Half-integer quantized anomalous thermal Hall effect in the Kitaev material candidate α-RuCl3.

Half-integer thermal quantum Hall conductance has recently been reported for the two-dimensional honeycomb material α-RuCl3 We found that the half-integer thermal Hall plateau appears even for a magnetic field with no out-of-plane components. The measured field-angular variation of the quantized thermal Hall conductance has the same sign structure as the topological Chern number of the pure Kitaev spin liquid. This observation suggests that the non-Abelian topological order associated with fractionalization of the local magnetic moments persists even in the presence of non-Kitaev interactions in α-RuCl3.

Majorana quantization and half-integer thermal quantum Hall effect in a Kitaev spin liquid.

The quantum Hall effect in two-dimensional electron gases involves the flow of topologically protected dissipationless charge currents along the edges of a sample. Integer or fractional electrical conductance is associated with edge currents of electrons or quasiparticles with fractional charges, respectively. It has been predicted that quantum Hall phenomena can also be created by edge currents with a fundamentally different origin: the fractionalization of quantum spins. However, such quantization has not yet been observed. Here we report the observation of this type of quantization of the Hall effect in an insulating two-dimensional quantum magnet1, α-RuCl3, with a dominant Kitaev interaction (a bond-dependent Ising-type interaction) on a two-dimensional honeycomb lattice2-7. We find that the application of a magnetic field parallel to the sample destroys long-range magnetic order, leading to a field-induced quantum-spin-liquid ground state with substantial entanglement of local spins8-12. In the low-temperature regime of this state, the two-dimensional thermal Hall conductance reaches a quantum plateau as a function of the applied magnetic field and has a quantization value that is exactly half of the two-dimensional thermal Hall conductance of the integer quantum Hall effect. This half-integer quantization of the thermal Hall conductance in a bulk material is a signature of topologically protected chiral edge currents of charge-neutral Majorana fermions (particles that are their own antiparticles), which have half the degrees of freedom of conventional fermions13-16. These results demonstrate the fractionalization of spins into itinerant Majorana fermions and Z2 fluxes, which is predicted to occur in Kitaev quantum spin liquids1,3. Above a critical magnetic field, the quantization disappears and the thermal Hall conductance goes to zero rapidly, indicating a topological quantum phase transition between the states with and without chiral Majorana edge modes. Emergent Majorana fermions in a quantum magnet are expected to have a great impact on strongly correlated quantum matter, opening up the possibility of topological quantum computing at relatively high temperatures.

Unusual Thermal Hall Effect in a Kitaev Spin Liquid Candidate α-RuCl_{3}.

The Kitaev quantum spin liquid displays the fractionalization of quantum spins into Majorana fermions. The emergent Majorana edge current is predicted to manifest itself in the form of a finite thermal Hall effect, a feature commonly discussed in topological superconductors. Here we report on thermal Hall conductivity κ_{xy} measurements in α-RuCl_{3}, a candidate Kitaev magnet with the two-dimensional honeycomb lattice. In a spin-liquid (Kitaev paramagnetic) state below the temperature characterized by the Kitaev interaction J_{K}/k_{B}∼80 K, positive κ_{xy} develops gradually upon cooling, demonstrating the presence of highly unusual itinerant excitations. Although the zero-temperature property is masked by the magnetic ordering at T_{N}=7 K, the sign, magnitude, and T dependence of κ_{xy}/T at intermediate temperatures follows the predicted trend of the itinerant Majorana excitations.

Determining the treatment strategy for colorectal neoplastic lesions: endoscopic assessment or the non-lifting sign for diagnosing invasion depth?

BACKGROUND AND STUDY AIMS: Assessment of the invasion depth of colorectal neoplasia is important in deciding between endoscopic and surgical resection treatment methods. Prior to attempting endoscopic resection, the lesion is lifted by submucosal injection, and a positive "non-lifting sign" is usually considered to indicate deeper submucosal infiltration. The purpose of this prospective multicenter study was to assess the predictive value of the non-lifting sign for differentiating between adenoma and early cancer (up to discrete submucosal infiltration [sm1]) and cancer with deeper infiltration (sm2). PATIENTS AND METHODS: During an 11-month period, a total of 271 colorectal neoplastic lesions in 239 patients were included in the study. Apart from the location, size, and macroscopic type of the lesion, the presence or absence of the non-lifting sign was recorded and compared with the endoscopic assessment of invasion depth. RESULTS: The non-lifting sign had a sensitivity of 61.5 %, a specificity of 98.4 %, a positive predictive value of 80.0 %, a negative predictive value of 96.0 %, and an accuracy of 94.8 %. Endoscopic diagnosis of deeper infiltration had a sensitivity of 84.6 %, a specificity of 98.8 %, a positive predictive value of 88.0 %, a negative predictive value of 98.4 %, and an accuracy of 97.4 %. Statistically significant differences were found in terms of sensitivity and accuracy. CONCLUSION: Because of its lower sensitivity and accuracy, the non-lifting sign will not replace endoscopic assessment. If a lesion does not lift, this can make resection technically difficult, but does not reliably predict deeper cancerous invasion.

