Biomedical subjects

W Dai

Publications and source records attributed to W Dai.

At least 37 records · Page 2Linked to original sources

PubMed2001

Lysosome proteins are redistributed during expression of a GTP-hydrolysis-defective rab5a.

The functioning of the endocytic pathway is influenced by a distinct set of rab GTPases, including rab5a, which regulates homotypic fusion of early endosomes. Expression of a dominant active, GTPase-defective rab5a accelerates endosome fusion, causing the formation of a greatly enlarged endocytic compartment. Here we present evidence that rab5a also regulates trafficking between endosomes and lysosomes and may play a role in lysosome biogenesis. The GTPase defective rab5aQ79L mutant was inducibly expressed as an EGFP fusion in HEK293 cells, and the distribution of lysosome proteins and endocytic markers then assessed by deconvolution fluorescence microscopy. During expression of EGFP-rab5aQ79L, the lysosome proteins LAMP-1, LAMP-2 and cathepsin D were found in dilated EGFP-rab5aQ79L-positive vesicles, which also rapidly labeled with transferrin Texas Red. Exogenous tracers that normally traffic to lysosomes after prolonged chase (dextran Texas Red and DiI-LDL) also accumulated in these vesicles. Dextran Texas Red preloaded into lysosomes localized with subsequently expressed EGFP-rab5a Q79L, suggesting the existence of lysosome to endosome traffic. Cells expressing EGFP-rab5a wt or the dominant negative EGFP-rab5aS34N did not exhibit these abnormalities. Despite the dramatic alterations in lysosome protein distribution caused by expression of EGFP-rab5a Q79L, there was little change in the endocytosis or recycling of a cell-surface receptor (beta2-adrenergic receptor). However, there was a deficiency of dense beta-hexosaminidase-containing lysosomes in cells expressing EGFP-rab5aQ79L, as assessed by Percoll gradient fractionation. These results suggest that expression of a GTPase-defective rab5a affects lysosome biogenesis by alteration of traffic between lysosomes and endosomes.

Cell Line↗

PubMed2001

[The protective effect of hepatocyte growth-promoting factor (pHGF) against carbon tetrachloride-induced acute liver injury in rats. II. Protective effects on cell membrane injury].

To examine the protective effects of hepatocyte growth-promoting factor (pHGF) against carbon tetrachloride (CCl4) -induced acute liver injury in rats, the pathological changes were observed by light and electron microcopy, and the serum GOT and GPT levels were measured. Acute liver injury was produced by the injection of CCl4 (2ml/kg BW) in two groups of animals, of which one received pHGF (300 microg/kg BW) via the tail vein after 4 hrs. In the group treated with CCl4 alone, serum GOT and GPT were significantly elevated (1280+/-228 and 187+/-73 IU/l, respectively) 6 hrs after injection, indicating the induction of liver injury by CCl4. They reached a peak (3836+/-654 and 1022+/-230 IU/l, respectively) at 48 hrs and declined thereafter, but did not completely recover after 72 hrs. PAS-negative cells were observed around the central veins after 6 hrs and most of the hepatocytes were PAS-negative at 12 hrs. PAS-positive cells began to appear and increased in number after 24 hrs. There were scarcely any PAS-negative cells remaining in the lobules after 72 hrs. In the group treated with CCl4 followed by pHGF, serum GOT and GPT levels were significantly lower than in the CCl4-treated group, and abundant PAS-positive hepatocytes were observed. Also, all hepatocytes were PAS-positive (as in normal liver) after 72 hrs. Administration of pHGF resulted in a decrease in the ultrastructural changes in rats with CCl4-induced liver injury such as vacuolation, cisternae formation and dilatation of the rough endoplasmic reticulum. These results suggest that pHGF acts to stabilize cell membranes, thereby providing protection against CCl4-induced hepatic injury.

Acute Disease↗

PubMed2001

Characterization of the laminated layer of in vitro cultivated Echinococcus vogeli metacestodes.

