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PubMed2006

Aberrant expression of krUppel-like factor 6 protein in colorectal cancers.

AIM: To investigate whether krUppel-like factor 6 (KLF6) plays an important role in the development and/or progression of colorectal cancer. METHODS: A total of 123 formalin-fixed and paraffin-embedded colorectal cancer specimens were analyzed by immunohistochemistry using tissue microarray for the expression of KLF6 protein. The specimens were collected over a 3-year period in the laboratories at our large teaching hospital in Seoul, Republic of Korea. The correlation of KLF6 expression with clinicopathologic parameters was analyzed by chi2 test and Bartholomew test. RESULTS: Normal colonic epithelium showed weak to moderate expression of KLF6, whereas reduced KLF 6 expression or loss of KLF6 expression was seen in 45 (36.6%) of the 123 colorectal carcinoma specimens. Interestingly, aberrant expression of KLF6 was detected in 25 (43.1%) of 58 cases with metastasis to regional lymph node and in 31 (47.0%) of 66 tumors more than 5 cm in size. Statistically, loss of KLF6 expression was significantly associated with tumor size (P < 0.05). However, there was no significant correlation between KLF6 expression and Dukes'stage (Bartholomew test, P > 0.05), tumor location and lymph node metastasis (chi2 test, P > 0.05). CONCLUSION: Loss of KLF6 expression may be a common and early event in colorectal carcinogenesis.

Colorectal Neoplasms↗
PubMed2006

Expression of NOS and HIF-1alpha in human colorectal carcinoma and implication in tumor angiogenesis.

AIM: To study CD34, CD105, inducible nitric oxide synthase (iNOS), endogenous nitric oxide synthase (eNOS), and hypoxia-inducible factor 1 (HIF-1) alpha expression in human colorectal carcinomas. METHODS: The tissue microarrays (TMAs) were made up of 80 cases of colorectal carcinoma and 80 cases of non-neoplasm colorectal mucosa. The expression of CD34, CD105, NOS and HIF-1alpha was detected by immunohistochemistry (S-P). RESULTS: iNOS and HIF-1alpha expression in colorectal carcinoma was significantly higher than in non-neoplasm colorectal mucosa (c2 = 43.166, P < 0.01; c2 = 10.4278, P < 0.01); eNOS expression in colorectal carcinoma was significantly lower than in non-neoplasm colorectal mucosa (c2 = 11.354, P < 0.01). The expression of iNOS correlated with differentiation (c2 = 18.141, P < 0.01), invasive depth (c2 = 4.748, P < 0.01), and Micro vessel density (MVD) (t = 2.327, P < 0.05). The expression of HIF-1alpha was correlated with infiltrating depth (c2 = 4.397, P < 0.05), Dukeos staging (c2 = 4.255, P < 0.05), and MVD (t = 2.272, P < 0.05). No correlation was found in eNOS expression. CONCLUSION: Over-expression of iNOS and HIF-1alpha in colorectal carcinoma is correlated with the biological character MVD.

Adenocarcinoma↗
PubMed2006

DEK Expression is controlled by E2F and deregulated in diverse tumor types.

Deregulation of the retinoblastoma (pRB) tumor suppressor pathway associated with aberrant activity of E2F transcription factors is frequently observed in human cancer. Microarray based analyses have revealed a large number of potential downstream mediators of the tumor suppressing activity of pRB, including DEK, a fusion partner of CAN found in a subset of acute myeloid leukaemia (AML) patients carrying a (6; 9) translocation. Here we report that the expression of DEK is under direct control of E2F transcription factors. Chromatin immunoprecipitation assays show that the DEK promoter is bound by endogenous E2F in vivo. The DEK promoter is transactivated by E2F and mutation of E2F binding sites eliminates this effect. Expression levels of DEK in human tumors have been investigated by tissue micro array analysis. We find that DEK is overexpressed in many solid tumors such as colon cancer, larynx cancer, bladder cancer, and melanoma.

Binding Sites↗
PubMed2005

Immunohistochemical and clinicopathologic characteristics of invasive ductal carcinoma of breast with micropapillary carcinoma component.