Clinical characteristics of synchronous colorectal cancer are different according to tumour location.

AIMS: The purpose of this study was to investigate the clinical characteristics of synchronous cancer patients, with particular attention given to variations in tumour location. METHODS: A retrospective evaluation of 249 synchronous cancer cases out of 3061 consecutive colorectal cancer patients. RESULTS: Multivariate analysis of risk factors for synchronous cancer according to tumour location revealed that male gender was a significant risk for synchronous lesions in the left colon only (odds ratio=2.05, 95% confidence interval 1.34-3.13). Meanwhile, aging was a risk factor for synchronous cancer in the right colon only (odds ratio=1.05, 95% confidence interval 1.02-1.08), and in both sides of the colon (odds ratio=1.03, 95% confidence interval 1.01-1.05), but not in the left colon only (odds ratio=0.98, 95% confidence interval 0.97-1.00). In addition, patients with synchronous lesions in the right colon only tended to have adenomas in the right colon, while those with synchronous lesions in the left colon only tended to have adenomas in the left colon (each P value <0.05). CONCLUSION: The risk factors and status of concurrent adenomas of synchronous cancer cases varied according to tumour location, suggesting that the colonic site susceptible to neoplasia varies according to patient characteristics.

Electric polarization, magnetoelectric effect, and orbital state of a layered iron oxide with frustrated geometry.

A layered iron oxide RFe2O4 (R denotes rare-earth-metal elements) is an exotic dielectric material with charge-order (CO) driven electric polarization and magnetoelectric effect caused by spin-charge coupling. In this paper, a theory of electronic structure and dielectric property in RFe2O4 is presented. Charge frustration in paired-triangular lattices allows a charge imbalance without inversion symmetry. Spin frustration induces reinforcement of this polar CO by a magnetic ordering. We also analyze an orbital model for the Fe ion which does not show a conventional long-range order.

Characteristics of metachronous multiple early gastric cancers after endoscopic mucosal resection.

BACKGROUND AND STUDY AIMS: Endoscopic mucosal resection (EMR) of early gastric cancer is a minimally invasive procedure. The incidence and characteristics of metachronous multiple gastric cancers were investigated in a retrospective study in patients with early gastric cancer after EMR treatment. PATIENTS AND METHODS: A total of 143 patients with early gastric cancer who had undergone EMR treatment were periodically followed up with endoscopic examinations for 24 months or longer. RESULTS: The median period of endoscopic follow-up was 57 months (range 24 - 157 months). None of the patients died of gastric cancer, and there were no treatment-related deaths. Five patients died of other diseases. Of 20 patients (14 %) with metachronous multiple gastric cancers, 15 were treated by EMR. One patient with differentiated submucosal cancer and four with undifferentiated cancers underwent surgery. Sixteen patients (11 %) had synchronous multiple early gastric cancer lesions within 1 year of the initial EMR. About half of the multiple lesions were located in the same third of the stomach as the primary lesion, and most lesions were similar in macroscopic type to the primary lesions. Most multiple lesions were of the differentiated type. CONCLUSIONS: Annual endoscopic examinations can preserve the whole stomach in most patients with early gastric cancer after successful EMR.

A phase I study of S-1 combined with weekly cisplatin for metastatic gastric cancer in an outpatient setting.

