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| 1 | Proteolytic-antiproteolytic balance and its regulation in carcinogenesis显示文摘Cancer development is essentially a tissue remodeling process in which normal tissue is substituted with cancer tissue. A crucial role in this process is attributed toproteolytic degradation of the extracellular matrix (ECM).Degradation of ECM is initiated by proteases, secreted by different cell types, participating in tumor cell invasion and increased expression or activity of every known class of proteases (metallo-, serine-, aspartyl-, and cysteine)has been linked to malignancy and invasion of tumor cells.Proteolytic enzymes can act directly by degrading ECM or indirectly by activating other proteases, which then degrade the ECM. They act in a determined order, resulting from the order of their activation. When proteases exert their action on other proteases, the end result is a cascade leading to proteolysis. Presumable order of events in this complicated cascade is that aspartyl protease (cathepsin D) activates cysteine proteases (e.g. cathepsin B) that can activate pro-uPA. Then active uPA can convert plasminogen into plasmin. Cathepsin B as well as plasmin are capable of degrading several components of tumor stroma and may activate zymogens of matrix metalloproteinases, the main family of ECM degrading proteases. The activities of these proteases are regulated by a complex array of activators,inhibitors and cellular receptors. Tn physiological conditions the balance exists between proteases and their inhibitors.Proteolytic-antiproteolytic balance may be of major significance in the cancer development. One of the reasons for such a situation is enhanced generation of free radicals observed in many pathological states. Free radicals react with main cellular components like proteins and lipids and in this way modify proteolytic-antiproteolytic balance and enable penetration damaging cellular membrane. All these lead to enhancement of proteolysis and destruction of ECM proteins and in consequence to invasion and metastasis. | Elzbieta Skrzydlewska Mariola Sulkowska Mariusz Koda Stanislaw Sulkowski | 2005 | World Journal of Gastroenterology2005，11，9： | 14 |
| 2 | Lipid peroxidation and antioxidant status in colorectal cancer显示文摘AIM: Reactive oxygen species (ROS) can induce carcinogenesis via DNA injury. Both enzymatic and non-enzymatic parameters participate in cell protection against harmful influence of oxidative stress. The aim of the present study was to assess the levels of final lipid peroxidation products like malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE) in primary colorectal cancer. Moreover, we analysed the activity of main antioxidative enzymes, superoxide dismutase (Cu, Zn-SOD),catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GSSRG-R) and the level of nonenzymatic antioxidants (glutathione, vitamins C and E).METHODS: Investigations were conducted in 81 primary colorectal cancers. As a control, the same amount of sample was collected from macroscopically unchanged colon regions of the most distant location to the cancer.Homogenisation of specimens provided 10% homogenates for our evaluations. Activity of antioxidant enzymes and level of glutathione were determined by spectrophotometry.HPLC revealed levels of vitamins C and E and served as a method to detect terminal products of lipid peroxidation in colorectal cancer.RESULTS: Our studies demonstrated a statistically significant increase in the level of lipid peroxidation products (MDA-Adc.muc.-2.65±0.48 nmol/g, Adc. G3-2.15±0.44 nmol/g, clinical Ⅳ stage 4.04±0.47 nmol/g, P<0.001 and 4-HNE-Adc.muc.-0.44±0.07 nmol/g, Adc. G3-0.44±0.10 nmol/g, clinical Ⅳstage 0.52±0.11 nmol/g, P<0.001) as well as increase of Cu,Zn-SOD (Adc.muc.-363±72 U/g, Adc. G3-318±48 U/g,clinical Ⅳ stage 421±58 U/g, P<0.001), GSH-Px (Adc.muc.-2143±623 U/g, Adc. G3-2005±591 U/g, clinical Ⅳ stage 2467±368 U/g, P<0.001) and GSSG-R (Adc. muc.