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)

SCC-RA is one of the fractions of TA-4, extracted and purified from uterine cervical squamous cell carcinoma. I studied SCC-RA in order to evaluate its significance as a tumor marker for esophageal carcinoma. In 32 of 75 (42.7%) esophageal cancer patients, serum SCC-RA was positive. As compared with IAP and CEA, SCC-RA was the best marker to monitor esophageal cancer. SCC-RA positive patients tended to die earlier than negative ones, and it was considered to be one of the prognostic factors. In the immunohistochemical study using anti SCC-RA monoclonal antibody, both the normal epithelium and the carcinoma tissue reacted with SCC-RA. In the carcinoma tissue. SCC-RA reactivity was observed in 27 of 31 specimens (87%). However there was no correlation among the reactivity, the serum level and clinical stage. Furthermore, I studied the relationship between the tumor growth and the serum SCC-RA levels in the nude mice bearing human esophageal squamous cell carcinoma xenografts. The SCC-RA levels in mice sera gradually increased and they correlated well to the tumor volume. In conclusion, SCC-RA reflected the tumor volume and clinical stage, and SCC-RA is useful for monitoring esophageal cancer patients.
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PMID:[Clinical and fundamental study of a squamous cell carcinoma related antigen (SCC-RA) for esophageal squamous cell carcinoma]. 187 May 66

Serum levels of CA 125 and markers reputed as specific for cancers in relevant locations (squamous cell carcinoma, SCC, carcinoembryonic antigen, CEA, CA 19.9, alpha-fetoprotein, AFP) were determined in 107 patients with gastrointestinal (GI) carcinomas. The aim of this study was to assess their individual and combined sensitivities, and the power of CA 125 in excluding primary ovarian epithelial cancer from GI primary. Serum CA 125 levels (in U/ml) ranged from nondetectable to 400 in patients with esophageal, to 570 in those with gastric, and to 300 in patients with colorectal carcinoma. The levels for liver secondaries, pancreatic, and hepatocellular carcinoma were 480, 2,720 and 1,100 U/ml, respectively. Serum SCC antigen was elevated in all patients with esophageal cancer, CEA or CA 19.9 in 52% of patients with gastric cancer and in 63% with liver secondaries, and CEA in 95% of patients with colorectal cancer; whereas serum CA 125 above 65 U/ml was found in 25% of this subgroup, but only in those with already an elevated concentration of specific marker(s). Serum CEA or CA 19.9 was elevated in 71%, CA 125 in 59% of patients with pancreatic cancer; the latter mostly in those with already elevated CEA or CA 19.9. Serum AFP was elevated in 84% and CA 125 in 40% of patients with hepatoma; the latter mostly in those with already an elevated AFP. CA 125 values exceeding 1,000 U/ml were found in 1 patient with pancreatic cancer (2,720 U/ml) and in 2 with hepatoma (1,050 and 1,100 U/ml). These findings illustrate the nonspecificity of the CA 125 antigen, its small if any advantage compared to the specific markers, and they diminish its role as a marker for primary ovarian cancer from GI primary unless it exceeds 2,800 U/ml.
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PMID:Serum levels of CA 125 in patients with gastrointestinal cancers. 248 Jun 31

Mouse monoclonal antibody (MAb) 3F8E3 (IgG3k) was developed against the head and neck cancer cell line LICR-LON-HN2. Subjected to indirect immunofluorescence, the MAb reacted exclusively with SCC cell lines and showed no reactivity with normal or transformed mouse and human non-SCC cell lines and hematopoietic cell lines. The radiolabelled MAb showed an affinity constant of 1.8 x 10(8) M-1 with HN2 cells and identified 2.07 x 10(4) sites/cell by Scatchard analysis. It identified 2 peptides from membrane extracts of HN2 cells by Western blotting. Avidin-biotin-complexed immunoperoxidase staining on cryostat sections of tumors from various tissues revealed that 3F8E3 reacted mainly with the membrane antigens of well differentiated SCC cells of oral cavity, larynx, esophagus, lung, uterine cervix, metastatic nodes of patients with oral cancer, and dysplastic cells in oral leukoplakia. The MAb did not react with poorly differentiated cells of Ca esophagus, adenocarcinoma of breast, stomach and colon, renal-cell carcinoma and soft-tissue sarcoma.
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PMID:Monoclonal antibody against human squamous-cell-carcinoma-associated antigen. 258 66

