Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidermal growth factor receptor (EGFR) was studied in ovarian tumours with immunohistochemical (IH) and ligand-binding assay (LBA). Two different monoclonal antibodies (MoAbs: 2E9, EGFR1) with respect to detecting EGFR with different ligand-binding affinities (low, high and low) were used. When comparing the IH data of MoAbs, 2E9 and EGFR1 a significant correlation was found (2P < 0.0001). Both antibodies stained 77% of the adenocarcinoma samples. The incidence of positivity as well as the mean percentage of stained cells was increased in metastases when compared with primary lesions. In 12.5% overexpression of EGFR (score 3) was noticed in some of the tumour cells. This was not due to amplification of the EGFR gene in any of the 25 ovarian tumours studied (including 6 which showed high expression of EGFR in IH). EGFR was detected in 66% of the adenocarcinomas analysed with LBA. A statistically significant correlation was found between the maximum binding capacities of EGFR obtained from Scatchard plots and the percentage of positive tumour cells determined by MoAb EGFR1 (2P < 0.0001). A weaker correlation was found between the reactivity of MoAb 2E9 and LBA (2P < 0.1). Clinical studies are necessary to determine the possible prognostic impact of EGFR determined with either method, or whether a combination of both will give a better discrimination between high- and low-risk patients.
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PMID:Epidermal growth factor receptor in ovarian tumours: correlation of immunohistochemistry with ligand binding assay. 145 40

Epidermal growth factor receptor (EGF-R) expression was studied immunohistologically in 38 patients with esophageal squamous cell carcinoma. The EGF-R was faintly expressed in basal and parabasal layers of normal esophageal epithelia and in cancer nests of 20 patients; it was strongly expressed in all areas of dysplastic epithelia and in cancer nests of 18 patients. The patients with strongly expressed EGF-R had lymph node metastases more frequently, and their prognosis was poorer than those with faintly expressed EGF-R. The EGF-R expression showed a mosaic pattern in 17 patients and a diffuse pattern in 21 patients. The patients with a mosaic pattern had lymph node metastases more frequently and a worse prognosis than those with a diffuse pattern. Expression of EGF-R in metastatic lymph nodes was similar to that in strongly expressing areas of primary cancers with a mosaic pattern. Thus EGF-R expression may be an important indicator for malignancies of esophageal squamous cell carcinomas because primary cancer cells with strongly expressed EGF-R metastasize to lymph nodes more frequently.
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PMID:Immunohistologic detection of the epidermal growth factor receptor in human esophageal squamous cell carcinoma. 170 47

Epidermal growth factor receptor expression in fresh-frozen uterine tissues was studied with the use of monoclonal antibody 528, which recognizes an epitope on the external domain of the epidermal growth factor receptor. Immunohistochemically detectable epidermal growth factor receptor was seen in all uterine cell types in 19 of 20 normal uteri. Staining of endometrial glands and endometrial stromal cells was consistently greater than that of myometrium, and no variation in intensity or distribution of staining was seen during the menstrual cycle. Immunohistochemically detectable epidermal growth factor receptor was found less frequently in endometrial adenocarcinomas than in normal endometrium (p less than 0.01). Thirteen of 40 endometrial adenocarcinomas (32.5%) did not express detectable receptor. Epidermal growth factor receptor expression did not correlate with histologic grade, depth of myometrial invasion, estrogen-progesterone receptor status, the presence of extrauterine metastases, or the development of recurrent disease.
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PMID:Epidermal growth factor receptor expression in normal and malignant endometrium. 248 65

The subjects in this study consisted of 40 preoperative untreated esophageal squamous cell carcinoma patients. While p53 did not significantly correlate with the clinicopathological factors, E-cadherin significantly correlated with lymphatic invasion, vascular invasion, the depth of invasion, the degree of lymph node metastasis, the histological stage, and the number of lymph node metastases. Epidermal growth factor receptor (EGFR) significantly correlated with age, the depth of invasion, and the number of lymph node metastases. The 5-year cumulative survival rate was 45.7% in the p53-positive cases and 61.9% in the p53-negative cases, with no significant difference, and 87.8% in the E-cadherin-positive cases and 19.1% in the -negative cases, and the difference was significant. The prognosis was significantly poor in EGFR-positive subjects: the 5-year survival rate was 38.6% in EGFR-positive cases and 68% in -negative cases. The 5-year survival rate in E-cadherin-negative, EGFR-positive cases was 0%, while it was 91.7% in the reverse pattern, and this difference was significant. These findings suggest that both E-cadherin and EGFR are important prognostic factors, and a more precise prognosis can thus be obtained by combining them. Such a combined technique may be very useful as an indicator for grading the biological malignancy of esophageal cancer.
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PMID:Evaluation of malignancy and the prognosis of esophageal cancer based on an immunohistochemical study (p53, E-cadherin, epidermal growth factor receptor). 1038 63