-880±194 U/g,Adc. G3-795±228 U/g, dinical Ⅳ stage 951±243 U/g, P<0.001)in primary tumour comparison with normal colon (MDA1.39±0.15 nmol/g, HNE-0.29±0.03 nmol/g, Cu, Zn-SOD-117±25 U/g, GSH-Px-1723±189 U/g, GSSG-R-625±112 U/g)especially in mucinous and G3-grade adenocarcinomas as well as clinical Ⅳ stage of colorectal cancer. We also observed a decrease of CAT activity (Adc.muc. -40±14 U/g,clinical Ⅳ stage 33±18 U/g vs84±17 U/g, P<0.001) as well as a decreased level of reduced glutathione (clinical Ⅳ stage 150±48 nmol/g vs 167±15 nmol/g, P<0.05) and vitamins C and E (vit. C-clinical Ⅳ stage 325±92 nmol/g vs 513±64 nmol/g, P<0.001; vit. E-clinical Ⅳ stage 13.3±10.3nmol/g vs37.5±5.2 nmol/g).CONCLUSION: Colorectal carcinogenesis is associated with serious oxidative stress and confirms that gradual advancement of oxidative-antioxidative disorders is followed by progression of colorectal cancer. | Elzbieta Skrzydlewska Stanislaw Sulkowski Mariusz Koda Bogdan Zalewski Luiza Kanczuga-Koda Mariola Sulkowska | 2005 | World Journal of Gastroenterology2005，11，3： | 12 |
| 3 | Interleukin-28B Polymorphism Improves Viral Kinetics and Is the Strongest Pretreatment Predictor of Sustained Virologic Response in Genotype 1 Hepatitis C Virus显示文摘 | Alexander J. Thompson Andrew J. Muir Mark S. Sulkowski Dongliang Ge Jacques Fellay Kevin V. Shianna Thomas Urban Nezam H. Afdhal Ira M. Jacobson Rafael Esteban Fred Poordad Eric J. Lawitz Jonathan McCone Mitchell L. Shiffman Greg W. Galler William M. Lee | 2010 | Gastroenterology2010，，1： | 7 |
| 4 | Evaluation of serum catnepsin B and D in relation to diniGopatnological staging of colorectal cancer显示文摘AIM: Proteolytic degradation of the extracellular matrix facilitates cancer invasion and promotes metastasis. The study aims at evaluation of preoperative and postoperative serum cathepsins B and D levels in correlation with selected anatomoclinical features of colorectal cancer.METHODS: Blood samples were collected from 63colorectal cancer patients before curative operation of the tumor 10 d later. Blood that was obtained from 20healthy volunteers, served as a control. The activity of cathepsin B was measured with Bz-DL-arginine-pNA as a substrate at pH 6.0, while cathepsin D activity was determined with urea-denatured hemoglobin (pH 4.0).RESULTS: The preoperative and postoperative activities of cathepsin B were significantly (P<0.00001) lower in serum of colorectal cancer patients than in control group.However, postoperative values of this protease were significantly increased in comparison with preoperative ones (P = 0.031). Activity of cathepsin D appeared to be significantly higher in colorectal cancer sera (P<0.00001)compared with controls. No statistically significant differences between preoperative and postoperative activity of cathepsin D were noted (P = 0.09). We revealed a strong linkage of cathepsins' levels with lymph node status and pT stage of colorectal cancer.CONCLUSION: Blood serum activities of cathepsin B and D depend on the time of sampling, tumor size and lymph node involvement. Significantly, increased activity of cathepsin D could indicate a malignant condition of the large intestine. In our work, the serum postoperative decrease of cathepsin B activity appears as an obvious concomitant of local lymph node metastasis-the wellknown clinicopathological feature of poor prognosis. | Elzbieta Skrzydlewska Mariola Sulkowska Andrzej Wincewicz Mariusz Koda Stanislaw Sulkowski | 2005 | World Journal of Gastroenterology2005，11，27： | 6 |