This study was carried out to evaluate whether the preoperative levels of serum glycoproteins (CEA, SCC, TPA, IAP, ACT, ASP and sialic acid) and HLA antigens (class I and II) could be potential aids in the selection of suitable gastric and esophageal cancer patients for postoperative adjuvant immunotherapy of PSK. Gastric cancer patients underwent gastrectomy and received postoperative adjuvant chemotherapy (MMC, FT and ADR) with or without PSK. One hundred and forty esophageal cancer patients in cooperative study groups (organizing chairman; Dr. Hiroshi Satoh) underwent esophagectomy and received postoperative adjuvant radiotherapy and chemotherapy (FT, BLM) with or without PSK. The efficacy of PSK was recognized in the patients with normal levels of all glycoproteins in gastric cancer, and with normal levels of CEA or SCC or TPA and abnormal levels of one or more APRs in both gastric and esophageal cancer, and with positive HLA-B40 antigen. The combination of tumor-associated factors, such as CEA, SCC and TPA and various non-specific reactants such as APRs was useful as a prognostic indicator. In addition, some of HLA antigens were also valuable. The pretreatment levels of glycoproteins and HLA antigens have potential aids in the selection of patients with gastric and esophageal cancer for PSK treatment.
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PMID:[Clinical effects of PSK on esophageal and gastric cancer patients and usefulness of serum levels of glycoproteins and HLA antigens as prognostic indicators]. 258 37

The CD4-CD8+ CTL (KE-4 CTL) cell line against autologous tumor cells was established in a patient with esophageal cancer. This KE-4 CTL recognized a peptide antigen on esophageal and lung squamous cell carcinomas in an HLA A2601-restricted manner, as evaluated by cytotoxicity against a panel of tumor cells, transfection experiments with HLA A2601 cDNA, and reconstitution with eluted peptides. None of the normal cells tested was lysed by this CTL. These results suggest the existence of HLA A2601-restricted CTL precursors recognizing a peptide antigen on SCC in a patient with esophageal cancer.
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PMID:HLA A2601-restricted CTLs recognize a peptide antigen expressed on squamous cell carcinoma. 767 Dec 30

Oesophageal cancer is the fifth most frequent cause of cancer death world wide and most of these cancers occur in developing countries. The survival rate for SCC or ADCs of the oesophagus is equally poor, mainly due to their late detection and the poor efficacy of the therapy. A short review of the natural history of these cancers, and in particular the occurrence of genetic and cellular alterations associated with cancer progression, is presented and discussed in the context of the relevance to aetiology and pathogenesis. SCCs and ADCs show a distinct pattern of TP53 mutations, namely a high prevalence of G > A transitions at CpG sites in ADCs whereas in SCCs a higher prevalence of G to T transversions and mutations at A:T base pairs is present. In both types of cancers TP53 mutations occur very early and are followed by the accumulation of other genetic alterations during the process of oesophageal carcinogenesis. The value of these genetic alterations in assessing the multifocal monoclonal origin of oesophageal cancer is also addressed.
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PMID:Molecular precursor lesions in oesophageal cancer. 1048 23

