Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent progress in molecular biology has revealed that the proliferation of breast cancer is controlled by various growth factors and their receptors. In particular, the amplifications and products of oncogenes which code growth factors and receptors can be different indicators of clinical malignancy from the conventional prognostic factors. We investigated the relation of c-erbB-2 and int-2 gene amplification, expression, ER and EGFR with clinical characteristics. In retrospective study, the cumulative 10-year survival rate of patients with c-erbB-2 and int-2 gene amplification was significantly lower than in patients without amplification. In 72 cases with tumor diameter less than 3.0 cm, which can be an indication of breast preservation surgery, the survival rates of patients in these gene amplified groups were significantly lower than in the non-amplified groups. As for prospective study, the results were the same as those from retrospective study. These data show that the cases with these gene amplification have a high biological malignancy and high risk of recurrence to distant organs, despite the small tumor diameter.
 ...
PMID:[Abnormalities and clinical characteristics of growth factors and receptor systems in breast cancer]. 791 99

Cell kinetic data are an important adjunct to histologically based tumor classifications and provide reliable information about future tumor behaviour. The growth fraction of 62 transitional cell carcinomas was assessed using Ki-67 and PCNA (Proliferating cell nuclear antigen/cyclin) immunostainings. Ki-67 recognises an unknown nuclear antigen expressed in dividing cells and requires the use of frozen sections. PCNA, a non histone nuclear protein, identifies proliferating cells within fixed, embedded tissue sections. The percentage of labeled cells was expressed as the labeling index (LI). The median LI in normal urothelium and transitional cell carcinoma were 0.5% and 8%, respectively for Ki-67, and 1.5% and 12% for PCNA. A general agreement between indices of cell proliferation and histological grade and stage was demonstrated. Although some discrepancies were observed, there was a strong correlation between Ki-67 and PCNA Lis (r = 0.8308, P < 0.01). In addition, tumor EGFR positive had PCNA values greater than those found in cancer EGFR negative (P = 0.01). These findings suggest that immunohistochemical nuclear labeling with anti-PCNA on routinely processed tissue is a simple technique for the assessment of transitional cell carcinomas.
 ...
PMID:PCNA/cyclin expression in transitional cell carcinomas of the human bladder: its correlation with Ki-67 and epidermal growth factor receptor immunostainings. 793 59

Recent data indicate that epidermal growth factor (EGF) is a potent mitogen to normal pituitary cells. Its receptor (EGFR or c-erbB-1), a cellular homologue of a viral oncoprotein erbB, is knonw to be overexpressed in many tumors, but little is known about the expression of EGF and EGFR in pituitary tumors. Immunocytochemical analyses of EGF, EGFR, and c-erbB-2 (an EGFR-related oncoprotein) were carried out on paraffin-embedded sections of 54 pituitary tumors. In sections from normal pituitary, EGF was localized mainly in the gonadotrophs and thyrotrophs. EGFR was detected in only 5-10% of the cells in all of the normal pituitary sections and was almost undetectable in all (34/34) of the hormone-secreting tumors (19 GH-, 9 ACTH-, 4 PRL- and 2 TSH-secreting tumors). However, in 16/20 of the samples from clinically nonfunctioning tumors, EGFR was markedly overexpressed. The EGFR found in these tumors and in the normal tissue was not the truncated form of the EGFR because all sections stained positively with monoclonal antisera to both the intra- and extracellular domains of the EGFR. EGF was coexpressed in the same NFT samples that stained positively for EGFR and was also found in 2/19 GH-, 2/4 PRL-, and 1/2 of TSH-secreting tumors. The expression of c-erbB-2 was detected in all normal tissue, all NFT, and about half of GH-secreting tumors. No correlation was found with clinical parameters other than tumor categories. Because the overexpression of structurally intact EGFR was confined to NFT, the response of the tumor cells to EGF in vitro was examined. The addition of 1 nM EGF to NFT-derived cells resulted in an increase in [3H]thymidine uptake to 237.5 +/- 19.8% (mean +/- SEM, n = 3) of the control value. EGF also stimulated EGFR messenger RNA levels, shown by Northern blot analysis. In contrast, the expression of glycoprotein hormone common alpha-subunit gene in the tumor cells was reduced by EGF, T3, and 17 beta-estradiol. The novel findings of overexpression of EGFR in most NFT combined with the in vitro response to EGF resulting in an increase in tumor cell growth, up-regulation of EGFR gene and suppression of hormone gene expression implicate a role for EGF and its receptor in the development and/or progression of NFT.
 ...
PMID:Expression of epidermal growth factor (EGF), its receptor, and related oncoprotein (erbB-2) in human pituitary tumors and response to EGF in vitro. 795 24

