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Ll patients were wild type in exon 12, and 10 out of 17 had the silent mutation C T in codon 824 GTCGTT, ValVal [rs10015469]. 2 samples of Dihexa biological activity non-neoplastic cervical tissue presented the intronic variation CA IVS12+22 [rs2307051] and all 3 presented the silent mutation in codon 824 [rs10015469]. In this table we show the results of only one lymphocytes donor, but all 8 donors were wild type for exon 12, and 3 out of 8 presented the polymorphism at codon 824.Page 5 of(page number not for citation purposes)Cancer Cell International 2006, 6:http://www.cancerci.com/content/6/1/aviability160 140 120 100 80 60 40 20 0 control PDGFBB Imatinib Imatinib + PDGFBB*^*^bp-PDGFR ActinControlPDGFBBImatinibImatinib + PDGFBBFigure of a) Effect3 imatinib in cervical cell line growth a) Effect of imatinib in cervical cell line growth.


CaLo cells were grown for two days in the absence of serum and then re-plated for treatment with imatinib, PDGF or both for five days. PDGFBB stimulated cell gowth as compared to the untreated control. On the contrary imatinib induced growth inhibition and when cells were co-treated with the ligand and imatinib, the growth-inducing activity of the PDGFBB was partly blocked by imatinib (comparison are marked with * or ^, all these differences were statistically significant p 0.001). Their corresponding pictures of the plates stained with crystal violet is shown below. b) Inhibition of phosphorylation of PDGFR by imatinib. CaLo cells were stimulated with PDGFBB at 10 ng/mL, for 10 min; treated with imatinib at 10 M for 2 hours; treated with imatinib for two hours and then with PDGFBB for 15 min; or no treatment as control. Equal loading confirmed with actin. Receptor phosphorylation is increased in the PDGFBB lane and inhibited by imatinib treatment.Page 6 of(page number not for citation purposes)Cancer Cell International 2006, 6:http://www.cancerci.com/content/6/1/has led to investigate the participation of these two receptors in several solid malignancies, particularly in small cell lung cancer and prostate carcinoma which over-express the c-kit receptor. However, early results using imatinib as a single agent have not been encouraging [35-37] which suggests that the sole presence of the putative target may not be sufficient to achieve tumor responses, besides, it is necessary to demonstrate that the pathway is functional and of relevance for one or more characteristics of the malignant phenotype in the tumor to be targeted. So far, the role of the PDGFR pathway for the development of cervical cancer has been only studied in in vitro models, derived from the observation of the interaction between the E5 papilloma virus protein with the PDGFR [19,20]. There is a single study showing that the four primary cervical cancers analyzed by immunohistochemistry expressed the PDGFR [22]. In several tumors, where the participation of PDGF family has been demonstrated, a simultaneous expression of the receptors and the ligands seems to be important, suggesting an autocrine stimulation mechanism [38]. In the present study we evaluated a larger sample of primary tumors for the expression of the ligands and receptors of PDGF at both the malignant and stroma components of the biopsy. The expression of these growth factor family PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27597769 members in stroma is important as they are regulators of mesenchymal cell proliferation and migration during development, and therefore could play important roles in stromal fibroblast recruitment and tumor progre.