The metacestode (larval) stages of the cestode parasites Echinococcus vogeli and E. multilocularis were isolated from the peritoneal cavity of experimentally infected C57BL/6 mice and were cultured in vitro for a period of up to 4 mo under conditions normally applied for the in vitro cultivation of E. multilocularis metacestodes. In contrast to E. multilocularis, E. vogeli did not exhibit extensive exogenous budding and proliferation but increased in size with a final diameter of up to 10 mm. Most metacestodes contained protoscoleces, singly or in groups, either associated with brood capsules or growing directly out of the germinal layer. Each individual metacestode was covered by an acellular translucent laminated layer that was considerably thicker than the laminated layer of E. multilocularis metacestodes. The ultrastructural characteristics, protein content, and carbohydrate composition of the laminated layer of in vitro cultivated E. vogeli and E. multilocularis were assessed using transmission electron microscopy, lectin fluorescence labeling, and lectin blotting assays. The laminated layer of E. vogeli is, as previously described for E. multilocularis metacestodes, largely composed of N-acetyl-beta-D-galactosaminyl residues and alpha- and beta-D-galactosyl residues, as well as of the core structure of O-linked carbohydrate chains, N-acetylgalactosamine-beta-1,3-galactose. However, in contrast to E. multilocularis, N-linked glycopeptides and alpha-D-mannosyl and/or glucosyl residues were also associated with the laminated layer of E. vogeli. The laminated layer from both species was isolated from in vitro cultivated metacestodes, and the purified fractions were comparatively analyzed. The protein:carbohydrate ratio (1:1) was similar in both parasites; however, the protein banding pattern obtained by silver staining following sodium dodecyl sulfate polyacrylamide gel electrophoresis suggested intrinsic differences in protein composition. A polyclonal antiserum raised against the E. multilocularis laminated layer and a monoclonal antibody, G11, directed against the major E. multilocularis laminated layer antigen Em2 did not cross-react with E. vogeli, indicating distinct compositional and antigenic differences between these 2 parasites.

Animals↗

PubMed2001

Identification of the human homologue of the early-growth response gene Snk, encoding a serum-inducible kinase.

Murine serum inducible kinase (mSnk) was recently cloned and characterized as an early-growth response gene involved in cell proliferation. Here we report the isolation and characterization of its human homologue, named hSnk. Sequence comparison shows that hSnk is highly conserved and its deduced protein sequence shares a significant amino acid identity with mSnk and rSnk proteins, as well as with other polo family kinase gene products. A survey of hSnk expression reveals that while a wide variety of human tissues express a low to moderate level of hSnk transcripts, fetal tissues, testis, and spleen express the most abundant hSnk transcripts. In addition, serum stimulation rapidly induces hSnk expression in fibroblast cells, reaching the peak level of induction within one hour post treatment. Considering that Plk and Prk, two other known human polo-family kinases, control cell cycle checkpoint and cell cycle progression, our current observations suggest that hSnk may also play an important role in cells undergoing rapid cell division or having a high mitotic index.

Adenosine Triphosphate↗

PubMed2001

[IFN-r/IL-4 expression in peripheral blood mononuclear cells of the patients with chronic severe hepatitis].

OBJECTIVE: To understand the expressions of interferon-r (INF-r) and interleukin-4 (IL-4) in peripheral blood mononuclear cells (PBMCs) of the patients with chronic severe hepatitis (CSH). METHODS: PBMCs from the patients with CSH were separated routinely and stimulated by PMA/Ionomycin/Monensin. The production of IFN-r/IL-4 by CD4+ T cells in PBMC was determined by fluorescence activated call sorting (FACS) analysis and fluorescence-quantitative PCR assay for quantification of HBV DNA. RESULTS: The percentage of IFN-gamma-producing T cells in CD4+ T cells was higher in patients with CSH (7.2%-26.3%) than in normal controls (2.2%-11.9%) (P<0.01). The percentage of Th1 cells increased significantly with the raise of hepatic inflammation activity. The percentage of IL-4-producing T cells in CD4+ T cells did not differ significantly between patients with CSH and normal controls. The quantification of HBV DNA decreased significantly with the increase of the percentage of IFN-gamma-producing T cells. CONCLUSIONS: Th1 cell is associated with hepatic inflammatory activity and IFN-gamma depresses HBV replication.

Adult↗

PubMed2000

Incomplete cytokinesis and induction of apoptosis by overexpression of the mammalian polo-like kinase, Plk3.

The polo-like kinases (Plks) are a family of conserved serine/threonine kinases that play a critical role in the normal progression of cells through mitosis. The Plk3 serine/threonine kinase is a mammalian member of this family. Overexpression of Plk3 in mammalian cells suppresses proliferation and inhibits colony formation. Subsequent analysis demonstrated that overexpression of Plk3 induces chromatin condensation and apoptosis. This phenotype could not be inhibited by coexpression of Bcl-2 and was partially dependent on the COOH-terminal domain of Plk3 but not on the catalytic activity of Plk3. Analysis of EGFP-Plk3 subcellular localization revealed that Plk3 localizes to the cellular cortex and to the cell midbody during exit from mitosis and is consistent with a role in cytokinesis. These data suggest that overexpression or ectopic suppression of Plk3 interferes with cellular proliferation by impeding cytokinesis.