Epidermal growth factor receptor (EGF-R) is known as an indicator of endocrine independence of breast cancer. However, a small proportion of EGF-R expressing tumors was found to respond to endocrine treatments. On the other side, a cut-off point of EGF-R positivity is not yet defined. In the aim to find out whether there exists a cut-off value that sharply discriminate the endocrine sensitive and endocrine insensitive breast cancers, the quantitative EGF-R content was analyzed in a group of 42 female patients with metastatic disease, being routinely treated with chemo-, chemo-endocrine, or endocrine therapy alone. Steroid receptors (SR) and EGF-R were determined by biochemical methods in tissue samples of an unselected group of patients. Patients with metastatic disease, either at diagnosis, or developed after the treatment of operable or locally advanced breast cancer, were included in the present analysis. According to the treatments used, and their therapeutic response, all patients were divided in endocrine sensitive or resistant, and chemo-sensitive or resistant. The SR and EGF-R status and content was analyzed in relation to the sensitivity to both systemic treatments. The EGF-R content was significantly lower in responders to endocrine treatments, compared to non-responders, while there was no difference in EGF-R level, in relation to the sensitivity to chemotherapy. In addition, the EGF-R content was significantly higher in chemo-sensitive tumors, than in endocrine sensitive. On the contrary, ER content was significantly higher in endocrine sensitive, than in endocrine resistant, and in chemo sensitive patients, as well. Similar differences were found in PR content, but they were less pronounced. While the individual ER contents in endocrine sensitive and endocrine resistant tumors overlapped, the EGF-R ranges were different: no one endocrine sensitive tumor exceeded the EGF-R content of 26 fmol/mg, thus suggesting the EGF-R cut-off point of endocrine sensitivity. The clinical use of EGF-R, with the cut-off point of 26 fmol/mg, in addition to clinical criteria of endocrine sensitivity and SRs, would significantly improve the correct endocrine sensitivity prediction (from 52 to 78%). In conclusion, in a group of metastatic breast cancer patients, treated routinely by systemic therapies it was found, that the use of higher cut-off point for EGF-R positivity can improve the prediction of endocrine sensitivity. The prognostic relevance of this cut-off value remains to be analyzed.
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PMID:Content of epidermal growth factor receptor in metastatic breast cancer: its role in endocrine sensitivity prediction. 1098 76

Head and neck squamous cell carcinoma is a clinically challenging disease that resulted in more than 500,000 cases worldwide in 2001. In the United States, head and neck squamous cell carcinoma has accounted for approximately 40,000 cases with 12,000 deaths reported in 2001, which makes it the fifth leading cause of cancer incidence and the sixth leading cause of cancer-related deaths. Patients with recurrent or metastatic disease have a median survival rate of approximately 6 months; and there is little evidence from randomized trials that survival advantages have been achieved over the community standard of cisplatin and infusional 5-fluorouracil combination. Despite significant improvements in diagnosis, local management, and chemotherapy of head and neck cancer, there has been no significant increase in long-term survival rates over the past 30 years. As little progress has been made, new management approaches are required. Novel biologic agents have been developed to target multiple specific regions of the cancer cell. Epidermal growth factor receptor blockers have been investigated, such as anti epidermal growth factor receptor monoclonal antibodies, tyrosine kinase inhibitors, ligand conjugates, immunoconjugates, and antisense oligonucleotides. Farnesyl transferase inhibitors are a class of compounds that inhibit a critical enzymatic step in the constitutive expression of mutated ras genes, which are present in more than 27% of oral cancers. Strategies targeting the p53 gene and protein may halt or reverse the process of tumorigenesis and metastasis as p53 mutations occur in 45 to 70% of head and neck squamous cell carcinoma patients. Continued development of these novel agents may help improve the overall response and survival rate of patients with head and neck cancer.
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PMID:Novel therapeutics for head and neck cancer. 1198 Dec 81

