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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 | 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 |
| 4 | 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 |
| 5 | Evaluation of apoptosis markers in conjunctival and eyelid benign and malignant tumors显示文摘 | Reszec J Sulkowska M Kanczuga-koda L | 2003 | Ann N Y Acad Sci2003，1010，10： | 1 |
| 6 | Expression of leptin, leptin receptor, and hypoxia-inducible factor 1 alpha in human endometrial cancer 显示文摘 | Koda M Sulkowska M Wincewicz A | 2007 | Ann N Y Acad Sci2007，1095，： | 1 |
| 7 | P53 correlates positively with VEGF in preoperative sera of colorectal cancer patients显示文摘 | Famulski W Sulkowska M Wincewicz A | 2006 | Neoplasma2006，53，1： | 1 |
| 8 | Role of endothelins in lung pathology 显示文摘 | Sulkowska M | 1997 | Roci-Akad-Med-Bialymst1997，42，1： | 1 |
| 9 | Tumor necrosis factor-ainduces em physema like pulmonary tissue rebuilding: changs in type II alveolar epithelial cell显示文摘 | Sulkowska M Sulkowski S Terlikowshi S | 1997 | Pol J Pathal1997，48，3： | 1 |
| 10 | Competitive binding of phenylbutazone and colchicine to serum albumin in multidrug therapy显示文摘 | SULKOWSKA A MACIAZEK-JURCZYK M BOJKO B | 2008 | J Mol Struct2008，881，13： | 1 |
| 11 | Interaction of anticancer drugs with human and bovine serum albumin 显示文摘 | Sulkowska A Rownicka J Sulkowski W | 2003 | Journal of Molecular Structure2003，，： | 1 |
| 12 | Gap junction intercellular communication and carcinogenesis 显示文摘 | sulkowski S Sulkowska M Skrzydlewska E | 1999 | Pol J Pathol1999，，4： | 1 |
| 13 | Analysis of the relationship between cancer procoagulant activity and PCNA and Ki 67 expression in cases of common and cellular uterine leiomyomas显示文摘 | Szajda SD Jówik M Sulkowska M | 2006 | Eur J Gynaecol Oncol2006，27，5： | 1 |
| 14 | Competitive binding of phenylbutazone and colchicine to serum albumin in multidrng therapy 显示文摘 | Sulkowska A Maciazek - Jurczyk M Bojko B | 2008 | Journal of Molecular Structure2008，881，13： | 1 |
| 15 | Evaluation of apoptosis markers in conjunctival and eyelid benign and malignant tumors显示文摘 | Reszec J Sulkowska M Kanczuga-Koda L | 2003 | Ann N Y Acad Sci2003，1010，： | 1 |
| 16 | Clinicopathological significance and linkage of the distribution of HIF - 1 alpha and GLUT - 1 in human primary colorectal cancer显示文摘 | WINCEWICZ A SULKOWSKA M KODA M | 2007 | Pathol Oncol Res2007，13，1： | 1 |
| 17 | Tumor necrosis factor-αinduces emphyse ma-like pulmonary tissue rebuilding:changes in type Ⅱ alveolar epithelial cell显示文摘 | Sulkowska M Sulkowski S Terlikowshi S | 1997 | Pol J Pathal1997，48，： | 1 |
| 18 | P53 correlates positively with VEGF in preoperative sera of colorectal cancer patients显示文摘 | Famulski W Sulkowska M Wincewicz A | 2006 | Neoplasma2006，53，1： | 1 |
| 19 | Competitive binding of phenylbutazone and colchicine to serum albumin in muhidrug therapy显示文摘 | Sulkowska A Maciazek-Jurczyk M Bojko B | 2008 | J Mol Struct2008，881，13： | 1 |
| 20 | Synthesis and spectroscopic studies of cyclo- and polyphosphazenes显示文摘 | W Sulkowski A Sulkowska B Makarucha | 2000 | Euro Polym J2000，36，： | 1 |
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