Alleles↗

PubMed2000

Cyclosporin A inhibits creatine uptake by altering surface expression of the creatine transporter.

The immunosuppressive drug cyclosporin A (CsA) inhibited the hCRT-1 cDNA-induced creatine uptake in Xenopus oocytes and the endogenous creatine uptake in cultured C(2)C(12) muscle cells in a dose- and time-dependent manner. FK506, another potent immunosuppressant, was unable to mimic the effect of CsA suggesting that the inhibitory effect of CsA was specific. To delineate the mechanism underlying, we investigated the effect of CsA on the K(m) and V(max) of creatine transport and also on the cell surface distribution of the creatine transporter. Although CsA treatment did not affect the K(m) (20-24 microm) for creatine, it significantly decreased the V(max) of creatine uptake in both oocytes and muscle cells. CsA treatment reduced the cell surface expression level of the creatine transporter in the muscle cells by approximately 60% without significantly altering its total expression level, and the reduction in the cell surface expression paralleled the decrease in creatine uptake. Taken together, our results suggest that CsA inhibited creatine uptake by altering the surface abundance of the creatine transporter. We propose that CsA impairs the targeting of the creatine transporter by inhibiting the function of an associated cyclophilin, resulting in an apparent loss in surface expression of the creatine transporter. Our results also suggest that prolonged exposure to CsA may result in chronically creatine-depleted muscle, which may be a cause for the development of CsA-associated clinical myopathies in organ transplant patients.

Animals↗

PubMed2000

p55CDC/hCDC20 is associated with BUBR1 and may be a downstream target of the spindle checkpoint kinase.

Eukaryotic cells have evolved a mechanism that delays the progression of mitosis until condensed chromosomes are properly positioned on the mitotic spindle. We have been studying genes that regulated the spindle checkpoint in human cells. Enforced expression of human BUBR1, but not a BUBR1 mutant allele, enhances accumulation of mitotic cells. Yeast two-hybrid system and GST-pulldown analyses show that p55CDC/hCdc20, a protein known to link spindle checkpoint components such as MAD2 to anaphase promoting complex (APC), interacts with BUBR1. In addition, p55CDC is capable of pulling down BUBR1 in sf-9 cells infected with both p55CDC and His6-BUBR1 recombinant baculoviruses but not in the cells infected with p55CDC baculoviruses or with the baculoviral vector alone. Moreover, immunoprecipitation followed by Western blot analyses confirmed that native p55CDC is associated with BUBR1 in HeLa cells. Spindle checkpoint activation by nocodazole treatment enhances the association between p55CDC and His6-BUBR1. In nocodazole-arrested mitotic cells, both CDC16 and hyperphosphorylated CDC27, two APC components, preferentially associate with His6-BUBR1 resins, but not the control resins. Furthermore, BUBR1 phosphorylates p55CDC in vitro, and the phosphorylation of p55CDC by BUBR1 appears to be correlated with spindle checkpoint activation. Together, our studies strongly suggest that BUBR1 may target APC via p55CDC.

Alleles↗

PubMed2000

A novel membrane-anchored Rab5 interacting protein required for homotypic endosome fusion.

The ras-related GTPase rab5 is rate-limiting for homotypic early endosome fusion. We used a yeast two-hybrid screen to identify a rab5 interacting protein, rab5ip. The cDNA sequence encodes a ubiquitous 75-kDa protein with an N-terminal transmembrane domain (TM), a central coiled-coil structure, and a C-terminal region homologous to several centrosome-associated proteins. rab5ip lacking the transmembrane domain (rab5ipTM(-)) had a greater affinity in vitro for rab5-guanosine 5'-O-2-(thio)diphosphate than for rab5-guanosine 5'-3-O-(thio)triphosphate. In transfected HeLa cells, rab5ipTM(-) was partly cytosolic and localized (by immunofluorescence) with a rab5 mutant believed to be in a GDP conformation (GFP-rab5(G78A)) but not with GFP-rab5(Q79L), a GTPase-deficient mutant. rab5ip with the transmembrane domain (rab5ipTM(+)) was completely associated with the particulate fraction and localized extensively with GFP-rab5(wt) in punctate endosome-like structures. Overexpression of rab5ipTM(+) using Sindbis virus stimulated the accumulation of fluid-phase horseradish peroxidase by BHK-21 cells, and homotypic endosome fusion in vitro was inhibited by antibody against rab5ip. rab5ipTM(-) inhibited rab5(wt)-stimulated endosome fusion but did not inhibit fusion stimulated by rab5(Q79L). rab5ip represents a novel rab5 interacting protein that may function on endocytic vesicles as a receptor for rab5-GDP and participate in the activation of rab5.