It has been reported that circulating anti-p53 antibodies (p53-Ab) in the serum are detected in some cancers. To investigate the usefulness of detecting p53-Ab, we measured the circulating p53-Ab in comparison with squamous cell carcinoma antigen (SCC-Ag) in patients with esophageal carcinoma. Serum specimens from 46 esophageal cancer patients (42 squamous cell carcinomas, 3 mucoepidermoid carcinomas and 1 basaloid squamous carcinoma) and 13 healthy subjects were studied. Serum p53-Ab was measured by an enzyme-linked immunosorbent assay. Surgically resected specimens from 43 patients were immunohistochemically stained for p53. Serum SCC-Ag was measured by a radioimmunoassay. The results were analyzed with the clinical data and outcome. Serum p53-Ab was detected in 13 (28%) of the 46 patients, but not in any of the healthy subjects. The positive rate was 0% (0/6) in stage I, 60% (3/5) in stage IIA, 30% (3/10) in stage IIB, 29% (7/24) in stage III and 0% (0/1) in stage IV. There was no difference in the outcome between the p53-Ab-positive and p53-Ab-negative patients. Immunohistochemically, 30 (70%) of the 43 specimens stained positively for p53. Serum p53-Ab was detected in 43% (13/30) of the patients with tumors which stained positively for p53. There was a close correlation between positivity for p53 immunostaining and positivity for p53-Ab (p<0.01). An elevated level of SCC-Ag was found in only 13%of the patients, and most patients positive for SCC-Ag already had advanced disease with lymph node metastasis and invasion to the adventitia. In conclusion, serum p53-Ab was detected in Japanese esophageal cancer patients at a frequency similar to that reported in Western countries. Serum p53-Ab may be a potentially useful molecular marker for detection and screening of esophageal cancer. Further studies of a large population may be required to elucidate the true diagnostic usefulness of measuring the serum p53-Ab.
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PMID:Detection of circulating anti-p53 antibodies in esophageal cancer patients. 1075

AIM:To determine the extent of apoptosis and its possible relationship with the changes of p53, Waflp21, bcl-2, and c-myc at different stages of esophageal carcinogenesis.METHODS:Two hundred and forty-one esophageal biopsy samples from symptom-free subjects and 38 surgically resected esophageal carcinoma tissues from a high-risk population for esophageal cancer in Henan, China were used in this study.Apoptotic cells and apoptotic bodies were identified by well-established morphological criteria. The extent of apoptosis and its possible relationship with the rate of cell proliferation (PCNA) and changes of p53, Waf1p21, bcl-2,and c-myc were analyzed in samples with esophageal precancerous and cancerous lesions.RESULTS:The apoptotic cells, identified morphologically, were located in the same proliferative compartment of hyperproliferative cell population in the esophageal epithelia as the cells immunostaining-positive for p53, bcl-2, c-myc and PCNA.The apoptotic indices (total number of apoptotic cells and apoptotic bodies per mm(2) of the tissue section) were low in the normal epithelia,and increased significantly as the lesions progressed from BCH to DYS and to SCC.The extent of apoptosis correlated well with the cell proliferation indices based on PCNA. The total number of positive cells for p53 stain was much higher than that of apoptotic cells. No difference in apoptotic indices was found between p53-positive and p53-negative samples. Waf1p21-positive cells resided in cell layers were higher in number than p53 and PCNA-positive cells. The number of immunostaining positive cells for Waflp21 increased slightly from normal to BCH,but decreased in DYS and SCC. Positive staining samples for bcl-2 and c-myc increased as the lesions progressed from BCH to DYS and to SCC. No apparent correlation between apoptosis and Waf1p21, bcl-2 or c-myc expression was observed.CONCLUSION:The extent of apoptosis was low in normal esophageal epithelium and increased as the lesions progressed. The apoptotic cells were located in the same hyperproliferative cell compartment as cells immunostaining-positive for p53, bcl-2,c-myc and PCNA,but no apparent correlation between apoptosis and these parameters was observed,possibly due to the complexities of molecular changes in esophageal carcinogenesis.
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PMID:Apoptosis and its relationship with cell proliferation, p53, Waf1p21, bcl-2 and c-myc in esophageal carcinogenesis studied with a high-risk population in northern China. 1181 1