A dose-escalation study was conducted for patients with metastatic gastric cancer to determine the recommended dose of weekly intravenous (i.v.) cisplatin combined with a fixed dose of a new oral dihydropyrimidine dehydrogenase-inhibitory fluoropyrimidine, S-1, on an outpatient basis. Secondary endpoints were to define the toxicity profile and to determine tumour responses. S-1 was fixed at a dose of 70 mg/m(2)/day and was administered for 2 weeks followed by a 1-week rest. Three dose levels of cisplatin (10, 15 and 20 mg/m(2)) were studied. Cisplatin was infused over 30 min on days 1 and 8. 20 patients were enrolled. No dose-limiting toxicities (DLTs) were recorded during the administration of cisplatin up to 20 mg/m(2), except for grade 3 diarrhoea and stomatitis in one patient at dose level 3. No grade 4 adverse events occurred. However, grade 2 gastrointestinal adverse reactions, such as nausea and anorexia, were seen in 7 of 13 patients at dose level 3 within the first two treatment cycles. This was determined to be the maximum acceptable level that would not negate the advantages observed with use of an oral drug such as S-1. An objective tumour response was seen at all dose levels, and the overall response rate in the 18 patients evaluated was 61%. A higher response rate of 78% was observed in 9 patients who had received no prior chemotherapy. Oral S-1 with weekly cisplatin is a feasible and promising combination regimen that is appropriate for an outpatient setting. A randomised phase II study comparing this combination with S-1 alone in chemo-nai;ve patients is warranted.

Enhanced expression of decay-accelerating factor and CD59/homologous restriction factor 20 in intestinal metaplasia, gastric adenomas and intestinal-type gastric carcinomas but not in diffuse-type carcinomas.

AIMS: Variable expression of the complement regulatory proteins, decay-accelerating factor, CD59/homologous restriction factor 20 (HRF20) and membrane cofactor protein has been shown in human gastrointestinal malignancies, but their expression in gastric cancer has not been fully described. Thus, we immunohistochemically defined the distribution of these proteins in human normal gastric mucosa, intestinal metaplasia, adenomas and gastric cancers. METHODS AND RESULTS: Gastric tissues were obtained by endoscopic biopsy or surgical resection and stained with mouse monoclonal antibodies to decay-accelerating factor, CD59/HRF20, and membrane cofactor protein. In the normal gastric mucosa, membrane cofactor protein was diffusely stained on the basolateral surface of epithelial cells, whereas the expression of decay-accelerating factor and CD59/HRF20 was inconspicuous. In intestinal metaplasia, adenoma and intestinal-type gastric carcinoma cells, decay-accelerating factor and HRF20 were intensely stained on the apical surface; membrane cofactor protein retained its location on the basolateral surface. In diffuse-type gastric carcinomas, the expression of decay-accelerating factor, CD59/HRF20 was lost, but membrane cofactor protein was present on the tumour cell surface. CONCLUSIONS: These findings suggest that membrane cofactor protein plays a primary role in the regulation of complement activation in normal and neoplastic gastric cells and that the expression pattern of the complement regulatory proteins is closely related to gastric carcinoma development.

Epidermal growth factor induces expression of decay-accelerating factor in human colonic cancer cells via the mitogen-activated protein kinase pathway.

The expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced in colorectal cancer. In this study, to elucidate mechanisms for enhanced DAF expression, we studied the effects of growth factors on DAF expression in HT-29 human colonic cancer cells. Cells were treated with epidermal growth factor (EGF), insulin-like growth factor-I, platelet-derived growth factor, and transforming growth factor-beta. DAF protein expression and mRNA expression were determined with enzyme immunoassay and Northern blot analysis. The signaling pathways that target DAF expression in response to growth factor stimulation were characterized by using various inhibitors of the signal transduction pathway. EGF induced significant increases in DAF protein and mRNA expression in HT-29 cells; the other growth factors had a weak effect or no effect. The EGF-induced DAF expression was inhibited by mitogen-activated protein (MAP) kinase kinase inhibitor PD 98059 but not by phosphatidylinositol-3 kinase inhibitor, phospholipase Cgamma inhibitor, or protein kinase C inhibitor. When we analyzed the phosphorylation state of the MAP kinase by immunoblot analysis, phosphorylated p44/p42 MAP kinase was detected in EGF-stimulated HT-29 cells, and the addition of PD 98059 abrogated the phosphorylation. These results indicate that EGF regulates DAF expression in HT-29 cells via the signaling pathway that depends on the activation of MAP kinase.

A randomized open trial for comparison of proton pump inhibitors, omeprazole versus rabeprazole, in dual therapy for Helicobacter pylori infection in relation to CYP2C19 genetic polymorphism.