Amino Acid Sequence↗

PubMed2000

[Study on the molecular mechanism of genetic damages in body cells in mice treated with organic mutants in drinking water].

The genetic toxicity of some volatile compounds of chlorinated by-products have been determined in animal studies. But little is known at present about the genetic toxicity of nonvolatile matter in drinking water in vivo assay. In a sub-acute experiment, the mice were exposed to the organic compounds extracted from in-home tap water. The pathologic changes in the liver and kidney tissues were observed under microscope and electron microscope. The frequencies of micronuclei in polychromatic erythrocytes in mice chest bone marrow in the three treated groups were tested. The point mutants in p53 gene of liver, kidney and colon tissues in the high dosage group were examined by PCR-SSCP. Especially, the frequencies of mutations in exon 7 of p53 gene in those mice were higher than those in exon 5 of p53 gene. It showed that the study on the molecular genetic toxicity of organic mutants in vivo assay was possible.

Animals↗

PubMed2000

Transforming activity of receptor tyrosine kinase tyro3 is mediated, at least in part, by the PI3 kinase-signaling pathway.

Protein tyrosine phosphorylation is an integral part of cytokine-induced proliferation and differentiation of hematopoietic cells. The authors previously reported cloning and characterization of the receptor tyrosine kinase Tif, also termed Tyro3. Using the yeast 2-hybrid technology, they recently identified that the p85 subunit of phosphatidylinositol 3-kinase (PI3 kinase) interacted with the cytoplasmic domain of Tyro3. On treatment with epidermal growth factor (EGF), NIH3T3 cells expressed EGFR/Tyro3 (a fusion receptor with the extracellular domain from epidermal growth factor receptor and the transmembrane and cytoplasmic domains from Tyro3), and EGFR/Tyro3 was rapidly phosphorylated on tyrosine residues. The interaction between Tyro3 and p85 was also confirmed by glutathione S-transferase (GST) pull-down experiments. Co-immunoprecipitation followed by Western blot analysis revealed that PI3 kinase was associated with and phosphorylated by the activated Tyro3. Tyro3-associated PI3 kinase exhibited an enhanced kinase activity. In addition, EGF treatment of EGFR/Tyro3-expressing cells led to enhanced phosphorylation of Akt, a downstream component of PI3 kinase. Treatment of NIH3T3 cells expressing a full length of rat Tyro-3, but not NIH3T3 cells, with protein S also resulted in phosphorylation of Akt. Soft agar colony assays showed that the addition of EGF to EGFR/Tyro3-transfected cells, but not to the parental NIH3T3 cells, resulted in a concentration-dependent increase in the formation of anchorage-independent colonies. Tyro3-mediated transformation of NIH3T3 cells was significantly blocked by wortmannin, a PI3 kinase-specific inhibitor. Results of these combined studies strongly suggested that the oncogenic transforming ability of Tyro3 was mediated at least in part by the PI3 kinase pathway. (Blood. 2000;95:633-638)

3T3 Cells↗

PubMed2000

PRK, a cell cycle gene localized to 8p21, is downregulated in head and neck cancer.

The human PRK gene encodes a protein serine/threonine kinase of the polo family and plays an essential role in regulating meiosis and mitosis. We have previously shown that PRK expression is downregulated in a significant fraction of lung carcinomas. Our current studies reveal that PRK mRNA expression is downregulated in a majority (26 out of 35 patients) of primary head and neck squamous-cell carcinomas (HNSCC) compared with adjacent uninvolved tissues from the same patients, regardless of stage. In addition, PRK transcripts were undetectable in one of the two HNSCC cell lines analyzed. Ectopic expression of PRK, but not a PRK deletion construct, in transformed A549 fibroblast cells suppresses their proliferation. Furthermore, fluorescence in situ hybridization analyses show that the PRK gene localizes to chromosome band 8p21, a region that exhibits a high frequency of loss of heterozygosity in a variety of human cancers, including head and neck cancers, and that is proposed to contain two putative tumor suppressor genes. Considering that PRK plays an important role in the regulation of the G2/M transition and cell cycle progression, our current studies suggest that deregulated expression of PRK may contribute to tumor development. Genes Chromosomes Cancer 27:332-336, 2000.

