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

Transforming growth factor-alpha (TGF-alpha) is a polypeptide growth factor that binds to the epidermal growth factor receptor and is though to stimulate cell proliferation. It has been believed to play a role in tumor initiation by inducing the reversible transformed phenotype; overexpression of TGF-alpha may be important for tumor progression via autocrine stimulation and oncogene overexpression. Expression of TGF-alpha and the epidermal growth factor receptor has been documented in several nontumorous tissues and in a variety of tumors. This study used immunohistochemistry to localize TGF-alpha expression in normal and neoplastic endocrine tissues. Transforming growth factor-alpha was found in nontumorous hypothalamus, pituitary, thyroid, parathyroid, adrenal cortex and medulla, and pancreatic islets. Immunoreactivity was detected in most benign and malignant tumors of these tissues, as well as in endocrine neoplasms of the lung and gastrointestinal tract. Hypothalamic gangliocytomas, pheochromocytomas, and adrenal cortical carcinomas showed consistently greater immunoreactivity than their normal counterpart, but there was no correlation between degree of reactivity and tumor grade, stage, or hormone content. These results suggest that in endocrine tissues, TGF-alpha is unlikely to prove useful as a tumor marker but that the growth factor may play a role in both normal physiology and tumorigenesis.
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PMID:Transforming growth factor-alpha in normal and neoplastic human endocrine tissues. 146 72

Using an immunoradiometric assay, Cathepsin D (Cath D) levels were measured in the cytosol of 23 normal and 39 neoplastic human laryngeal tissues. Scattered Cath D levels (from 2.2 to 17.8 pM/mg protein; median = 7.6) were found in normal mucosa specimens. Cath D concentrations range from 2.0 to 29.3 pM/mg protein (median = 8.5) in laryngeal tumors. When a comparison between Cath D levels in normal and neoplastic tissue specimens from the same patient was done, Cath D levels were significantly higher in laryngeal cancers than in their normal counterparts (P = 0.03). No correlation with clinico-pathological parameters and steroid hormone and epidermal growth factor receptor status was found. Further studies should investigate whether the production of Cath D by laryngeal tumors could have a clinical relevance for this neoplasia.
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PMID:Cathepsin D in primary squamous laryngeal tumors: correlation with clinico-pathological parameters and receptor status. 148 62

In the search for sensitive and specific tumor markers for bladder carcinoma, expression of various oncogenes and gene products (such as c-erb B-2, p53) and epidermal growth factor receptor merits particular attention. Although the results are not yet conclusive, important predictive markers are about to emerge from ongoing studies in this field. Bacillus Calmette-Guerrin treatment in superficial bladder cancer is probably the most successful immunotherapy in humans. But there is still a large knowledge deficit in the issues of optimal dose schedule and mechanisms of action. Although promising results of neoadjuvant chemotherapy in patients with invasive bladder cancers are reported, we must be cautious about changing our conventional approach until the results of large scale, controlled, randomized studies evaluating the survival are published.
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PMID:Bladder cancer. 149 53

We have investigated the expression of epidermal growth factor receptor (EGF-R) in invasive cervical cancer tissue of the uterus to determine whether there is a relationship between the expression of EGF-R and lymph node metastasis. Frozen sections of surgical specimens from twenty patients with invasive cervical cancer were immunohistochemically stained by the alkalinephosphatase anti-alkalinephosphatase method. The monoclonal antibody 528 we employed reacts with the receptor binding epitope within the EGF molecule, indicating that monoclonal antibody 528 is competitive with ligands such as EGF. Immunohistochemical staining was carried out before and after dissociation of ligands from the cellular surface of the tumor by acid treatment. However, the staining was resulted in no difference between before and after acid treatment. Consequently, the expression of EGF-R was detected in all cancer tissues as well in some normal tissue such as basal cell layers of epidermis. The expression of EGF-R was related inversely with lymph node metastasis by Wilcoxon rank sum test (p less than 0.05). These findings suggest that the expression of EGF-R in cervical cancer does not always lead to tumor growth or tumor invasion, although it does in some types of cancer.
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PMID:[Immunohistochemical study on the expression of epidermal growth factor receptor (EGF-R) in invasive cervical cancer of the uterus]. 150 31

Altered expression of growth factors and growth factor receptors is frequently described in human tumors and human tumor cell lines. This further supports the hypothesis that oncogenesis is due to the subversion of mitogen-responsive pathways. The aim of this study was to investigate the expression of epidermal growth factor receptor (EGFR) and transforming growth factor alpha (TGF alpha) in 13 larynx carcinomas and 2 carcinomas of the oral cavity. We found receptor overexpression in 7 out of 15 tumors at mRNA and/or protein level but low expression in the majority of the normal adjacent tissues. TGF alpha was expressed only in 1 case, but no tyrosine kinase activity of the receptor was detected by antiphosphotyrosine antibody.
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PMID:Expression of epidermal growth factor receptor and transforming growth factor alpha in human larynx carcinoma. 151 34