Nine cases of malignant gliomas were selected for the presence of double minutes (dmin) or homogeneously staining regions (hsr) detected by conventional cytogenetics. Analyses were performed on fresh (2 cases) or xenografted (5 cases) tumors or both (2 cases). A modified comparative genomic hybridization technique (mCGH) was applied exhibiting a single amplified locus in 8 tumors and 4 amplified loci in one tumor. Recurrent sites of amplification were detected in 7p11-p12 (5 cases) and 1q32.1 (2 cases). Signals were also observed in 4q11-q12, 5p15.1, 7q31, 8q24.1 and 9p2 in one tumor each. Southern blotting demonstrated that the genes for EGFR (epidermal growth factor receptor), PDGFRA (platelet derived growth factor receptor alpha), MET and MYC oncogenes were involved in 7p11-p12, 4q11-q12, 7q31 and 8q24.1 amplifications, respectively. These amplifications were found by in situ hybridization on tumor spreads, in dmin or episomes for EGFR, dmin for PDGFRA and MET, and hsr and dmin for MYC genes. Other mCGH signals, for which no target genes could be proposed, were confirmed by chromosome paintings on tumor metaphases. In one of the tumors, the coamplification of DNA from 5p15.1 and 9p2 bands in the same dmin was demonstrated.
 ...
PMID:Oncogene amplification in human gliomas: a molecular cytogenetic analysis. 805 36

Our primary objectives were to: 1) develop a system for the study of prostatic tumor evolution; and 2) examine the role of the epidermal growth factor/epidermal growth factor receptor (EGF/EGFR) pathway in prostate tumor progression. Adult human prostate epithelial cells previously immortalized by transfection with the SV40 T antigen gene (P69SV40T) produced tumors in only 2/18 mice with a 6 month latency period. Reinjection of cells recovered from these tumors after 1 or 2 cycles of growth in nude mice produced tumors in 2/4 and 2/3 mice with markedly decreased latent intervals of 12, 25, 25 and 25 days each. The chromosomal complement of each tumor was human, consistently pseudodiploid, and retained the Y chromosome. In both anchorage-independent and adherent cell growth assays, EGF stimulated proliferation by approximately 2-fold in both the parental P69SV40T line and the tumor sublines. The tumor sublines expressed less EGFR protein than the parental line, as assessed by Western immunoblotting and flow cytometric analysis. Immunoprecipitation revealed increased production of the 18 and 25 kDa TGF-alpha precursors parallel to decreases in detectable EGFR. The growth of both the parental P69SV40T line and the tumor sublines was inhibited by a neutralizing antibody to TGF-alpha under serum-free defined conditions. Inclusion of the TGF-alpha neutralizing antibody consistently inhibited the proliferation of the tumor sublines more than P69SV40T in both proliferation and [3H]thymidine incorporation assays. This finding suggests that the increased tumorigenicity and decreased latent interval observed among the human prostate tumor cells is partially due to activation of the TGF-alpha/EGFR autocrine network.
 ...
PMID:Tumorigenicity of SV40 T antigen immortalized human prostate epithelial cells: association with decreased epidermal growth factor receptor (EGFR) expression. 807 59

Esophageal cancer is one of the 10 most prevalent human cancers worldwide. The incidence of esophageal adenocarcinoma is on the rise and patients with this disease typically have very poor prognosis. Informative biomarkers would benefit the clinical management of this disease. We examined 13 cases with esophageal adenocarcinomas and 5 cases with Barrett's esophagus for amplification of the EGFR and erbB-2 genes. We detected multiple copies of the EGFR gene in 30.8% of the tumors and multiple copies of the erbB-2 gene in 15.4% of the tumors. Of the cases with amplification of the erbB-2 gene, co-amplification of the EGFR gene was found. Multiple copies of the EGFR gene were also found in one case of Barrett's esophagus. Immunohistochemical staining of the tissues revealed increased expression of the erbB-2 protein in Barrett's mucosa and adenocarcinoma, but no associations between staining intensity and degree of EGFR or erbB-2 gene amplification, histology, or tumor stage were found. Differential polymerase chain reaction was examined as a method for pre-operative detection of gene amplification in esophageal tumors and Barrett's mucosa.
 ...
PMID:Amplification and over-expression of the EGFR and erbB-2 genes in human esophageal adenocarcinomas. 809 13

Cancer has been defined as a fundamental disorder of cellular growth control. Which arises in some cells through changes in genes (DNA-level: geneamplification, mutation and rearrangement) or their expression (RNA- and protein-level), and gives these cells a growth advantage in comparison to the surrounding cells. Since the last decade we know the identity of these genes and the nature of the changes they underwent in the cancer cell. Only a few of the known oncogenes play a role in head and neck cancer. These are the EGFR (epidermal growth factor receptor), c-myc, the ras gene family, int-2, hst- 1 and bcl- 1. In some clinical disorders, like childhood neuroblastoma and breast cancer, oncogenes play already an important role in tumor staging as well as a prognostic parameter. The aim for the future is the therapeutic application of oncogenes better known as gene therapy.
 ...
PMID:Oncogenes related to head and neck cancer. 813 94