| 5 | Connexin 26 correlates with Bcl-xL and Bax proteins expression in colorectal cancer显示文摘AIM: To evaluate of Cx26 in correlation with Bcl-xL and Bax proteins in colorectal cancer.METHODS: Immunohistochemical staining using specific antibodies was performed to evaluate the protein expression of Cx26, Bax and Bcl-xL in 152 colorectal cancer samples and the correlations among studied proteins as well as the relationships between the expression of Cx26,Bax, Bcl-xL and clinicopathological features were analyzed.RESULTS: Both normal epithelial cells and carcinoma cells expressed Cx26, Bax and Bcl-xL, but Cx26 in cancer cells showed aberrant, mainly cytoplasmic staining. Expression of Cx26, Bax and Bcl-xL was observed in 55.9%, 55.5%and 72.4% of evaluated colorectal cancers respectively.We found the positive correlation between Cx26 and Bax expression (r = 0.561, P<0.0001), Cx26 and Bcl-xL (r = 0.409, P<0.0001) as well as between Bax and Bcl-xL (r = 0.486, P<0.0001). Association of Cx26, Bax and Bcl-xL expression with histological G2 grade of tumors was noted (P<0.005, P<0.001 and P<0.002 respectively).CONCLUSION: Cytoplasmic presence of Cx26 and its association with apoptotic markers could indicate a distinct role from physiological functions of Cx26 in cancer cells and it could suggest that connexins might be a target point for modulations of apoptosis with therapeutic implications. | Luiza Kanczuga-Koda Stanislaw Sulkowski Mariusz Koda Elzbieta Skrzydlewska Mariola Sulkowska | 2005 | World Journal of Gastroenterology2005，11，10： | 5 |
| 6 | Factors That Predict Response of Patients With Hepatitis C Virus Infection to Boceprevir显示文摘 | Fred Poordad Jean–Pierre Bronowicki Stuart C. Gordon Stefan Zeuzem Ira M. Jacobson Mark S. Sulkowski Thierry Poynard Timothy R. Morgan Cliona Molony Lisa D. Pedicone Heather L. Sings Margaret H. Burroughs Vilma Sniukiene Navdeep Boparai Venkata S. Goteti | 2012 | Gastroenterology2012，，3： | 5 |
| 7 | Factors That Predict Response of Patients With Hepatitis C Virus Infection to Boceprevir显示文摘 | Fred Poordad Jean–Pierre Bronowicki Stuart C. Gordon Stefan Zeuzem Ira M. Jacobson Mark S. Sulkowski Thierry Poynard Timothy R. Morgan Cliona Molony Lisa D. Pedicone Heather L. Sings Margaret H. Burroughs Vilma Sniukiene Navdeep Boparai Venkata S. Goteti | 2012 | Gastroenterology2012，，3： | 2 |
| 8 | The new paradigm of hepatitis C therapy: integration of oral therapies into best practices显示文摘 | N. H. Afdhal S. Zeuzem R. T. Schooley D. L. Thomas J. W. Ward A. H. Litwin H. Razavi L. Castera T. Poynard A. Muir S. H. Mehta L. Dee C. Graham D. R. Church A. H. Talal M. S. Sulkowski I. M. Jacobson | 2013 | J Viral Hepat2013，，11： | 2 |
| 9 | Increased expression of connexins 26 and 43 in lymph node metastases of breast cancer显示文摘 | Kanczuga-Koda L Sulkowski S Lenczewski A | 2006 | J Clin Pathol2006，59，4： | 1 |
| 10 | Hepatitis C virus infection as an opportunistic disease in persons infected with human immunodeficiency显示文摘 | Sulkowski MS Mast EE Seeff LB | 2000 | Virus Clin Infect Dis2000，30，： | 1 |
| 11 | Prevalence of type 2 diabetes mellitus among persons with hepatitis C virus infection in the United States显示文摘 | Mehts SH Brancati FL Sulkowski MS | 2000 | Ann Intem Med2000，133，8： | 1 |
| 12 | Daclatasvir plus sofosbuvir for previously treated or untreated chronic HCV infection显示文摘 | Sulkowski MS Gardiner DF Rodriguez-Torres M | 2014 | N Engl J Med2014，370，3： | 1 |
| 13 | Viral hepatitis and HIV eoinfection 显示文摘 | Sulkowski MS | 2008 | J Helm- tol2008，48，2： | 1 |
| 14 | Management of adverse effects of Peg - IFN and ribavirin therapy for hepatitis C显示文摘 | Sulkowski M S Cooper C Hunyady B | 2011 | Nat Rev Gastroenterol Hepatol2011，8，4： | 1 |
| 15 | Needlestick transmission of hepatitis C 显示文摘 | Sulkowski MS Ray SC Thomas DL | 2002 | JAMA2002，287，18： | 1 |
| 16 | Ethanol-induced neurotoxicity is counterbalanced by increased cell proliferation in mouse dentate gyrus显示文摘 | Pawlak R Skrzypiec A Sulkowski S | 2002 | Neurosci Lett2002，327，： | 1 |
| 17 | Treatment algorithm for the management of hepatitis C in HIV-coinfected persons显示文摘 | Sulkowski MS | 2006 | J Hepatol2006，44，1： | 1 |
| 18 | Hepatitis C in the HIV-infectedperson 显示文摘 | Sulkowski MS Thomas LD | 2003 | Ann Intern Med2003，138，3： | 1 |
| 19 | Characterization of receptors for murine pregnancy specific glycoproteins 17 and 23显示文摘 | Sulkowski GN Warren J Ha CT | | 0，，08： | 1 |
| 20 | Morbidity and mortal- ity in patients with esophageal atresia 显示文摘 | Sulkowski JP Cooper JN Lopez JJ | 2014 | Surgery2014，156，8： | 1 |
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