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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Int J Cancer 1993 May 08
PMID:Amplification and over-expression of the EGFR and erbB-2 genes in human esophageal adenocarcinomas. 809 13

Activation of cellular or c-oncogenes and loss of function of suppressor genes appears to be the key event in the formation of most human cancers. Altered forms of these genes or their protein products have the potential to provide a new generation of cancer markers. As cancer markers, the most useful application of c-oncogenes and suppressor genes so far, has been in providing prognostic information. The correlation of N-myc gene amplification with poor prognosis in neuroblastoma was one of the first examples of prognostic data supplied by a c-oncogene. Most, but not all investigators, find that either amplification or increased expression of c-erbB-2 gene correlates with poor prognosis in breast cancer. Other potential prognostic markers in breast cancer include amplification of the c-myc gene, and increased expression of both EGFR and p53 protein. Although c-oncogenes and suppressor genes have the potential to supply prognostic information in a broad range of cancers, many of the results are still preliminary with conflicting conclusions.
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PMID:Cellular oncogenes and suppressor genes as prognostic markers in cancer. 812 58

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.
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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)
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PMID:Overview of the biologic markers of breast cancer. 815 Jul 84

Epidermal Growth Factor in a polypeptide growth factor of which receptor EGFR has a prognosis value for some malignant tumours. Data are limited concerning the EGFR value in cervix tumours. EGFR was measured in biopsies obtained in cervix cancer patients before any treatment. Twenty-two patients (18 squamous carcinomas, 4 adenocarcinomas) were studied. EGF binding was characterized in seven tumour samples. Scatchard representation identified a single family of binding sites. Kd value revealed high affinity for EGF binding: 0.645 +/- 0.769 nmol/l. EGFR values were determined by a simplified competition method using a radiolabeled ligand. EGFR was found to be more elevated in tumours (n = 20) than in normal tissue (n = 4): (59.5 vs 10.5 fmol/mg proteins). There was a tendency for higher EGFR values in squamous tumours (m = 83.5 fmol/mg proteins) as compared to adenocarcinomas (m = 35.5 fmol/mg proteins), P = 0.09. There was no difference in the distribution of EGFR values according to tumour differentiation and staging. This work confirms the presence of EGFR in cervix tumours. Interestingly, we found that tumours with high EGFR values were more radiosensitive than tumours with low values.
Bull Cancer 1993 Mar
PMID:[Demonstration and characterization of EGF receptors in cancer of the uterine cervix]. 817 74

A series of rat monoclonal antibodies (MAbs) has been generated against the extracellular domain of the receptor for EGF which block the binding of EGF and TGF alpha to the receptor and inhibit the growth in vitro of a range of carcinoma cell lines that over-express the receptor for EGF. Some of these antibodies were able also to induce the complete regression of xenografts of EGFR-over-expressing tumours when treatment was started, either at the time of tumour inoculation or later when the tumours were established. The most effective of these antibodies was ICR62, which was also able to activate host immune effector functions. We conclude that antibodies which block growth-factor-ligand interaction can have a profound influence on the proliferative capacity of tumour cells in vivo and may have useful clinical application.
Int J Cancer Suppl 1994
PMID:Immunotherapy with antibodies to the EGF receptor. 819 87

Radioreceptorial assessment of EGFR expression was prospectively performed on 60 primary human endometrial tumors. Of these, 26 were EGFR-positive while 13 expressed high EGFR levels. High EGFR levels correlated well with poor histopathological grading. No correlation with histopathological type, stage, myometrial invasion, lymph-node involvement or steroid hormone receptor status was observed. Disease-free survival rate was significantly shorter in the cases with high than in the cases with low EGFR levels. These results suggest a potential role of EGFR expression assessment in prognostic characterization of endometrial cancer patients.
Int J Cancer 1994 Jan 02
PMID:Significance of epidermal growth factor receptor expression in primary human endometrial cancer. 826 74

EGFR is a member of the tyrosine kinase family of cell surface receptors with a wide range of expression throughout development and in a variety of different cell types. The receptor can transmit signals to cells: i) upon interaction with ligands such as EGF, TGF alpha, amphiregulin or heparin binding EGF, ii) upon truncation or mutation of extracellular and/or intracellular domains, iii) upon amplification of a basal receptor activity (in the absence of ligand) through cooperation with other cellular signaling pathways or nuclear events (e.g. expression of v-erbA). The activated EGFR can exert pleiotropic functions on cells, depending on their tissue origin and state of differentiation. Under certain conditions it can also contribute to neoplasia and development of metastases. Such conditions can exist upon aberrant receptor/ligand expression and activation (e.g. in the wrong cell; at the wrong time; in the wrong amounts). Aberrant signalling can also occur through constitutive EGFR activation. Oncogenic potential of EGFR has been demonstrated in a wide range of experimental animals. EGFR is also implicated in human cancer, where it may contribute both to the initiation (glioblastoma) and progression (epithelial tumors) of the disease. EGFR may influence key steps in the processes of tumor invasion and dissemination. Involvement of EGFR in tumor spread may indicate a potential use of this receptor as a target for antimetastatic therapy.
Cancer Metastasis Rev 1993 Sep
PMID:EGF receptor in neoplasia and metastasis. 828 12

AGS human gastric cancer cells were characterized to possess EGF receptors. Scatchard analysis revealed a half saturation constant of 0.6 nM and 9000 receptors per cell. Exogenously added EGF stimulated gastric cancer cell growth in a dose-dependent manner with a maximum effect of +38% at 10 nM EGF. Inhibition of the EGFR-associated tyrosine kinase by genistein and the tyrphostins RG-13022, RG-14620 and RG-50864 resulted in a dose-dependent growth inhibition with half maximal inhibition at 10 microM, 7 microM and 23 microM, respectively. EGF mediated growth stimulation was dose-dependently reversed by coincubation with genistein. At genistein concentrations exceeding 6 microM serum-stimulated growth of AGS cancer cells was also inhibited. We conclude that EGF is an important growth factor for AGS gastric cancer cells. Inhibition of the EGFR-associated tyrosine kinase seems to be an effective antiproliferative principle in EGFR-positive human gastric cancer cells.
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PMID:Antiproliferative effect of tyrosine kinase inhibitors in epidermal growth factor-stimulated growth of human gastric cancer cells. 829 23

mRNA expression of stromelysin-3 (ST3) and 72K type IV collagenase (cIVase) in 4 human breast cancer cell lines and 55 resected breast tumors were examined using Northern blot analysis. In 4 cell lines ST3 was not expressed at all, while cIVase gene expression was detected in 3 of them. The ST3 expression was found more specifically in malignant tumors (39/40, 97.5%) than in benign ones (4/15, 26.7%), although cIVase was expressed in all tumor specimens. The quantitative analysis showed that ST3 expression in malignancies was significantly greater than that in benign tumors (P = 0.0007), while cIVase expression was not (P = 0.1381). ST3 gene expression was also closely related to the presence of lymph node metastasis (P = 0.047), while cIVase was not (P = 0.1091). These results suggest, therefore, that ST3 is expressed more specifically by stromal cells surrounding cancer cells than cIVase. Since ST3 mRNA expression was independent of the EGFR, ER and erbB2 protein expression, ST3 may be a new potent prognostic guide for breast carcinomas, which can detect highly malignant subpopulations.
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PMID:Stromelysin-3 mRNA expression and malignancy: comparison with clinicopathological features and type IV collagenase mRNA expression in breast tumors. 829 52


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