Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0546837 (esophageal cancer)
 8,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

K-SAM gene was originally isolated as an amplified gene in a stomach cancer cell line by in-gel DNA renaturation method. K-SAM encodes a membrane receptor with tyrosine kinase and is often amplified in poorly differentiated type of stomach cancer, while c-ERBB-2 is often amplified in well differentiated type of stomach cancer. There are several forms of K-SAM mRNAs which are generated by alternative splicing, and two types of K-SAM protein without transmembrane region. The ligand of K-SAM is considered to be growth factor(s) belonging to fibroblast growth factor (FGF) or heparin binding growth factor (HBFG) family. We have also frequently found amplification of HST-1 or HSTF1 gene in esophageal cancer. HST-1 gene, originally found as a transforming gene, is located on human chromosome 11q13, and it locates 35 kbp apart from its related gene, INT-2. Neither of the genes was expressed even in cancer cells with the co-amplification. By cosmid walking, we have identified at least two genes, designated tentatively as EXP1 and EXP2, on the same amplicon as HST-1 and INT-2, and the mRNAs for EXP1 and EXP2 genes were increased in amounts proportional to the degree of amplification.
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PMID:Biological significance of gene amplification in carcinogenesis. 184 51

We investigated the amplification and expression of oncogenes in human malignant tumors. The survival rates of patients with c-erbB, c-erbB-2, and int-2 oncogene amplification/expression were significantly lower than those of the patients without gene amplification/expression. Many distant organ metastases were observed in esophageal cancer patients with int-2 amplification, in gastric cancer patients with c-erbB-2 over-expression, and in breast cancer patients with int-2 and c-erbB-2 amplification. These results suggest that the amplification/expression of these oncogenes may serve as good markers for determining the biological malignancy of cancers.
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PMID:[Cancer metastasis and recurrence from the standpoint of amplification and expression of oncogenes in human malignant tumors]. 194 61

The clinical significance of the measurement of c-erbB-2 oncogene product was evaluated. The subjects consisted of 404 patients, including 248 with cancer of the digestive organs and 128 with benign digestive diseases. Serum c-erbB-2 protein levels were measured by sandwich immunoenzyme assay. The positive rates of c-erbB-2 protein, at a cut-off value of 17.0 U/ml, were, for cancers: hepatocellular carcinoma 61.6%, biliary tract cancer 54.8%, pancreatic cancer 25.0%, esophageal cancer 33.3%, gastric cancer 16.9%, and colorectal cancer 5.0%. For benign digestive diseases, the rates were: liver cirrhosis 63.3%, chronic hepatitis 43.2%, acute hepatitis 42.9%, other liver diseases 42.8%, cholelithiasis 30.0%, and chronic pancreatitis 0%. Serum c-erbB-2 protein levels were significantly correlated with the markers of hepatic functional reserve, the indocyanine green retention rate and the hepaplastin test. These findings suggest that serum c-erbB-2 protein levels are greatly influenced by liver dysfunction and that their clinical usefulness as a serum tumor marker is questionable.
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PMID:Serum levels of c-erbB-2 protein in digestive diseases. 752 80