The level of transforming growth factor beta1 (TGFbeta1) and transforming growth factor betaII receptor (TGFbetaRII) was determined immunohistochemically in normal tissues and tissues with different severities of lesions (basal cell hyperplasia, BCH; dysplasia, DYS; carcinoma in situ, CIS; and squamous cell carcinoma, SCC) from surgically resected human esophagi and esophageal biopsies of symptom-free subjects. The samples were from an area with high esophageal cancer incidence in northern China (Linzhou, formerly Linxian, and nearby county Huixian in Henan Province). Peroxidase immunostain (ABC) and conventional hematoxylin and eosin stain were used. The tissue sections were incubated with antibodies of TGFbeta1 and TGFbetaRII overnight. The immunoreactivity was observed in cytoplasm of the esophageal specimen. From normal to BCH to DYS to CIS and to SCC, the positive immunostaining rates for TGFbeta1 increased significantly (P < 0.05). A linear correlation between the positive immunostaining rates of TGFbeta1 and the different lesions was observed (P < 0.05). From well- to moderately- and poorly differentiated SCC, the positive immunostaining rates for TGFbeta1 decreased gradually, but the difference was not significant (P > 0.05). In contrast, with the lesions progressing from normal to BCH to DYS to CIS and to SCC, the positive immunostaining rates for TGFbetaRII decreased significantly (P < 0.05). From well- to moderately- and poorly differentiated SCC, the positive immunostaining rates for TGFbetaRII decreased significantly (P < 0.05). There was a linear correlation between the positive rates of TGFbetaRII and different lesions and SCC differentiation (P < 0.05). The present results indicated that the alterations of TGFbeta1 and TGFbetaRII is a frequent event in esophageal multistage carcinogenesis, the absent or lower expression of TGFbetaRII may lead to the loss of cell proliferation control by TGFbeta1 and the overexpression of TGFbeta1 may be a negative feedback response caused by the lower expression of TGFbetaRII protein.
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PMID:Changes of TGFbeta1 and TGFbetaRII expression in esophageal precancerous and cancerous lesions: a study of a high-risk population in Henan, northern China. 1206 47

We performed an integrated cytogenetic study using a combination of comparative genomic hybridization (CGH), spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) to analyze chromosomal aberrations associated with 8 human esophageal squamous cell carcinoma (EC-SCC) cell lines, and used real-time quantitative PCR (Q-PCR) to study the copy number changes of two candidate genes of chromosome 3q, PIK3CA and TP63, in 20 primary tumors of EC-SCC. The pooled CGH results revealed frequent gain abnormalities on chromosome arms 1p, 1q, 3q, 5p, 6p, 7p, 7q, 8q, 9q, 11q, 12p, 14q, 15q, 16p, 16q, 17q, 18p, 19q, 20q, 22q, and Xq, while frequent losses were found on 3p, 4, 5q, 6q, 7q, 9p, and 18q. SKY detected 195 translocations, 13 deletions and 2 duplications. Among the 374 breakpoints, most clustered at the centromeric regions, such as 8q10, 13q10, 7q10, 9q10, 14q10, 15q10, 16q10, 21q10, and 22q10, but also at other regions, including 3q (3q21, 3q22, 3q25), 7p (7p22, 7p14, 7p12), 7q (7q21, 7q31, 7q32), 8q (8q21.1, 8q23), 11q (11q21, 11q24), 13q (13q14) and 18q (18q21). There was a good correlation between the number of aberrations identified by CGH and SKY (r=0.667; p=0.035). Combined CGH and SKY analyses indicated that chromosomes 3, 7, 9, 11, 14, 16, 18, 19, 20, and 22 harbored higher frequency of chromosomal aberrations than expected. FISH using BAC clones containing oncogene PIK3CA and TP63 found that both genes were amplified in 6 and 5 cell lines, respectively. Q-PCR analysis of primary tumors revealed amplification of PIK3CA and TP63 in 100% and 80% of the cases. Average copy number of PIK3CA per haploid genome was greater than that of TP63 (6.27 vs 2.73), and the difference showed statistical significance (p<0.001). Combination of CGH, SKY and FISH could reveal detailed chromosomal changes associated with esophageal cancer cells, and Q-PCR could assess the change of the candidate genes in clinical samples in a high throughput way.
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PMID:Genotypic analysis of esophageal squamous cell carcinoma by molecular cytogenetics and real-time quantitative polymerase chain reaction. 1296 65


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