BACKGROUND AND AIM: The genetic polymorphism of cytochrome P450 (CYP) 2C19 has been shown to influence the efficacy of Helicobacter pylori eradication therapy with a proton pump inhibitor (PPI) and amoxicillin (so-called dual therapy). Omeprazole, a widely used PPI, and rabeprazole, a new PPI, are metabolized in different pathways in terms of CYP2C19 genetic polymorphisms. In this study, we compared the efficacy of omeprazole and rabeprazole in a 2-week dual therapy in relation to CYP2C19 polymorphism. METHODS: One hundred and ninety-nine patients with peptic ulcer disease were randomly assigned to receive one of the following regimens: 500 mg t.i.d. amoxicillin together with either 20 mg b.i.d. omeprazole or 10 mg b.i.d rabeprazole. The eradication of H. pylori was evaluated by using a bacterial culture and a [(13)C]-urea breath test at 1--2 months after completion of treatment. Cytochrome P4502C19 polymorphism was analyzed by using polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Intention-to-treat-based cure rates for the omeprazole or rabeprazole regimens were 66.3% (95% CI, 56--75) and 62.4% (95% CI, 52--71), respectively, without significant difference. Cytochrome P4502C19 genetic polymorphism did not influence the cure rates in either of these regimens. We analyzed various factors associated with treatment failure (PPI, CYP2C19 genotype, and smoking habit) by using multiple logistic regression; smoking was the only significant independent factor for treatment failure. CONCLUSION: Omeprazole and rabeprazole were equally effective in combination with amoxicillin in eradicating H. pylori, irrespective of the PPI used (omeprazole or rabeprazole) and CYP2C19 genetic polymorphism. Smoking significantly decreased the cure rate of H. pylori infection in the dual therapy.

Polymorphic expression of decay-accelerating factor in human colorectal cancer.

BACKGROUND: We have previously shown that expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced immunohistochemically on the luminal surface of cancer glands in human colorectal cancer and is detected in stool specimens of patients with colorectal cancer. The amount of DAF present in the stools might be influenced by the stability of DAF on the cell surface which is regulated by biochemical properties such as glycosylation of the protein. In the present study, to help elucidate the mechanism for the release of DAF from human colorectal cancers, we biochemically analyzed DAF expression by western and northern blotting by using surgically resected specimens of colorectal cancers. METHODS: Surgically resected colorectal cancer tissues were obtained from 10 patients. Expression of DAF was determined by western and northern blotting, and glycosylation of DAF protein was analyzed with glycosidase digestion. RESULTS: Northern blot analysis demonstrated that the expression of DAF mRNA in colorectal cancer was enhanced two- to threefold compared with normal tissues. In western blotting, expression of DAF protein in the cancer tissue was increased, and heterogeneity in the apparent molecular weight of DAF was observed among patients. When o-linked sugars were removed, this heterogeneity of DAF size diminished. CONCLUSIONS: The polymorphic expression of DAF in colorectal cancer is likely to reflect variability in the o-glycosylation of the protein. We speculate that this variability could affect the stability of DAF on the surfaces of cancer cells and, in turn, the amount of DAF shed into the stools of colorectal cancer patients.

[Multimodality therapy for synchronous liver metastases of gastric cancer--significance of aggressive hepatic resection of liver lesions].

We analyzed 15 gastric cancer patients with synchronous liver metastases, and studied the significance of hepatic resection with multimodality therapy. 1. Both gastric and hepatic resections followed by intra-arterial or systemic chemotherapy were performed for six patients, two of whom had intra-operative MCT or EIT. The survival time of four patients without recurrence was 5 Y 4 M, 4 Y 5 M, 2 Y 4 M and 11 M. Two patients died of recurrence in the retroperitoneum or residual liver 3 Y 10 M and 8 M after therapy, respectively. The three-year survival rate was 83%. 2. The longest survival among the five patients treated with gastric resection without hepatic resection followed by intra-arterial or systemic chemotherapy was 1 Y 1 M. 3. Four patients with non-curative factors (P, N, M) were treated with systemic chemotherapy only, and the longest survival was 1 Y 1 M. In conclusion, when local control is obtained during surgery in patients with gastric cancer with synchronous liver metastasis, aggressive hepatic resection supported with MCT or EIT should be performed on liver lesions to improve the prognosis.

Cytokine-stimulated release of decay-accelerating factor (DAF;CD55) from HT-29 human intestinal epithelial cells.