Esophageal cancer is an important problem in the United States. It results in more deaths (over 10,000 annually) than rectal cancer. Furthermore, the incidence of esophageal adenocarcinoma is increasing at a rate faster than that of nearly any other cancer and the reasons for the increase are not well understood. A variety of tumor-suppressor genes (including p53, APC, DCC and Rb) and proto-oncogenes (including prad1, EGFR, c-erb-2 and TGF alpha) may be involved in the development and progression of esophageal cancer. Clinical prognostic factors include stage, Karnofsky performance status, sex, age, anatomic location of the tumor, and degree of weight loss. A new staging system based on depth of wall penetration and lymph node involvement correlates well with prognosis for patients undergoing esophagectomy. Newer staging procedures including endoscopic ultrasound as well as the use of minimally invasive surgery, such as thoracoscopy and laparoscopy, may allow accurate staging without esophagectomy. Surgical resection provides excellent palliation; however, the chance for cure with esophagectomy alone is only 10% to 20%. Adjuvant treatment with pre- or postesophagectomy radiation may improve local-regional control but does not improve survival. Nor has preoperative chemotherapy been shown to improve survival; however, it remains an active area of investigation. Multimodality therapy, namely, chemotherapy and radiation (chemoradiation), given concurrently prior to surgical resection shows promise, with one study indicating a 5-year survival of 34%. A complete pathologic response to chemoradiation correlates with improved survival. Chemoradiation has been shown to be superior to radiation as primary management of esophageal cancer. There has been no successfully completed randomized trial of surgery versus definitive radiation or chemoradiation. However, chemoradiation represents a reasonable alternative to esophagectomy in the primary management of squamous cell carcinoma of the esophagus and chemoradiation also appears to be effective in the treatment of patients with adenocarcinoma of the esophagus, offering significant palliation and a chance for long-term survival as well. Randomized studies of preoperative chemoradiation versus surgery or versus chemoradiation alone are needed. The treatment of advanced esophageal cancer must be directed toward palliation of symptoms. Newer endoscopic techniques, including the use of expansile metal stents, laser ablation, intraluminal high-dose rate brachytherapy, BICAP tumor probe, or photodynamic therapy, offer selected patients short-term palliation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Esophageal cancer. 753 69

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.
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PMID:Amplification and over-expression of the EGFR and erbB-2 genes in human esophageal adenocarcinomas. 809 13

The relation between the concentration of epidermal growth factor (EGF) receptor and the effects of EGF on cell proliferation were studied using 16 newly established human esophageal cancer cell lines. According to 125I-EGF binding assay, the amount of EGF receptor was found to vary from 6 x 10(4) to 1.2 x 10(7) (sites/cell). Changes in EGF-stimulated tyrosine-specific protein kinase activity almost paralleled changes in the number of EGF receptors per cell. Amplification of EGF receptor gene was detected in only one cell line. Under monolayer culture conditions, we found three types of growth responses of esophageal cell lines to EGF; growth in 5 cell lines was inhibited and that in 4 cell lines was stimulated while that in the other 7 cell lines remained unaffected. Relation was observed between the number of EGF receptors per cell and the growth response to EGF. On the other hand, cell lines whose growth was inhibited by EGF in monolayer culture were stimulated by EGF in soft agar culture, though the opposite was not necessarily true.
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PMID:Relation of epidermal growth factor receptor concentration to growth of human esophageal cancer cell lines. 827 53

An improved cDNA selection method was established to isolate expressed genes efficiently from an amplified chromosome region in human cancer. Biotinylated yeast artificial chromosome DNA containing c-ERBB-2 was hybridized in solution with PCR-amplifiable cDNAs of an esophageal cancer cell line bearing the c-ERBB-2 amplification. After capturing the hybrids on avidin-coated magnetic beads, the cDNAs were amplified by PCR. Four new genes (A39, C51, CAB1, and GRB-7) coamplified with c-ERBB-2 were isolated from the enriched cDNA library. CAB1, GRB-7, and c-ERBB-2 were overexpressed in gastric and esophageal cancer cells in correspondence with the amplification. The deduced amino acid sequence of the CAB1 gene had significant homology to the recently discovered steroidogenic acute regulatory protein, StAR, which plays an essential role in cholesterol transport to mitochondria. It was established that multiple overexpressed genes are frequently present in a single amplicon.
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PMID:Isolation of a candidate gene, CAB1, for cholesterol transport to mitochondria from the c-ERBB-2 amplicon by a modified cDNA selection method. 927 27