CONTEXT: A micropapillary carcinoma (MC) component is generally considered to behave aggressively. Although several reports have described the prognostic significance of MC in breast carcinomas, immunohistochemical findings of MC, especially as compared to non-MC, are rarely described. OBJECTIVE: We compared clinicopathologic and immunohistochemical findings between 38 cases of invasive breast carcinoma with an MC component (IMC) and 217 cases of invasive breast carcinoma without an MC component (NIMC). DESIGN: We constructed a tissue microarray from 38 cases of IMC and performed immunohistochemical stainings for cytokeratin (CK) 7, CK20, estrogen receptor, progesterone receptor, p53, c-Erb-B2, CD34, CK5, epidermal growth factor receptor, and c-Kit in both MC and non-MC components. RESULTS: Cases with IMC were associated with greater tumor size, more frequent lymphovascular invasion, nodal metastases, greater mean numbers of positive lymph nodes, and higher stage than those with NIMC, but were not associated with poorer survival rates. On immunohistochemistry, only p53 reactivity was statistically different between MC and non-MC components in IMC cases. Estrogen receptor positivity tended to be lower in MC than non-MC, but the difference was not significant. Most of the MCs and non-MCs in IMC cases were positive for CK7, but none of them were positive for CK20, CK5, epidermal growth factor receptor, or c-Kit. CONCLUSIONS: Based on the frequent nodal metastases and association with higher stage found in IMC as compared with NIMC cases, as well as higher p53 positivity and lower frequency of estrogen receptor expression, MC could be considered an aggressive histologic type of breast carcinoma. In both MC and non-MC components in IMC cases, no basallike immunostaining pattern was detected.

Adult↗
PubMed2006

Immunohistochemical classification of de novo, transformed, and relapsed diffuse large B-cell lymphoma into germinal center B-cell and nongerminal center B-cell subtypes correlates with gene expression profile and patient survival.

CONTEXT: Diffuse large B-cell lymphoma (DLBCL) can be assigned to prognostic subgroups, including germinal center B-cell (GCB) and activated B-cell subgroups, by using gene expression profiling and, reportedly, immunohistochemistry for CD10, Bcl-6, and multiple myeloma-1/interferon regulatory factor-4 (MUM1/IRF4). OBJECTIVE: To compare 2 commercial MUM1/IRF4 antibody formulations for accuracy in subtyping DLBCL against gene expression profiling, compare subtyping to patient survival, and evaluate the usefulness of GCB and non-GCB subtyping in relapsed and transformed DLBCL. DESIGN: Evaluation of 2 commercial MUM1/IRF4 antibodies, ICSTAT/M17 and Mum-1p, by using 40 cases of de novo, relapsed, and transformed DLBCL; and comparison of the results obtained with gene expression profiling and survival. RESULTS: Immunohistochemistry predicted the gene expression profiling subtype 71.8% and 69.2% of the time overall with use of the Mum-1p and ICSTAT/M17 antibodies, respectively, and 100% and 91.7% of the time when MUM1/IRF4 expression determined subtype. Gene expression profiling and immunohistochemistry revealed nearly identical 5-year overall survival rates for the GCB vs non-GCB subtypes (68.0% for GCB vs 24.7% for non-GCB with use of gene expression profiling [P = .03] and 70.2% vs 18.4%, respectively, with use of immunohistochemistry [P < .001]). When de novo, transformed, and relapsed cases were analyzed separately, 5-year overall survival rates were also significantly different. CONCLUSIONS: Immunohistochemistry can be used to subclassify DLBCL, including a very small series of transformed and relapsed cases, into GCB and non-GCB subtypes and predict survival rates similar to those predicted by use of gene expression profiling. The 2 MUM1/IRF4 antibodies performed similarly.

B-Lymphocytes↗
PubMed2006

The CD117 immunohistochemistry tissue microarray survey for quality assurance and interlaboratory comparison: a College of American Pathologists Cell Markers Committee Study.