Breast cancer is a complex but increasingly well-understood disease. Clearly, multiple alterations from normal mammary cells are required to achieve a transformed phenotype. Furthermore, there may be several possible alterations within broad categories that will produce the transformations leading to the malignant state. The specific set of alterations within a given cancer may thus provide necessary information about how it is unique and how it may best be treated. Several of the newer biologic markers of breast cancer may provide very specific treatment information. erbB-2 may predict for improved response to doxorubicin, rather than CMF. hsp 27 may predict for failure of doxorubicin. pS2 or EGFR may provide supplemental information predicting response to hormonal therapy. Each of these variables has strong evidence to support its use in this manner, but that evidence has been obtained on limited numbers of patients treated in a limited number of ways. The most established markers, with multiple studies indicating their prognostic benefit, are erbB-2, cathepsin D, and proliferation markers. Of the several proliferation markers there may be no one choice that is best. However, very clearly, any marker must be carefully assessed for appropriate cut-off values, and cut-off values established by one cohort of patients should be verified against another cohort of patients. The oncoproteins associated with cell cycle regulation (cyclin D, p53, Rb, and c-myc) have shown strong promise of providing important prognostic information. The limited studies to date indicate that these markers are independent of one another. Cell cycle regulation may be an area in which any defect may serve to deregulate the cell, and therefore several defects in one cell would be unlikely. The specific nature of the defect in a given cancer may be very important. With the advent of immunohistochemical methods to measure most of the markers, more information may become available. Finally, the burgeoning area of tumor-stromal interactions is replete with potentially important markers of cancer prognosis. The growth factors, which are marginally a part of this area owing to the probable importance of paracrine effects on cancer cell growth, have progressively developed a body of literature supporting their prognostic potential. However, they have rarely been studied in conjunction with the other aspects of tumor-stromal cooperation. The markers of metastatic potential, nm23 and angiogenesis, have been shown in small cohorts to have considerable prognostic import.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Overview of the biologic markers of breast cancer. 815 Jul 84

In 68 cases of surgically resected gastric carcinomas, expression of human epidermal growth factor (EGF) and its receptor (EGFR) were examined immunohistologically using the Avidin-Biotin Peroxidase Complex Method, and their relation with DNA contents and nuclear protein synthesis in the tumor progression were studied by measuring DNA ploidy patterns and nucleolar organizer regions (NORs), respectively with cytofluorometry and AgNO3 stain method. EGF and EGFR expression were respectively found only in 2 (7%) and 1 (4%) in 28 early cancers, and significantly increased in advanced cancers, 25 (63%) and 9 (23%) out of 40 cases. The ratio of aneuploid tumor and the NORs numbers per tumor cell also increased in advanced cancers, compared with in early cancers. EGF and EGFR respectively expressed in 19 (51%) and 9 (23%) in 37 aneuploid cancers, significantly more frequent than 8 (26%) and 1 (3%) in 31 diploid cancers. In the EGF-positive tumors, the NORs numbers showed 4.11 +/- 0.72, significantly higher than 2.68 +/- 0.61 in the EGF-negative tumors. These results suggested that expression of EGF and EGFR in the gastric carcinomas increases during the tumor progression from the early to advanced stage, stimulates synthesis of DNA and nuclear protein, and consequently enhances (strengthens, heightens, or intensifies) the proliferative activity of the tumors.
 ...
PMID:[Expression of human epidermal growth factor and its receptor of the gastric carcinomas with special reference to DNA ploidy patterns and nucleolar organizer regions]. 817 99

Nine human malignant gliomas (2 astrocytomas grade III and 7 glioblastomas) were analyzed using comparative genomic hybridization (CGH). In addition to the amplification of the EGFR gene at 7p12 in 4 of 9 cases, six new amplification sites were mapped to 1q32, 4q12, 7q21.1, 7q21.2-3, 12p, and 22q12. Nonrandom chromosomal gains and losses were identified with overrepresentation of chromosome 7 and underrepresentation of chromosome 10 as the most frequent events (1 of 2 astrocytomas, 7 of 7 glioblastomas). Gain of a part or the whole chromosome 19 and losses of chromosome bands 9pter-23 and 22q13 were detected each in five cases. Loss of chromosome band 17p13 and gain of chromosome 20 were revealed each in three cases. The validity of the CGH data was confirmed using interphase cytogenetics with YAC clones, chromosome painting in tumor metaphase spreads, and DNA fingerprinting. A comparison of CGH data with the results of chromosome banding analyses indicates that metaphase spreads accessible in primary tumor cell cultures may not represent the clones predominant in the tumor tissue.
 ...
PMID:Comparative genomic hybridization of human malignant gliomas reveals multiple amplification sites and nonrandom chromosomal gains and losses. 820 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>