We used TaqMan PCR to detect quantitative anomalies of tumor markers in both tumor and serum DNA from esophageal cancer patients. We demonstrated the potential of this methodology by detecting erbB-2 amplifications in a plurality of esophageal tumor samples. These amplifications were corroborated by Southern blots. We then showed the potential of this methodology to detect quantitative anomalies of erbB-2 in serum DNA from individuals with a corresponding amplification in the tumor. The capability of TaqMan PCR to detect abnormalities in serum of esophageal cancer patients creates an opportunity to diagnose esophageal cancer and to monitor the outcome of treatment with a blood test.
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PMID:Detection of erbB-2 amplifications in tumors and sera from esophageal carcinoma patients. 1038 22

The epidermal growth factor receptor family consists of four closely related transmembrane receptors: epidermal growth factor receptor (EGF-R), c-erbB-2, c-erbB-3, and c-erbB-4. Overexpression of each receptor may lead to cell transformation and contributes to tumor progression in various malignancies. Although these factors have been analyzed in many cancers separately, little is known about their concomitant expression in esophageal cancer. Based on the finding that EGF-R and c-erbB-2 form highly active transmembranous heterodimers that enhance cell growth and proliferation, we used Northern blot analysis and immunohistochemistry to analyze the concomitant expression of EGF-R, c-erbB-2, and c-erbB-3 in tissue samples obtained from 39 patients undergoing esophagectomy for esophageal cancer. Northern blot analysis revealed a fourfold increase (p < 0.01) in EGF-R mRNA levels in the esophageal cancer samples in comparison with normal tissue samples. The c-erbB-2 receptor was only 1.25-fold elevated in the esophageal cancers, which failed to be statistically significant (p = 0.31). In contrast, c-erbB-3 mRNA levels were 3.5-fold lower (p < 0.01) in the esophageal cancers than in the normal tissues. Immunohistochemical analysis showed weak EGF-R, c-erbB-2, and c-erbB-3 immunostaining in the normal esophageal tissue. In esophageal cancer samples, immunoreactivity for EGF-R, c-erbB-2, and c-erbB-3 was mainly located in the cancer cells. Strong EGF-R, c-erbB-2, and c-erbB-3 immunoreactivity was present in 59%, 64%, and 64% of the esophageal cancer samples, respectively. In consecutive tissue sections, identical cancer cell clusters often exhibited these three closely related receptors simultaneously. However, correlation of the immunohistochemical findings with the clinicopathologic patient parameters revealed that the presence of EGF-R, c-erbB-2, or c-erbB-3 had no influence on patient survival (p > 0.05). In addition, the simultaneous presence of these receptors did not influence survival. Our findings indicate that in esophageal cancer the presence of EGF-R, c-erbB-2, and c-erbB-3 alone or in combination seems to have no major influence on patient prognosis and does not alter tumor growth behavior significantly.
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PMID:Concomitant analysis of the epidermal growth factor receptor family in esophageal cancer: overexpression of epidermal growth factor receptor mRNA but not of c-erbB-2 and c-erbB-3. 1051 40

Esophageal cancer is one of the most frequently occurring malignancies and the seventh leading cause of cancer-related deaths in the world. Esophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer worldwide. Our goal in this study was to detect c-myc, p21(WAF/CIP1), p53, C-erbB-2 and COX-2 immuno-expression in ESCC. Archival formalin-fixed, paraffin-embedded tissues of 18 cases of ESCC (13 biopsies and 5 surgical specimens) were studied, retrospectively, by immunohistochemistry. p53 protein was observed in 50% of the cases, while c-myc was found in 6 of 18 samples (33.33%). All samples (100%) were negative for p21(WAF/CIP1). C-erbB-2 oncoprotein and the COX-2 protein were detected in 5.5% (1/18) and 16.66% (3/18) of the cases, respectively. Taken together, our results suggest that c-myc, p53, C-erbB-2 and COX-2 proteins do not correlate with cancer stage or follow-up in ESCC as revealed by immunohistochemistry.
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PMID:Correlation analysis of c-myc, p21(WAF/CIP1), p53, C-erbB-2 and COX-2 proteins in esophageal squamous cell carcinoma. 2317 19


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