Expression of DAF (CD55) is enhanced on colonic epithelial cells of patients with ulcerative colitis (UC), and stool DAF concentrations are increased in patients with active disease. Cytokines are known to modulate DAF expression in various human cells, and lesions of UC reveal altered profiles of cytokine production. In this study, we evaluate the effects of various cytokines, IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, and interferon-gamma (IFN-gamma), on the synthesis and kinetics of DAF protein in HT-29 human intestinal epithelial cells. Using flow cytometry and an ELISA, we found that HT-29 cells constitutively express DAF on the cell surface and spontaneously release DAF into the culture supernatant under standard culture conditions. When the culture supernatant was centrifuged at 100000g, nearly a half of DAF was precipitated, indicating that one half of the released DAF was present as a membrane-bound form and the other half as a soluble form. Analysis of the culture supernatant of biotin surface-labelled HT-29 cells suggested that the soluble form DAF was derived by secretion from within the cell or by cleavage from the cell surface. Among the cytokines, IL-4 markedly, and IL-1beta moderately, enhanced the expression and the release of DAF. Actinomycin D, cycloheximide, and brefeldin A inhibited the increase in DAF release induced by IL-4 and IL-1beta stimulation. These results suggest that DAF is released from intestinal epithelial cells in response to cytokine stimulation and that IL-4 and IL-1beta are possible cytokines involved in DAF release into the colonic lumen of patients with UC.

Decay-accelerating factor (DAF) in stool specimens as a marker of disease activity in patients with ulcerative colitis (UC).

Colonic epithelial cells of patients with UC express DAF in relation to the severity of mucosal inflammation. The aim of this study was to determine whether this factor in stool could be used as a marker of disease activity in UC patients. Stool DAF was measured by use of an immunoassay in 181 stool specimens obtained from 55 patients with UC of various levels of disease activity. Stool DAF concentrations in patients whose UC was active (0.0-785.6 ng/g stool; median 47.1 ng/g; n = 115) were significantly higher than concentrations in patients whose disease was inactive (0.0-48.6 ng/g; median 0.0 ng/g; n = 66) (P < 0.0001). Values in active UC patients also were higher than those in control patients with diarrhoea (0.0-30.0 ng/g; median 0.0 ng/g; n = 26) (P < 0.0001) and in control subjects without apparent colorectal disease (0-20.4 ng/g; median 0.0 ng/g; n = 44) (P < 0.0001). The elevated levels of stool DAF obtained from UC patients in relapse declined markedly in specimens collected after the disease went into remission following medical therapy. Stool DAF levels correlated with the severity of endoscopic and histological findings and the degree of DAF expression on the colonic epithelia. Our results suggest that the measurement of stool DAF is useful as a non-invasive means of monitoring intestinal disease activity in patients with UC.

Immunohistochemical analysis of intercellular adhesion molecule-1 expression in human gastric adenoma and adenocarcinoma.

In this study, we examined the distribution of intercellular adhesion molecule-1 (ICAM-1) in gastric adenomas and carcinomas immunohistochemically at the light and electron microscopic levels. ICAM-1 was expressed on tumour cells in 12 of 28 gastric carcinomas and in 3 of 11 adenomas but not on most normal gastric epithelial cells. ICAM-1 was localized on luminal sites of neoplastic glands in adenomas and in intestinal-type carcinomas, and rarely on the surface of tumour cells of diffuse carcinomas. Expression of ICAM-1 on the tumour cells was more frequent in intestinal-type than diffuse carcinomas (P < 0.005). At the ultrastructural level, ICAM-1 was present prominently on the apical membrane and weakly on the lateral surface of the tumour cells of the intestinal-type carcinoma and also localized on the perinuclear membrane and the membrane of the endoplasmic reticulum of cancer cells. There was no significant association between ICAM-1 expression and HLA antigen expression or the number of infiltrating lymphocyte subsets. These results may implicate the synthesis of ICAM-1 by gastric cancer cells, but the expression is infrequent and may not be sufficient for host immune surveillance of the tumour cell.

Distribution of activated complement, C3b, and its degraded fragments, iC3b/C3dg, in the colonic mucosa of ulcerative colitis (UC).