CONTEXT: We have developed tissue microarray-based surveys to allow laboratories to compare their performance in staining predictive immunohistochemical markers, including proto-oncogene CD117 (c-kit), which is characteristically expressed in gastrointestinal stromal tumors (GISTs). GISTs exhibit activating mutations in the c-kit proto-oncogene, which render them amenable to treatment with imatinib mesylate. Consequently, correct identification of c-Kit expression is important for the diagnosis and treatment of GISTs. OBJECTIVE: To analyze CD117 immunohistochemical staining performance by a large number of clinical laboratories. DESIGN: A mechanical device was used to construct tissue microarrays consisting of 3 x 1-mm cores of 10 tumor samples, which can be used to generate hundreds of tissue sections from the arrayed cases, suitable for large-scale interlaboratory comparison of immunohistochemical staining. RESULTS: An initial survey of 63 laboratories and a second survey of 90 laboratories, performed in 2004 and 2005, exhibited >81% concordance for 7 of 10 cores, including all 4 GIST cases, which were immunoreactive for CD117 with >95% staining concordance. Three of the cores achieved less than 81% concordance of results, possibly due to the presence of foci of necrosis in one core and CD117-positive mast cells in 2 cores of CD117-negative neoplasms. CONCLUSIONS: There was good performance among a large number of laboratories performing CD117 immunohistochemical staining, with consistently higher concordance of results for CD117-positive GIST cases than for nonimmunoreactive cases. Tissue microarrays for CD117 and other predictive markers should be useful for interlaboratory comparisons, quality assurance, and education of participants regarding staining nuances such as the expression of CKIT by nonneoplastic mast cells.

Biomarkers, Tumor↗
PubMed2006

Beta-catenin nuclear expression correlates with cyclin D1 expression in primary and metastatic synovial sarcoma: a tissue microarray study.

CONTEXT: The association between aberrant (nuclear) beta-catenin expression and cyclin D1 accumulation has been demonstrated in diverse neoplasms. In synovial sarcoma (SS), aberrant beta-catenin expression has prognostic relevance, but the association with cyclin D1 has not been established. The SYT-SSX fusion protein, unique to SS, may independently increase cyclin D1. OBJECTIVE: To determine whether nuclear beta-catenin is associated with cyclin D1 overexpression in SS and whether primary and metastatic SS differ in the expression of these markers. DESIGN: We incorporated 82 tumors initially diagnosed as SS into a tissue array. Fluorescence in situ hybridization with custom probes was used to select t(X;18) positive tumors. Clinical data, tumor type and outcome were tabulated. The tumors were tested for the association between nuclear beta-catenin and cyclin D1 immunostaining. Primary and metastatic tumors were compared. RESULTS: Fifty-one tumors (41 primary and 10 metastatic) from 43 patients demonstrated t(X;18). Cyclin D1 staining was identified in 21 (59%) primary and 8 (80%) metastatic tumors, respectively, and nuclear beta-catenin in 24 (41%) primary and 7 (70%) metastatic tumors, respectively. No significant difference was noted between primary and metastatic tumors with respect to the above markers. The presence of nuclear beta-catenin showed a significant association with cyclin D1 expression (P < .001). A small number of cyclin D1 cases were negative for nuclear beta-catenin but positive for phosphorylated Akt. CONCLUSIONS: Increased cyclin D1 in SS may be driven by abnormally expressed beta-catenin, similar to other neoplasms. The pattern of expression of these markers is established early during tumorigenesis.

Adolescent↗
PubMed2006

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Gene Expression Regulation, Neoplastic↗
PubMed2003

Gleevec (STI-571) inhibits lung cancer cell growth (A549) and potentiates the cisplatin effect in vitro.

BACKGROUND: Gleevec (aka STI571, Imatinib) is a recently FDA approved anti-tumor drug for chronic myelogenous leukemia. Gleevec binds specifically to BCR-ABL tyrosine kinase and inhibit the tyrosine kinase activity. It cross-reacts with another two important membrane tyrosine kinase receptors, c-kit and PDGF receptors. We sought to investigate if Gleevec has a potential role in treatment of non-small cell lung cancer. RESULTS: We have shown that Gleevec alone can inhibit the A549 lung cancer cell growth in dose-dependent manner, and the optimal concentration of Gleevec inhibition of A549 cell growth is at the range of 2-3 microM (IC50). We have also shown that A549 cells are resistant to cisplatin treatment (IC50 64 microM). Addition of Gleevec to the A549 cells treated with cisplatin resulted in a synergistic cell killing effect, suggesting that Gleevec can potentiate the effect of cisplatin on A549 cells. We also showed that the A549 lung cancer cells expresses the platelet derived growth factor receptor alpha, and the inhibitory effects of Gleevec on A549 cells is likely mediated through inhibition of PDGFR alpha phosphorylation. We further tested 33 lung cancer patients' tumor specimens to see the frequency of PDGFR-alpha expression by tissue micro-arrays and immunohistochemistry. We found that 16 of the 18 squamous carcinomas (89%), 11 of the 11 adenocarcinomas (100%), and 4 of the 4 small cell lung cancers (100%) expressed PDGFR-alpha. CONCLUSION: These results suggest a potential role of Gleevec as adjuvant therapeutic agent for treatment of non-small cell lung cancer.

