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Thus, company astrazeneca amount of the selectin ligand sLea on three colon cancer cell lines correlated with their metastatic potential and blocking of sLea reduced metastasis formation (26). SLea and sLex expression showed a positive correlation with the metastatic risk in breast cancer patients and was an independent prognostic indicator of survival, regardless of the size of the primary tumour and lymph node involvement (27-30).

In our study, cells of all breast cancer cell lines expressed sLex, but a n e m i a considerable difference between the cell lines was detected. Expression of sLea was also very similar in breast cancer cells; MCF7 cells grown in vitro reacted weakly, T47D and HBL100 cells grown in vitro and a n e m i a tumours of all three cell lines did not react with with anti-sLea antibody. Thus, the analysis of selectin binding and ligand expression was not able to differentiate between metastatic breast cancer cells developing pulmonary metastases and non-metastatic breast cancer cells, when xenografted into SCID mice.

HPA and selectin histochemistry of the investigated cancer cells were different in staining intensity and staining pattern. A n e m i a results suggest that HPA and selectins did not bind to identical glycotopes. Although the importance of selectins for tumour cell adhesion and metastatic spread is beginning to be well established, a n e m i a of malignant cells to selectins in histochemistry and expression of selectin ligands is of limited predictive value for the metastatic potential of these cells in our xenograft model, also depending on the tumour entity.

The experiments performed here in xenograft models did not show a n e m i a correlation between binding of cells to AAA and E-selectin fusion protein. Furthermore, AAA-positivity of breast and colon cancer cells was not associated with their metastatic potential. In parallel no significant differences in reactivity for the lectin AAA were shown for normal and malignant colorectal tissues (31).

These results indicate that fucose residues, recognized by the AAA lectin, are at least not exclusively linked to glycoproteins specifically involved in processes of metastasis formation. In colon cancer cells, histochemistry with the lectins, selectins and selectin ligands showed generally stronger staining when cells were grown in vitro than in corresponding primary tumours. This observation confirms that the expression of carbohydrate structures on tumour cells grown in vitro and in vivo can vary as a result of transformational a n e m i a such as hypoxia, 3D growth and high cell density (33).

Thus, HPA- and selectin-binding of cancer cells, indicating the metastatic potential of these cells, can also be influenced by the environment of articles medicine cells (34). It is now established that the epithelial-mesenchymal transition (EMT) and the reverse process (MET) are central regulators of cellular plasticity in carcinomas and play an important role in cancer metastasis (35-37).

When epithelial tumour cells a n e m i a, they lose their contact with the neighbouring epithelial cells and basal lamina, and acquire a more mesenchymal character with migratory and invasive properties (35-37).

Cells grown in vitro and cells in the primary tumours grown in SCID mice might represent such different states of tumour cells undergoing EMT and MET, respectively, and hence differ in their carbohydrate residues. In summary, the carbohydrate residues of the breast and colon cancer cells recognised by HPA seem to be different to the glycotopes binding to the selectins.

Histochemical analysis of selectin fusion protein binding and agency for toxic substances and disease registry for selectins are of limited predictive value for the metastatic potential in our xenograft model, depending on the tumour entity. Thus, E-selectin binding, as well as CA19-9 and CD15s immunohistochemistry, arm differences in metastatic and non-metastatic colon cancer cells grown in vitro, while metastatic and non-metastatic breast cancer cells exhibited a n e m i a slight differences in P-selectin binding.

The different glycotope expressions, in particular of especially colon cancer cells gluconate potassium in vitro and in vivo indicate that selectin- and HPA-binding properties a n e m i a carcinoma cells are not static, but dynamic and might be related to the EMT and MET of cancer cells. Thereby, cancer cells grown in culture seem to reflect the mesenchymal and thus metastasizing phenotype, whereas xenografted cells in solid tumours rather possess epithelial characteristics.

View this table:View inlineView popupDownload powerpointTable I. Characterization of different cancer cell lines. Materials and Methods Cell culture. View this table:View inlineView popupDownload powerpointTable II. Acyclovir (Zovirax)- Multum In this study, the binding of different lectins and selectins, and expression of selectin ligands in metastasizing and non-metastasizing colon and breast cancer cell lines were examined by immunohistochemistry.

Discussion HPA binds primarily to GalNac residues and with a lower affinity to GlcNac residues. Histochem J 29: 677-684, 1997. OpenUrlCrossRefPubMedBrooks SA, Leathem AJ: Prediction of lymph node involvement in breast cancer by detection of altered glycosylation in the primary tumour. Lancet 338: 71-74, 1991. OpenUrlCrossRefPubMedBrooks SA, Lymboura M, Schumacher U, Leathem AJ: Histochemistry to detect Helix pomatia lectin binding in breast cancer: methodology makes a difference.

J Histochem Cytochem 44: 519-524, 1996. Cancer 74: 3104-3107, 1994. Cancer Lett 219: 233-242, 2005. OpenUrlCrossRefPubMedSchumacher U, Mitchell BS: Use of clinically relevant human-SCID-mouse models in metastasis research. Trends Biotechnol 15: 239-241, 1997. OpenUrlPubMedBrooks SA, Hall DM, Buley I: GalNAc glycoprotein expression by breast cell lines, primary breast cancer and normal breast epithelial membrane.

Br J Cancer 85: 1014-1022, 2001. Int J Cancer 95: 79-85, 2001. J Am Chem Soc 123: 10705-10714, 2001. OpenUrlCrossRefPubMedKonno A, Hoshino Y, Terashima S, Motoki R, Kawaguchi T: Carbohydrate expression profile of colorectal cancer cells is relevant to metastatic pattern and prognosis.

A n e m i a Exp Metastasis 19: 61-70, 2002. Br J Cancer 102: 602-609, 2010. OpenUrlCrossRefPubMedRemmele W, Stegner HE: Recommendation for uniform definition of an immunoreactive score (IRS) for immunohistochemical estrogen receptor detection (ER-ICA) in breast cancer tissue.

Pathologe 8: 138-140 (in German), 1987. OpenUrlPubMedLaidler P, Litynska A n e m i a Tumor cell N-glycans in metastasis. Acta Biochim Pol 44: 343-357, 1997. OpenUrlPubMedKonstantopoulos K, Thomas SN: Cancer cells in transit: the vascular interactions of tumor cells. Annu Rev Biomed Eng 11: 177-202, 2009.

OpenUrlCrossRefPubMedMannori G, Santoro D, Carter L, Corless C, Nelson RM, Bevilacqua MP: Inhibition of colon carcinoma cell lung colony formation by a soluble form of Glucotrol XL (Glipizide Extended Release)- Multum.

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