Carcinoma, Squamous Cell↗

PubMed2000

Protective effects of calcitonin gene-related peptide on guinea-pig cardiac anaphylaxis.

Anaphylactic events occurring in cardiac tissues can result in cardiac dysfunction via vasoconstriction and arrhythmias. Calcitonin gene-related peptide (CGRP) is the most potent vasodilator and possesses anti-arrhythmic action. We examined the influence of CGRP on cardiac anaphylaxis in guinea-pigs. In the Langendorff-perfused heart of passively sensitized guinea-pigs, antigen challenge evoked a decrease in coronary flow, left ventricular pressure and its maximum first derivatives (+/-dP/dtmax) and an increased heart rate. Antigen challenge also induced atrioventricular conduction block. Treatment with CGRP (1 or 3 nM) significantly improved the recovery of cardiac function and reduced the incidence and duration of atrioventricular block without influencing the increased heart rate. Pretreatment with capsaicin caused effects similar to those of CGRP and markedly elevated the content of CGRP in coronary effluent. Ischaemic preconditioning, induced by two cycles each of 5 min global ischaemia and 5 min reperfusion, also improved cardiac function and raised the level of CGRP in coronary effluent. The protective effects of ischaemic preconditioning were abolished in the presence of the CGRP receptor antagonist CGRP8-37. Histamine release did not differ significantly during any of the interventions. The findings of the present study indicate that, in guinea-pig hearts, CGRP protects against cardiac anaphylaxis and that the cardioprotection by CGRP is independent of histamine release.

Anaphylaxis↗

PubMed2000

Cleaved antitrypsin polymers at atomic resolution.

Alpha1-antitrypsin deficiency, which can lead to both emphysema and liver disease, is a result of the accumulation of alpha1-antitrypsin polymers within the hepatocyte. A wealth of biochemical and biophysical data suggests that alpha1-antitrypsin polymers form via insertion of residues from the reactive center loop of one molecule into the beta-sheet of another. However, this long-standing hypothesis has not been confirmed by direct structural evidence. Here, we describe the first crystallographic evidence of a beta-strand linked polymer form of alpha1-antitrypsin: the crystal structure of a cleaved alpha1-antitrypsin polymer.

Biopolymers↗

PubMed2000

[Expression and immunological reactivity of recombinant HCV-core protein].

OBJECTIVE: To express HCV-core proteins in E.coli and to develop effective HCV-core DNA-based vaccine. METHODS: The vector that expresses the highly conserved HCV core genes were constructed. The pGEX-3X HCVCore constructs contained the 1-201 ncls (1-67aa, C201), 1-402 ncls (1-134aa, C402) and 1-591ncls ( 1-197aa, C591), then expressed in E.coli cells. RESULTS: The products of HCV C201 and C402 genes were expressed as a fusion protein with glutathione-S-transferase (GST, 26kDa) whose molecular weight were 3.1 x 10(4) and 3.9 x 10(4) separately. C591 gene was not effectively expressed in E.coli. The expressed proteins were sequestered within inclusion bodies (IB) and a variety of procedures designed to minimize IB formation proved unsuccessful. The method finally adopted involved the purification of inclusion bodies followed by the solubilization, purification, and refolding of the expressed protein. The purified C402 protein was antigenically reactive with serum from chronically infected HCV patients. BALB/C mice were immunized by a subcutaneous injection of C402 protein together with Freund's complete adjuvant which produced strong anti-HCV core humoral immune responses. CONCLUSION: It is important for the study of gene vaccine to construct a certain length of HCV core gene.

Animals↗

PubMed2000

[Construction of recombinant BCG bearing Schistosoma japonicum 26Ku antigen gene and study on its immunogenicity on mice].