During the past few decades medical science has accepted the concept that cancer is a fundamental disorder of cellular growth control. A disorder can originate in some cells through changes in genes (DNA level: gene amplification, mutation and rearrangement) or their expression (RNA and protein levels), and stimulates growth in contrast to surrounding cells. Over the last decade genes affected in the cancer cell have been identified as well as the nature of changes undergone. Only a few of the known oncogenes play a role in head and neck cancer. These are epidermal growth factor receptor, c-myc, the ras gene family, int-2, hst-1 and bcl-1. In some clinical disorders, such as childhood neuroblastoma and breast cancer, oncogenes have been shown to play an important role in tumor staging or as a prognostic parameter. The aim for future therapy is the effective application of oncogenes (or "gene therapy") in clinical practice.
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PMID:[Oncogenes and their significance for head and neck cancers]. 151 16

A 94 year old man with an invasive ductal carcinoma of the breast (T4N2M1, stage IV), underwent a modified radical mastectomy to improve his quality of life. The estrogen receptor status of both the breast tumor and the metastatic axillar lymph nodes was high. Immunohistochemical staining for epidermal growth factor, epidermal growth factor receptor, or c-erbB-2 protein was negative. The patient received only tamoxifen continuously for 3 months, and later apparently showed a complete remission. Therefore, in advanced male breast cancer with a high estrogen receptor status, operation in conjunction with hormone therapy may lead to a favorable result in some cases.
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PMID:A 94 year old male stage IV breast cancer patient showing complete remission under tamoxifen treatment after operation. 151 97

The expression of epidermal growth factor receptor (EGFR) was investigated in 67 cases of odontogenic cysts and 35 cases of odontogenic tumors using monoclonal antibody to EGFR (Biomarker, Israel) to determine the presence and significance of this transmembrane growth factor receptor. The cystic epithelial cells of odontogenic cystic lesions (keratocyst 60%; primordial cyst 75%; radicular cyst 35%; and follicular cyst 47.4%) were positive to EGFR staining. Cytochemical characterization of EGFR in those cystic epithelium was cell membrane positive type as in the normal epithelium. No expression of EGFR was found in the odontogenic tumors. This diversity of EGFR represents no binding activity of EGF, or loss of EGFR in the tumor cell upon EGFR mediated growth in odontogenic tumors was suggested a different tumor cell growth factor status or microenvironment in cell proliferation mechanism at the cellular level in cysts and tumors of odontogenic origin.
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PMID:Epidermal growth factor receptor in odontogenic cysts and tumors. 152 33

The epidermal growth factor receptor (EGFR) and its ligands are thought to be important in the control of proliferation of many epithelial systems, including the exocrine pancreas. Abnormalities in expression of two of the known ligands of the EGFR, transforming growth factor alpha and epidermal growth factor, occur frequently in ductal adenocarcinoma of the human pancreas. We have examined an archival series of cases of pancreatic pathology for expression of the EGFR using the anti-EGFR antiserum 12E and found that there is almost ubiquitous overexpression of EGFR in pancreatic cancer and in chronic pancreatitis. Southern blot analysis showed no evidence of amplification or rearrangement of the EGFR gene. We conclude that an autocrine loop involving the EGFR system may be involved in the genesis of both neoplasia and reactive hyperplasia of pancreatic ductal epithelium.
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PMID:The epidermal growth factor receptor in human pancreatic cancer. 153 76

Lipotrope-deficient (methyl-deficient) diets cause fatty livers and increased liver-cell turnover and promote carcinogenesis in rodents. In rats prolonged intake of methyl-deficient diets results in liver tumor development. The mechanisms responsible for the cancer-promoting and carcinogenic properties of this deficiency remain unclear. The results of the experiments described here lend support to the hypothesis that intake of such a diet, by causing depletion of S-adenosylmethionine pools, results in DNA hypomethylation, which in turn leads to changes in expression of genes that may have key roles in regulation of growth. In livers of rats fed a severely methyl-deficient diet (MDD), lowered pools of S-adenosylmethionine and hypomethylated DNA were observed within 1 week. The extent of DNA hypomethylation increased when MDD was fed for longer periods. The decreases in overall levels of DNA methylation were accompanied by simultaneous alterations in gene expression, yielding patterns that closely resembled those reported to occur in livers of animals exposed to cancer-promoting chemicals and in hepatomas. Northern blot analysis of polyadenylated RNAs from livers of rats fed control or deficient diets showed that, after 1 week of MDD intake, there were large increases in levels of mRNAs for the c-myc and c-fos oncogenes, somewhat smaller increases in c-Ha-ras mRNA, and virtually no change in levels of c-Ki-ras mRNA. In contrast, mRNAs for epidermal growth factor receptor decreased significantly. The elevated levels of expression of the c-myc, c-fos, and c-Ha-ras genes were accompanied by selective changes in patterns of methylation within the sequences specifying these genes. Changes in DNA methylation and in gene expression induced in livers of rats fed MDD for 1 month were gradually reversed after restoration of an adequate diet. In hepatomas induced by prolonged dietary methyl deficiency, methylation patterns of c-Ki-ras and c-Ha-ras were abnormal. Although human diets are unlikely to be as severely methyl deficient as those used in these experiments, in some parts of the world intake of diets that are low in methionine and choline and contaminated with mycotoxins, such as aflatoxin, are common. Even in industrialized nations, deficiencies of folic acid and vitamin B12 are not uncommon and are exacerbated by some therapeutic agents and by substance abuse. Thus, it seems possible that interactions of diet and contaminants or drugs, by inducing changes in DNA methylation and aberrant gene expression, may contribute to cancer causation in humans.
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PMID:Methyl groups in carcinogenesis: effects on DNA methylation and gene expression. 154 43


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