Antineoplastic Agents↗
PubMed2005

[Correlation of clusterin expression to prognosis of bladder carcinoma].

BACKGROUND & OBJECTIVE: Clinically, molecular prognostic markers for bladder carcinoma are still rare. Recently, up-regulation of clusterin protein has been suggested to relate with development and prognosis of several human cancers, but its relation with bladder cancer is unclear. This study was to analyze correlation of expression of clusterin protein to clinicopathologic parameters and prognosis of bladder cancer with tissue chip. METHODS: A tissue microarray containing 81 cases of bladder carcinoma was constructed. The expression of clusterin was detected by immunohistochemistry; its correlation with clinicophathologic parameters was analyzed. RESULTS: Of the 81 cases of bladder cancer, 69 were detectable by immunohistochemistry, 32 (46.4%) of which showed overexpression of clusterin protein. Overexpression rate of clusterin was significantly higher in poorly differentiated (G3 grade) tumors than in well differentiated (G1-G2 grades) tumors (75.0% vs. 34.7%, P=0.002), and was significantly higher in invasive (T2-T4 stages) tumors than in superficial (Ta-T1 stages) tumors (65.4% vs. 34.9%, P=0.014). Expression of clusterin was negatively correlated with prognosis of bladder cancer patients (log-rank=5.88, P=0.015); the recurrence-free survival time of patients with overexpression of clusterin was shorter than that of patients with normal expression of clusterin (37.3 months vs. 48.8 months). CONCLUSION: The overexpression of clusterin might be a molecular prognostic marker of bladder cancer.

Adenocarcinoma↗
PubMed2005

[Expression of KAI1, MRP-1, and FAK proteins in lung cancer detected by high-density tissue microarray].

BACKGROUND & OBJECTIVE: The genesis, development, invasion, and metastasis of tumor are closely correlate with alterations of multi-genes. At present, the roles of Kang-ai-1 (KAI1), motility-related protein-1 (MRP-1), and focal adhesion kinase (FAK) in lung cancer have seldom been reported. This study was designed to investigate the roles of KAI1, MRP-1, and FAK in tumorigenesis and development of lung cancer, and their values in diagnosis and predicting the prognosis of lung cancer. METHODS: The expression of KAI1, MRP-1, and FAK proteins in a high-density tissue microarray containing 240 spots were detected by SP immunohistochemistry. RESULTS: The positive rates of KAI1 and MRP-1 were significantly lower in primary lung cancer than in normal lung tissue (25.9% vs. 100%, 42.6% vs. 100%, P<0.05). The positive rate of FAK was significantly higher in primary lung cancer than in normal lung tissue (44.4% vs. 10.0%, P<0.05). The expression of KAI1, FAK, and MRP-1 in primary lung cancer had no correlation with age and gender of the patients, and macroscopic and histological type of tumor, but had correlations with tumor differentiation, clinical stage, and lymph node metastasis. In addition, the expression of MRP-1 had correlation with histological type of tumor; the positive rate of MRP-1 was significantly lower in small cell lung cancer than in non-small cell lung cancer (0 vs. 50.0%, P<0.05). KAI1 expression was negatively correlated to FAK expression (rs=-0.458, P<0.05); MRP-1 expression was positively correlated with KAI1 expression (rs=0.535, P<0.05), and negatively correlated with FAK expression (rs=-0.438, P<0.05). CONCLUSIONS: The abnormal expression of KAI1, MRP-1, and FAK proteins are related to invasion and metastasis of lung cancer. Combined detection of the 3 proteins may be useful in predicting the development and prognosis of lung cancer.

Adult↗
PubMed2005

[Correlation of lymphangiogenesis to progression of colorectal cancer].