The third component of complement (C3) is central to both the classical and alternative pathways in complement activation. In this study, involvement of C3 activation in the mucosal injury of UC was investigated. We examined the distribution of activated (C3b) and degraded fragments (iC3b/C3dg) of C3, terminal complement complex (TCC), and complement regulatory proteins in normal and diseased colonic mucosa including UC and other types of colitis using immunohistochemical techniques at the level of light and electron microscopy. While C3b and iC3b/C3dg staining was negligible in the normal mucosa, iC3b/C3dg and, to a lesser extent, C3b were deposited in UC mucosa along the epithelial basement membrane. The deposition was enhanced in relation to the severity of mucosal inflammation (C3b, P less than 0.05; iC3b/C3dg, P less than 0.01). Epithelial deposition of TCC was not observed in most UC mucosa. Immunoelectron microscopy showed that C3b and iC3b/C3dg were distributed mainly along the epithelial basement membrane and the underlying connective tissue in a granular, studded manner, and weakly present along the basolateral surface of epithelial cells. These C3 fragments were also deposited in inflammatory control mucosa such as ischaemic and infectious colitis. Our findings suggest that deposition of the C3 fragments occurs in inflamed colonic mucosa of diverse etiologies, including UC, but to define a role of the deposition in the development of mucosal injury in UC awaits direct study.

Relation of family history of cancer and environmental factors to the risk of colorectal cancer: a case-control study.

The relation of a family history of cancer and environmental factors to colorectal cancer was investigated in a case-control study conducted from 1992 to 1994 at 10 medical institutions in Japan using a self-administered questionnaire, and 363 cases of colorectal cancer were compared with 363 controls matched for sex and age. A family history of colorectal cancer was positively associated with colon cancer (odds ratio (OR) = 2.0, 95% confidence interval (CI) 1.03-3.87) and rectal cancer (OR = 2.1 CI 0.94-4.48), but a family history of other cancers did not increase the risk. The proportion of patients with a family history of colorectal cancer within first-degree relatives was 12.4%--appreciably higher than figures previously reported in Japan. On the other hand, the incidence of hereditary non-polyposis colorectal cancer was 1.4%, and lower than previous estimates. Among dietary factors, a western-style diet significantly increased the risk of both colon and and rectal cancer (OR = 2.3 CI 1.30-3.88 and OR = 2.1 CI 1.26-3.63, respectively). Consumption of rice was protective against both colon and rectal cancer (OR = 0.5 CI 0.31-0.82 and OR = 0.3 CI 18-0.65, respectively). Animal meat, oily food, fish, vegetables and fruit were shown to affect the risk, but no statistically significant correlation was found. Among other factors, constipation increased the risk of colon cancer (OR = 2.0 CI 1.02-3.76) and consumption of coffee raised the risk of rectal cancer (OR = 1.7 CI 1.07-2.82). Our findings suggest that a family history of colorectal cancer is an important risk factor for this disease, and does not contradict the hypothesis that the risk of colorectal cancer in Japan may be influenced by westernization of lifestyle. However, we were unable to find conclusive evidence that familial clustering of this disease is strongly affected by environmental factors or genetic diseases such as hereditary non-polyposis colorectal cancer.

Detection of decay-accelerating factor in stool specimens of patients with colorectal cancer.

BACKGROUND & AIMS: Colorectal cancers have an increased expression of decay-accelerating factor (DAF). The aim of this study was to determine whether stool specimens of patients with colorectal cancer contain increased amounts of DAF. METHODS: DAF was measured using an immunoassay in the stool specimens of 40 persons with colorectal cancer, 18 with colorectal adenomatous polyps, 13 with upper gastrointestinal cancer, and 41 without gastrointestinal disease. RESULTS: Stool DAF concentrations in patients with colorectal cancer (0-9.8 ng/g stool; median, 1.6 ng/g) were significantly higher than those in patients with adenoma (0-6.4 ng/g; median, 0 ng/g) (P < 0.05), patients with upper gastrointestinal cancer (0-3.1 ng/g; median, 0 ng/g) (P < 0.05), and subjects without gastrointestinal disease (0-3.4 ng/g; median, 0 ng/g) (P < 0.01). Resection of colorectal cancers caused a marked decrease in stool DAF concentrations. The stool DAF test was positive in a substantial portion of patients with colorectal cancer whose tumors were small ( < 2 cm), at an early TNM stage, or unassociated with fecal occult blood positivity. The sensitivity of the test for colorectal cancer was 55%, and the specificity was 85%. CONCLUSIONS: The measurement of stood DAF deserves evaluation as a test for detection of colorectal cancer.