OBJECTIVE: To construct recombinant BCG vaccine bearing Schistosoma japonicum 26Ku glutathione S-transferase (Sj26GST) gene and determine its immunogenicity on BALB/c mice. METHODS: Using techniques of molecular biology, human mycobacterium tuberculosis HSP70 promoter and Sj26GST gene were linked to produce a fused gene. The fused gene was cloned into an E. coli-Mycobacterium shuttle plasmid pBCG-2000 to construct an E. coli-Mycobacterium expression shuttle plasmid pBCG-Sj26 that could express Sj26GST gene. Then, the pBCG-Sj26 was introduced by electroporation into mycobacterium bovis BCG to construct a recombinant BCG vaccine bearing Sj26GST gene (rBCG- Sj26GST). The expression of Sj26GST gene in BCG was induced by heating. The lymphocyte stimulating index (SI), macrophage activity and IL-2, IFN-gamma levels of the serum and culture supernatant of spleen lymphocytes were tested after immunization of BALB/c mice with rBCG-Sj26GST vaccine. RESULTS: The fused gene of HSP70 promoter and Sj26GST cDNA was inserted into an E. coli-Mycobacterium shuttle expression plasmid by analysing electrophoresis results on PCR products using plasmid pBCG-Sj26 as a templet. The content of rSj26GST contained 15% of total bacterial protein of BCG. The SI of the experimental group was 2.26 +/- 0.43, which was significantly higher than those in the control group (1.61 +/- 0.28, P < 0.05), vector group (1.48 +/- 0.30, P < 0.05) and BCG group (1.42 +/- 0.26, P < 0.05). The macrophage NO level of the experimental group was (357.42 +/- 84.11) nmol/ml which was significantly higher than those in the control group (183 nmol/ml +/- 33 nmol/ml, P < 0.01) and vector group (203 nmol/ml +/- 56 nmol/ml, P < 0.01). The serum IL-2 level of the experimental group was (267 pg/ml +/- 130 pg/ml), which was significantly higher than those in the control group (45 pg/ml +/- 15 pg/ml, P < 0.01) and vector group (52 pg/ml +/- 29 pg/ml, P < 0.05. Compared with the control group, the serum IFN-gamma level increased by 20%, the IL-2 level of the culture supernatant of spleen lymphocytes increased by 44%. CONCLUSIONS: The foreign gene encoding Sj26 GST can be expressed in BCG. rBCG Sj26GST vaccine may induce stronger immune response in BALB/c mice than in control, vector and BCG groups.

Animals↗

PubMed2000

[Detection of remnants after removal of medullary thyroid carcinoma].

OBJECTIVE: To assess whether calcium stimulation test or somatostain-receptor (SS-R) imaging could early detect remnants after removal of medullary thyroid carcinoma (MTC). METHODS: Calcitonin stimulation (calcium element 3 mg/kg weight, i.v. 10 min), carcino-embryonic antigen (CEA), gastrin (GST) and vasoactive intestinal peptide (VIP) were tested in 14 patients with postoperative MTC. SS-R imaging was used to localize the remnants after removal of MTC in patients with elevated calcitonin. RESULTS: Calcitonin stimulation test showed that the peak value of serum calcitonin was elevated in all patients, of whom 7 had the elevated vatue of basic calcitonin and peak calcitonin. In the 7 patients, SS-R imaging showed normal CEA, GST and VIP. CONCLUSIONS: It is necessary for patients after removal of MTC to perform calcitonin stimulation test for detecting remnants early. SS-R imaging may be useful for localizing remnants and metastatic foci. CEA, GST and VIP are not significant in monitoring MTC after operation.

Adult↗

PubMed2000

[A clinical study on coincidence with hyperthyroidism and thyroid carcinoma].

OBJECTIVE: A retrospective study has been carried out to evaluate the prevalence of coincidence with hyperthyroidism and thyroid carcinoma. METHODS: 394 patients underwent surgery for hyperthyroidism and 245 patients suffered from thyroid cancer were chosen for the study in our hospital from January 1983 to June 1998. RESULTS: Thyroid cancer and hyperthyroidism coincided in 12 patients. The incidence of thyroid cancer was 3.0% (12/394) in hyperthyroidism, and the incidence of hyperthyroidism was 4.9% in thyroid cancer. There were 7 female and 5 male, with a diffuse goiter (n = 3), a diffuse goiter with a cold nodule (n = 3), multinodular goiter (n = 6). Among the 12 patients, 7 patients had an occult thyroid cancer with a diameter of 1 cm or less, most of them with papillary carcinoma, less frequently had metastases, 4 patients had thyroid cancer with a diameter of 3 cm or more, and 3 patients had metastases. CONCLUSIONS: The prevalence of coincidence with thyroid cancer and hyperthyroidism is more than that of thyroid cancer in population. Diagnostics for exclusion of thyroid cancer is required carefully even in the presence of hyperthyroidism.

Female↗