomes 1, 3p, 8p, 11p, 13q, 17q, 17, and 22q. The latter may correspond to losses or inactivations of tumor suppressor genes. Recently, two major distinct breast susptibility genes were isolated, namely BRCA1 and BRCA2. We performed PCR-SSCP analysis to determine the role of the BRCA1 gene in Japanese breast cancer and investigated how multiple genetic alterations contribute to tumor development and/or progression in primary breast cancer, using a large number of tumor materials.
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PMID:[Genetic alterations and DNA-based diagnosis in breast cancer]. 870 40

Pim-1, a protooncogene product, induced tumor in the combination with MYC. So far, two reports were published concerning Pim-1 function to apoptosis. One was that Pim-1 inhibit apoptosis in Pim-1 introduced transgenic mouse with a background of lpr/lpr, in which Fas was abrogated. However, the other that Pim-1 induced apoptosis in a transient expression system was also reported. In this communication, we survey the possible functions of Pim-1 in terms of the factor related to apoptosis and carcinogenesis.
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PMID:[Apoptosis related gene, Pim-1]. 874 85

We identified 126 tumor cell lines established from patients with small cell cancer at the NCI-Navy Medical Oncology Branch from 1977 through 1992. Extensive clinical information was available on 96 patients from whom these cell lines were established. These patients comprised approximately one fourth of the 407 patients treated on prospective therapeutic clinical trials during the same time period. The proportion of tumor cell lines established from previously untreated patients with both limited and extensive stage small cell lung cancer increased during the 16 years of the study (P = 0.008). MYC family DNA amplification was present in 16 of 44 (36%) tumor cell lines established from previously treated patients compared to 7 of 52 (11%) of tumor cell lines established from untreated patients (P = 0.009). MYC DNA amplification in tumor cell lines established from patients previously treated with chemotherapy continued to be associated with shortened survival (P = 0.001). The initiation of a policy to obtain tumor tissue for the purpose of selecting chemotherapeutic agents given to individual patients was associated with an increase in the proportion of patients from whom tumor cell lines could be established for both extensive and limited stage patients (P = 0.0001 and 0.05, respectively).
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PMID:MYC family DNA amplification in 126 tumor cell lines from patients with small cell lung cancer. 880 3

We intended to establish the frequency of exon-specific TP53 gene alterations and the relation to patient and tumor characteristics and clinical outcome of patients with breast cancer. By using polymerase chain reaction-single-strand conformation polymorphism analysis (PCR-SSCP) and sequencing techniques, TP53 gene alterations were found in 59 (32%) of the 187 samples studied. Most of the TP53 changes (37%) were observed in exon 7. In patients with known follow up (median, 107 months), there was no significant association of the frequency of TP53 mutation with menopausal or nodal status, tumor size, or progesterone receptor status. TP53 gene alterations were more frequently present in estrogen receptor (ER)-negative (ER-) tumors (P = 0.04) and in tumors with an amplified HER2/NEU oncogene (P = 0.03). Univariate analysis showed that patients with a mutated TP53 in their primary tumors had shorter relapse-free (P = 0.01) and overall (P = 0.03) survival. Patients with a TP53 gene mutation in exon 8 may be identified as having a particularly rapid rate of relapse. In Cox multivariate regression analysis, which included age, menopausal status, lymph node status, tumor size, steroid-hormone-receptor status, and oncogene amplifications, both TP53 gene alteration and MYC amplification independently predicted poor prognosis, with relative hazard rates for TP53 and MYC of 1.8 and 1.6, respectively, in analysis for relapse-free survival and of 1.7 and 1.6, respectively, in analysis for overall survival.
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PMID:TP53 and MYC gene alterations independently predict poor prognosis in breast cancer patients. 881 49

The protein product of the retinoblastoma tumor suppressor gene (pRb) has been demonstrated to bind transcriptional factors such as E2F and c-Myc protein in vitro. To determine whether pRb regulates both cellular (c-myc) and viral (HPV LCR) promoter activity in vivo, MYC-CAT or HPV LCR-CAT chimeric expression plasmids were generated and cotransfected with a pCMV-RB expression plasmid. pRb repressed both myc and LCR transcription but not SV40-CAT. Transcriptional repression induced by pCMV-RB was relieved by addition of pSV2-E7. Moreover, immunohistochemical assays indicate that in cervical intraepithelial neoplasia lesions, an increased pRb expression correlates with decreased c-myc oncogene expression. These results suggest that pRb can negatively regulate c-myc transcription in vivo in both normal tissue or early cervical lesions. However, in HPV induced invasive cervical carcinomas where viral DNA is integrated expressing its oncoproteins, pRb could be complexed by HPV E7 oncoprotein releasing the repression effect and promoting cell growth.
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PMID:The retinoblastoma gene product negatively regulates cellular or viral oncogene promoters in vivo. 884 42

The etiology of breast cancer involves a complex interplay of exogenous and endogenous factors, including genetic factors. The identification of oncogenes, tumor suppressor genes and human mismatch repair genes has helped to refine the characterization of breast carcinogenesis. The major types of genetic alterations in breast cancer are amplification of protooncogenes (ERBB2 and MYC) and DNA from chromosome band 11q13; mutation of p53; and loss of heterozygosity on 1p, 3p, 8p, 11p, 13q, 16q, 17p, 17q, 18q. The latter may imply inactivations of tumor suppressor genes. Recently, two distinct familial breast cancer susceptibility genes, BRCA1 and BRCA2, have been isolated. These findings enable to use these genes for genetic diagnosis in clinical oncology.
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PMID:[Cytogenetic abnormalities, genetic alterations, and applications for genetic diagnosis in breast cancer]. 897 25


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