BACKGROUND & OBJECTIVE: Lymphatic metastasis affects the prognosis of colorectal cancer patients. The binding of vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor receptor-3 (VEGFR-3) promotes lymphangiogenesis and lymphatic metastasis. This study was to investigate the interrelation of VEGF-C, VEGFR-3 and lymphangial density (LAD), and to identify their correlations to clinicopathologic factors of colorectal cancer. METHODS: The tissue microarrays containing 105 cases of colorectal cancer and 105 cases of normal colorectal tissue were produced separately. The expression of VEGF-C and VEGFR-3 was detected by immunohistochemistry; LAD was assessed through Podoplanin immunohistochemical staining. RESULTS: The positive rates of VEGF-C and VEGFR-3, and LAD were significantly higher in colorectal cancer than in normal colorectal tissue (61.0% vs. 22.8%, P<0.01; 55.2% vs. 20.0%, P<0.01; 8.91+/-3.75 vs. 6.68+/-1.38, P<0.01). The expression of VEGF-C had no correlation to that of VEGFR-3. LAD was significantly higher in VEGF-C-positive colorectal cancer than in VEGF-C-negative colorectal cancer (10.89+/-3.36 vs. 5.83+/-1.67, P<0.01). VEGF-C was up-regulated in colorectal cancer at Dukes'C stage, or with lymph node metastasis or distant metastasis; VEGFR-3 was up-regulated and LAD was higher in colorectal cancer at Dukes'C stage, or with lymph node metastasis. CONCLUSION: VEGF-C and VEGFR-3 are related with the lymphangiogenesis, lymphatic metastasis, and progression of colorectal cancer.

Aged↗
PubMed2005

Expression and significance of Survivin mRNA in lung cancer tissue microarray detected by FISH.

OBJECTIVE: To investigate the expression of Survivin mRNA in lung cancer tissue microarray (TMA) by fluorescence in situ hybridization (FISH) method, and determine the role and significance of it in lung cancer genesis and progress. METHODS: The expression of Survivin mRNA was detected by FISH method and TMA technology. Fifty-four cases of lung cancer and 10 cases of normal lung tissue were examined. RESULTS: Survivin mRNA was expressed in 66.7% (36/54) of lung cancer; the positive ratio of lung cancer was significantly higher than that of normal lung tissue (0/10; chi2 = 15.238, P < 0.05). The positive ratio of Survivin mRNA was significantly higher in poor differentiated cancer (20/24, 83.3%) than moderate and well differentiated cancer (16/30, 53.3%; chi2 = 5.40, P < 0.05). The positive ratio of Survivin mRNA was significantly higher in group with lymph node metastasis (27/32, 84.4%) than without lymph node metastasis (9/22, 40.9%; chi2 = 11.084, P < 0.05). The positive ratio of Survivin mRNA was significantly higher in stage III-IV(12/13, 92.3%) than stage I - II (24/41, 58.5%; chi2 = 5.066, P < 0.05). CONCLUSION: Survivin mRNA highly expresses in lung cancer, which is related to the progress and malignant behavior. Survivin may play a promoting role in lung cancer genesis and progress and provide a basis for estimating prognosis and treatment.

Adenocarcinoma↗
PubMed2005

[Development of ZM-1 tissue microarrayer].

ZM-1 tissue microarrayer designed by our group is manufactured in stainless steel and brass. It features an easier and faster preparation for tissue microarrays. By means of it, a group of biopsy needles are used to punch the donor tissue specimens respectively, and all the needles with the punched specimen cylinders are arranged into the array-board, where small holes have been digged to fit the needles. All the specimen cylinders arraying and the tissue microarray block's shaping are finished simultaneously. ZM-1 tissue microarrayer with a lower cost of manufacture, is capable of preparing the tissue microarrays conveniently, efficiently and quality-controllably.

Equipment Design↗
PubMed2005

High hRFI expression correlates with resistance to fluoropyrimidines in human colon cancer cell lines and in xenografts.

We previously reported that the over-expression of hRFI, a protein preferentially expressed in the digestive tract regions of several cancers, exhibited a tendency to inhibit TNF-alpha induced apoptosis. In this study, we sought to determine the potential effect of hRFI expression on the sensitivity to 5-fluorouracil (5-FU) and/or other fluoropyrimidines. For the whole lysates of 8 colon cancer cell lines, we performed Western blotting with anti-hRFI antibody and analyzed the correlations between the expression level of hRFI and the cell lines' sensitivity to 5-FU induced apoptosis. Furthermore, for a tissue microarray consisting of 32 xenograft derived human cancer cell lines, we examined the expression levels of hRFI and survivin by immunohistochemical staining, and analyzed the correlations between the expression of each protein and the sensitivity to several chemotherapeutic agents in the xenografts examined. Both in colon cancer cell lines and in xenografts, the expression level of hRFI was correlated with resistance to 5-FU and its derivatives. This evidence suggests that hRFI may be a marker predicting the response to fluorouracil derived chemotherapeutic agents and that the reduction of the expression level of hRFI might improve the outcome of chemotherapy.

Carrier Proteins↗