Epidermal growth factor receptor (EGFR) is a member of the ErbB family of receptors. Its stimulation by endogenous ligands, EGF or transforming growth factor-alpha (TGF-alpha) results in activation of intracellular tyrosine kinase, therefore, cell cycle progression. High levels of EGFR expression are correlated with poor prognosis and resistance to radiation therapy in a variety of cancers, mostly in squamous-cell carcinoma of the head and neck (SCCHN). Blocking the EGFR by a monoclonal antibody results in inhibition of the stimulation of the receptor, therefore, in inhibition of cell proliferation, enhanced apoptosis, and reduced angiogenesis, invasiveness and metastases. The EGFR is a prime target for new anticancer therapy in SCCHN, and other agents in development include small molecular tyrosine kinase inhibitors and antisense therapies.
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PMID:The epidermal growth factor receptor (EGFR) in head and neck cancer: its role and treatment implications. 1672 44

Bronchioloalveolar carcinoma is a fascinating and unusual variant of nonsmall-cell lung cancer that has a tendency towards an indolent course and to metastasize to the lung rather than distant organs. Chemotherapy has shown activity in advanced bronchioloalveolar carcinoma but response rates remain low. Epidermal growth factor receptor tyrosine kinase inhibitors have shown impressive activity against bronchioloalveolar carcinoma in trials. New data suggest that epidermal growth factor receptor mutations and gene copy number may predict subsets of patients who could most benefit from these novel agents. These new findings may point the way to a new era in which we can predict which patients will respond to epidermal growth factor receptor tyrosine kinase inhibitors and thus allow us to tailor therapy to the individual patient.
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PMID:A new era for bronchioloalveolar carcinoma: current state of the art and recent advances in biologically targeted therapy. 1706 26

Recurrent vulvar carcinoma with metastasis has few effective treatment options, which are mainly directed toward palliation of symptoms. A 70-year-old woman was originally treated in 1999 for vulvar squamous cell carcinoma (SCC) with radical vulvectomy and bilateral inguinofemoral groin dissection. She represented in 2005 with a new lesion distinct from the margin of her first disease occurrence. Although treatment of this area included surgical resection and chemoradiation, she recurred 3 months later. Despite radical surgical resection with an anal perineal resection, she presented 2 months later with widely metastatic disease. Epidermal growth factor receptor (EGFR) staining of the tumor cells showed 3+ staining in 100% of the cells. She was treated with palliative radiation therapy (RT) and a cetuximab plus cisplatin chemotherapy protocol. A partial response was obtained for 5 months with palliation of symptoms. Few treatment options exist for recurrent metastatic vulvar carcinoma. The combination of the EGFR antagonist cetuximab with cisplatin has shown modest success in other metastatic SCCs. The partial response experienced in our patient suggests its potential use in women with recurrent or metastatic vulvar carcinoma.
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PMID:Recurrent metastatic vulvar carcinoma treated with cisplatin plus cetuximab. 1802 Dec 14

Despite various effective local treatments for hepatocellular carcinoma (HCC), some patients do not meet the treatment criteria because of extrahepatic metastases or macroscopic vascular invasion at the time of their diagnosis. Furthermore, many patients treated with successful local treatments develop recurrences after treatment. Although these patients receive systemic treatment including chemotherapy, HCC is generally recognized as a chemo-resistant tumor. Recently, new molecular targets have been confirmed and various targeted agents are now being investigated for the treatment of HCC. Epidermal growth factor receptor (EGFR) is frequently expressed in human hepatoma cells, and EGF may be one of the mitogens that are needed for the growth of hepatoma cells. HCC is generally hypervascular, and vascular endothelial growth factor (VEGF) promotes HCC development and metastasis. Various inhibitors targeting EGFR and/or VEGF, VEGF receptor (VEGFR) have been developed as treatments of HCC. In phase-II studies of these growth factor inhibitors, the response rates are relatively low; however, high rates of disease control, enabling a good time to progression, have been achieved. Recently, a randomized phase III trial of sorafenib versus placebo conducted in patients with advanced HCC demonstrated the beneficial effects of this drug on the time-to-progression and overall survival of the patients, and the drug could become established as the standard chemotherapeutic agent for advanced HCC. Further clinical trials using biologic agents are warranted to prolong the survival in HCC patients.
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PMID:Growth factors as therapeutic targets in HCC. 1843 84


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